Diseases of the arteries, including angina pectoris

DEPARTMENT OF

BACTERIOLOGY AND IMMUNOLOGY

SCHOOL OF MEDICINE

UNIVERSITY OF PITTSBURGH

200 PENNSYLVANIA HALL

DO NOT CIRCUiATf

DEPARTMENT OF

BACTERIOLOGY AND IMMUNOLOGY

SCHOOL OF MEDICINE

UNIVERSITY OF PITTSBURGH

200 PENNSYLVANIA HALL

DISEASES OF THE ARTERIES

INCLUDING

ANGINA PECTORIS

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DISEASES OF THE
ARTERIES

INCLUDING

ANGINA PECTORIS

BY

Sir CLIFFORD ALLBUTT, K.C.B.

M.A., M.D., F.R.C.P., F.R.S., Hon. M.D., LL.D., D.Sc, Etc.

REGIUS PROFESSOR OF PHYSIC IN THE UNIVERSITY OF CAMBRIDGE
FELLOW OF GONVILLE AND CAIUS COLLEGE
HON. FELLOW NEW YORK ACAD. MED., ETC.

IN TWO VOLUMES
VOL. II

MACMILLAN AND CO., LIMITED

ST. MARTIN'S STREET, LONDON

1915

COPYRIGHT

CONTENTS

PAET I
ARTERIOSCLEROSIS

CHAPTER VIII

PAGE

Cardiosclerosis and Myocardial Values . . .1

CHAPTER IX

Diagnosis and Prognosis of Arteriosclerosis . . 59

CHAPTER X

Treatment of Arterial Disease . . . .80

PART II

SECTION I

Aortitis ....... 143

SECTION II.— ANGINA PECTORIS

CHAPTER I

Introductory . . . . . . .211

CHAPTER II

Simulations of Angina Pectoris . . . .221

■^A>\-a:

CONTENTS

CHAPTEK III

Tobacco Angina

PAGE

. 244

CHAPTER IV

Causes op Angina Pectoris .

249

CHAPTER V

Symptoms

. 279

CHAPTER VI

Hypotheses of Angina

. 350

Diagnosis

CHAPTER VII

. 491

Prognosis

CHAPTER VIII

. 511

Treatment

CHAPTER IX

. 521

INDEX

. 541

CHAPTER VIII

CARDIOSCLEROSIS AND MYOCARDIAL VALUES1

" Cardiosclerosis." — In all my papers, from the time that
I began to write on these subjects, I have urged that in arterio-
sclerosis closer and more discriminating attention should be given
to the conditions of the heart, and that our common phrases —
for instance, that of " cardiosclerosis," or in still finer language
" Myodegeneratio cardiosclerotica " — should be more considered.
By the indiscriminate use of this term, the heart is brought into
common condemnation with sclerosed vessels, a view which is
only partially justifiable.

Huchard1 s Views. — We are in a position to consider the
opinions of the late M. Huchard on this matter in their final
form as, by request, he presented them finally in 1908 and 1909 ;
in 1908 at the International Congress at Buda-Pest, in 1909
as " specially reported " by himself to a representative of the
Medical Press.2 On both occasions Huchard began by reiterating
his postulate, that all arteriosclerosis, whether regarded as an
anatomical lesion or as a clinical series, is one disease, a malady
attacking heart, arteries, and kidneys as a whole ; the affection
of the heart being homologous with that of the arteries. In his
view the heart goes down, not as vanquished in a strife against
odds, but in a co-ordinated retrogression. The mere senile heart
he explicitly withdrew from the category of arteriosclerosis. The
whole malady of arteriosclerosis originates, so he declared, in
certain intestinal toxins, pressor in action, which escape neutralisa-

1 " Myocardial Values," the substance of an address to the Chelsea Clinical
Society on March 12, 1912, under the title of " The Physician and the Patholo-
gist on Heart Failure," published in the medical journals near that date.

2 Medical Press, March 1909.

1

2 :< CARDIOSCLEROSIS " part i

tion by the liver. The distinguished author went on to present
a paradigm of the malady as a single and comprehensive morbid
series, as follows : —

" First stage : ' Presclerosis, due to renal causes ' — a ' cardio-
renal ' state with excessive pressures ' almost invariably.' The
heart is affected by toxins from the very beginning ; the cardio-
sclerosis, whatsoever its degree, dates from the initiation of the
first stage, advances pari passu with the affection of the arteries,
and is due directly to the intoxication."

" Second stage : Established myovalvular cardiosclerosis,
together with the same depravation of the arteries, and both
originating alike and together from the toxins."

" Third stage : The ' Mitro-arterial ' (when mitral incom-
petency sets in)."

" Fourth stage : That of ' Cardio-ectasis,' a stage which may
or may not be reached. Cerebral haemorrhage, or other incident,
may cut the life short. Cerebral hemorrhage however, the
alleged consequence of arteriosclerosis, occurs only in cases of
chronic interstitial nephritis " (I).1

Auto-intoxication, cardiosclerosis, arteriosclerosis ! " Three
words, Don Jorge ! and what may not be made out of three
words ? You have lived among us to little purpose if you think
we require more than three words to build a system with." But
let us seek into the grounds of this fair -seeming edifice which
seems at best to be speculative, and even at this to be in-
consistent and equivocal. When it was urged that if many
cases of arteriosclerosis are attended with high pressures, yet a
large number persist from first to last with pressures little, if at
all, above the ordinary, Huchard minimised the low-pressure
cases as much as possible, retaining them in the same category
but as transient phases, phases to be explained by cardiac
reduction, or degrees of portal congestion with intermittence of
that function of the liver which should neutralise intestinal
toxins ; as in another place 2 he put it " toxins primarily of
intestinal origin and associated with portal congestion." The

1 These pages were written during Huchard' s lifetime ; I desire now to
qualify my criticisms by a tribute of great respect for the memory of a
distinguished colleague, and of an earnest and devoted clinical physician.

2 Lancet, Sept. 4, 1909, p. 720.

chap, viii THE HEART IN HYPERPIESIA 3

interviewer seems to have demurred, as regards the first or
" presclerotic " stage, that there is often no evidence of renal
or hepatic affection, perhaps much to the contrary ; Huchard
then took refuge in a vague summary of " renal causes mixed
with abdominal toxins, and dietetic errors."

This is " Schematismus " indeed ! The difficulties are (a)
that in some 50 per cent of cases of arteriosclerosis exorbitant
pressures are never manifested from first to last ; many of them
indeed being not inconsistent with fair or even good health up
to advanced years ; (6) that if we accept such a term as " cardio-
sclerosis," this should include the coronary and myocardial
scleroses which occur no less in these low-pressure cases; (c) that
in high-pressure cases — and these are they, be it remembered,
which for Huchard made the main category of arteriosclerosis
in the first stage of which the heart with its vessels should
begin simultaneously to undergo degradation — the heart, instead
of yielding, when pressures might fall, is so charged with
intrinsic energy as to multiply its work, for a time out of its
normal and intact reserves, and afterwards by the abundant
hypertrophy which it still has at command ; a development
which may reach enormous dimensions, a robust capacity by
which it succeeds for some years in concealing even from the
patient all consciousness of the mischief on foot ; (d) that only
at length does this heart suffer defeat and begin to yield,
with the usual consequences of this discomfiture, involving
often of course the familiar forcing of the mitral valve ; (e) that
although in renal disease cerebral haemorrhage is frequent, yet
it is frequent also in high-pressure cases (hyperpiesia) in which
by ordinary clinical or pathological methods no renal disease
may be detected ; (/) that indeed it is rather in the low-
pressure kind that the general withering with interstitial
substitution all over the body takes place, as it does in
the kidney ; (g) that, as a matter of clinical and pathological
experience, in the high-pressure cases, including those of renal
disease, the heart's muscle, save for consequential strains,
largely retains the characters and resources of health, while not
infrequently its coronary arteries are practically efficient.

Now, do not these differences suffice to prove that the con-
ceptions which by Huchard's eloquence have held the field so long

4 " CAKDIOSCLEROSIS " part i

must be reconsidered and recast ? What are we to think of this
sentence, recently from the pen of a leading physician writing
specially on heart diseases ? — " Arteriosclerosis and atheroma
may cause fatty and fibrous degeneration of the cardiac walls
by obstruction of the coronary arteries, and at the same time
a general rise of the arterial pressure is common in this com-
plaint " (italics mine). If we have any use at all for the term
cardiosclerosis, it should signify rather the so-called " senile "
(decrescent) involution, coronary obliteration, and myocardial
fibrosis and decay, than the accumulation of stresses against
which, in chronic renal disease or in hyperpiesia, the cardio-
arterial system, the heart especially, makes a long and vigorous
and not inglorious resistance. From his carefully tabulated
experience Schabert x says of 15 cases of arteriosclerosis
without high pressures (" ohne Hypertension " ; he admits
my distinction) he found some cardiosclerosis in 12. " Cardio-
sclerosis " then is an omnibus word ; it may mean the
cardiofibrosis of Dehio, it may mean coronary atheroma, it
may mean valvular induration, and so forth ; changes which
are several, and have no regular correlations.

If the reader accepts my original separation of arteriosclerosis
mainly into the hyperpietic and the decrescent (or involutionary)
forms, he will perceive that throughout these two classes the
behaviour and conditions of the heart are widely different. In
Hyperpiesia, as we may see again and again, the heart is for
a long time little the worse ; it has more work to do, but for
a while it meets this demand without even a static dilatation
or great hypertrophy. For many weeks at least, in compara-
tively young persons, perhaps for some months or a year, I
cannot tell, the heart may meet a pressure of 180-200 without
demonstrable overgrowth. A normal left ventricle can continue
to expel its contents against a double aortic pressure, as may
be shown by the constancy of the diastolic pressure and of the
pulmonary arterial pressure.2 In trained men the heart learns
to meet large, though temporary, fluctuations of output.
Under regular exercise it learns quickly to modify its own

1 Schabert, Peter sb. med. WocJienschr., No. 4, 1911 ; quoted Deutsche med.
Wochenschr., March 2, 1911.

2 Leonard Hill, private letter January 2, 1908, with reference to Schafer's
Physiology, vol. ii. p. 151, fig. 91. So also Roy and others.

ch. viii HEART IN DECRESCENT SCLEROSIS 5

tone, and to throw out larger quantities, even against the
rising pressures of the outset of exertion, before peripheral
dilatation takes place ; all which degrees of filling it must do in
approximately equal times. This competence one observes in
the cases, which we see again and again, of high pressures in
renal disease of unknown, but not very long, duration without
appreciable cardiac hypertrophy ; though, on the other hand,
it is true that in urgent renal disease the left ventricle
is capable of considerable hypertrophy in a few weeks. A
comparatively young heart however, under a correspondingly
high-pressure coronary circulation, seems by its reserves to be
able for a while to keep up the balance without obvious statical
increase ; so that if the resistance be reduced, things may and
do fall back into their normal relations. The same is true also
of moderate degrees even of static hypertrophy, if of no very long
standing, of standing not sufficient to have strained the vessels
and established in these structures a new set. We see such
hearts come back within their normal limits, and the disorder
clear up ; prone as it may be, if not prevented, to return.
If this strain has taken place, if under excessive and persistent
arterial pressures irremediable alteration of both heart and
arteries has become established, and restoration to the normal
hopeless, if indeed dilatation of the heart under the irresistible
pressures is now ominous of defeat, and the patient is falling
into the abyss of " heart failure," even then the heart may die
— so to speak — sword in hand, die bravely and valiantly before
superior forces, without intrinsic infirmity. The myocardium in
such a case will probably show some fibrosis, and the coronary
arteries the effects of strain ; but the heart is one which has
succumbed hale and fighting ; and in subjects under 50 years of
age with permeable coronaries the myocardium often proves to
be practically sound. Dr. Janeway has aptly pointed out that
in these hearts auricular fibrillation is rare.1 Moreover in
high-pressure experiments on animals these enlarged hearts con-
sume a proportionate increase of oxygen ; whereas the chemistry
of a degenerate heart is degraded, it contains traces of lactic
acid and aldehyd, and considerable quantities of amino-acids
(Rohde, Ogawa and others).

1 Janeway, Arch. Inst. Med., Dec. 1913.

6 " CARDIOSCLEROSIS " part i

But in the decrescent form of arteriosclerosis the story is
otherwise ; in this series of changes the heart may indeed be
involved in a common fate with its vascular extensions. More
or less, as accidents may fall out, if it is suffering it is not
from overwork, for in these cases the arterial pressures are not
excessive, but from a more or less progressive and insidious
intrinsic decay. If, enfeebled by degeneration, loss of elasticity,
stiffness and tortuosity, and the formation of vortices or
otherwise, the arteries offer more frictional resistance, this
hindrance does not attain to large proportions ; the pressures
rise a little, and velocity falls a little ; the heart may perhaps
undergo some slight increase in volume, but the whole
arterial system is put under no extraordinary strain. What
happens is that the individual does less work ; and thus,
under economical conditions, he may live long enough, if less
effectually. Not infrequently, in a slow case, as life advances,
and the quality of the arteries becomes gradually a little worse,
the heart does not deteriorate pari passu with the vessels, but
takes upon itself a little more work, and does it quietly.
Thus by a gradual readjustment of conditions a moderate
accumulation of stresses is supportable, and life goes on fairly
well. Let us not then be too ready, even in old people, to talk
thoughtlessly of " cardiosclerosis " as a part of arteriosclerosis.

Morbid Anatomy of the Heart in Arteriosclerosis. — In discuss-
ing the arteries in this context we saw that it was not always easy
to discriminate differences of cause, if any, by their anatomical
changes. In respect of the heart however some such discrimina-
tion is more practicable. I have said that the heart in the series
I have called Hyperpiesia differs from the heart in the course
of that kind of arteriosclerosis which I have indicated by the
name of Decrescent. As in all fields of pathology, transition
cases occur to blur or to complicate the description, but here
not to any very confusing degrees.

How comes it then that in discussions of Arteriosclerosis we
are so familiar with the name " Cardiosclerosis," a sound too
often taken for sense ? Why, because it is one of those com-
fortable words which dispense with thought. I have tried to
extract, especially from our brilliant French colleagues, some
pathological definition, or at least some notion of its meaning as

ch. vin ANATOMY OF HEART IN SCLEROSIS 7

a name, but in vain. At length however, in an essay by a
leading physician of the French school, I lighted upon a defini-
tion ; it ran thus : " Cardiosclerosis signifies all those particular
states of the myocardium which lead to cardiac insufficiency —
say in Bright's disease, in diffuse arteriosclerosis, or in states of
high tension ; in a word, all final stages of the ' cardiopathies
arterielles ' of Huchard." That is to say, the name is as desti-
tute of precise meaning as I had been led by the indiscriminate
use of it to suppose. To offer us in exchange for it Huchard's
" cardiopathies arterielles " is to palm off on us one token for
another, neither of which has any intrinsic value. Huchard
and his disciples reiterated again and again that high tension,
cardiosclerosis, and arteriosclerosis were features of one uniform
and consistent process.

But from the facts we have learned, not that arteriosclerosis
is a " disease," or clinical series, involving heart and arteries
in a fairly uniform process, in a common decay ; nor again that
it is a cause of "high tension" bringing with it, more or less in-
evitably, strain and destruction of the cardioarterial machine ; they
tell us that we are dealing with, and confounding together, two
different processes, the one a process of mechanical strain with
consecutive lesion and destruction, the other a process degenera-
tive from its beginning, whether rooted in some original defect in
these parts, implied in prolonged wear and tear, or engendered by
some poison or crooked chemistry of the body. From a patho-
logical standpoint however there is something more to be said.

I have argued that in the arteriosclerosis of "high tension" —
my Hyperpiesia — the heart primarily is, and throughout the
readaptive stages of the malady continues to be, healthy.
Hypertrophied it is, but so long as by natural growth the
extraordinary work is done, hypertrophy is not disease. The
proverbial blacksmith's arm is not a diseased arm, nor does
it naturally carry in it the seeds of disease. There is more
stuff to nourish, and so far if, by arterial disease or other
defect or poison, the fuller tale of wholesome food should
fail, the arm is more liable to dwindle. But these are con-
ditions not essential but consequential. I must be forgiven &
I reiterate that a man may fall into hyperpiesia, and continue in
it for some time, perhaps for a few years — three or four ? — So that

8 " CARDIOSCLEROSIS " part i

his heart, contending against abatements of velocity, may wax
in sound fibre to degrees of considerable hypertrophy, and yet,
toxaemia apart,1 remain healthy (p. 9) ; and, if normal pressures
can be restored, may still be capable of returning to its normal
work and dimensions. In hyperpiesia neither heart nor vessels are
to blame, they are not the sinners but the sinned against ; and
the heart if defeated falls in a defence of the citadel. It may fall,
as I have said, sword in hand, or it may be reduced by the
plagues incident to beleaguered communities ; in this case, by
strain, or by incidental toxins, the gallant heart and its auxiliaries
may be compelled to surrender ; but this is not degeneracy. Ac-
cordingly, if by some chance a man die in an early stage of
hyperpiesia, or likewise of chronic renal disease, the left ventricle
of the heart will be found hypertrophied, but healthy ; at later
stages the right side of the heart may suffer a consecutive strain,
and, whether by strain alone or by toxic influences arising out
of disturbed nutrition, both ventricles may now show evidences
of injury, often in chronic cases by the substitution of a
worse for a better fibre. As Dr. Batty Shaw well says,2 " The
case is a cardiac case only in a secondary sense, and the heart
may be normal in cellular detail." Furthermore, the coronary
arteries may not yet have suffered much ; to the naked eye
they may remain fair, or present patches of decay of
little importance in respect of a supply of a due quantity of
blood, be it better or worse. Barcroft and Dixon have shown
that the consumption of oxygen per unit of heart is much less
than per unit of kidney, pancreas, or submaxillary gland ; and
Bollinger and other pathologists now admit that often in these
big overworked hearts no abnormal structure is to be found. As
after a single nephrotomy the other kidney enlarges, and with it
its arterial trunk, so the heart, and even its arteries, grow up to
the new demands ; but this is not degeneration. In the last
stage of the malady, it is true, the heart will be found big and
distorted, stretched beyond its elastic limits, deteriorated in
fibre, and, it may be, with its nutritive arteries damaged by
overwork so gravely that latterly their inelastic walls and
narrower channels had become unable to supply a sufficiency of
food to the myocardium. Thus the cheaper fibre may have
1 Davy, R., Lt., June 22, 1912. 2 Shaw, B., Clin. J., Mar. 27, 1907.

chap, viii MYOCARDIAL FIBROSIS 9

been laid down in the place of some of the active muscle, or
perhaps in support of it ; or the muscle may in part have
succumbed. The valves likewise are pretty sure, in a like fibroid
substitution, and a like loss of elasticity, to exhibit the effects
of strain. Notwithstanding, even then the heart does not
present the typical state due to a primary atheroma, or primary
degeneration ; in a collection of appropriate specimens it is easy
to separate the " high tension " hearts from those which were
primarily atheromatous in vessel or degenerate in tissue ; those
which fought a good fight to the last from those which, by their
own inherent imperfection, or perverted by some poison, had
deteriorated primarily.

Nevertheless it is true that in many of these hearts, particularly
in those of chronic hyperpiesia or renal disease, and when dilata-
tion has supervened, some alteration of histological constituents is
to be found, at death perhaps in most of them. The hypertrophy
seems to consist, as Dr. Gutch demonstrated in our laboratories,
and as Kolliker taught beforetime, rather in an enlargement of
the several muscular fibres than in a multiplication of them ;
frequently however additional fibres are to be seen, even in abun-
dance, not of muscle but of connective tissue. This " myo-
fibrosis" often very improperly called myocarditis, was perhaps
fully studied first by Dehio ; x he showed that if the patient had
died during a stage of adequate compensation, with but little
dilatation, the myofibrosis was nominal in degree ; but that
with the fag of the heart and its chronic dilatation, the connective
element increased. Dehio thought the immediate cause to be
viscosity of the nutritive blood. In mitral regurgitation the
myofibrosis is found more in the left ventricle, in mitral stenosis
in the right ventricle ; but it is always most in the auricles. It
may be found in hearts with quite normal coronary arteries, as
in valvular disease ; though in other cases disease of these vessels
may have conduced to its formation. As I have asked already :
When is fibrosis an effect ? — -when a cause ? In this myofibrosis
the connective fibres are sometimes uniformly distributed, like
an infiltration penetrating among the muscular elements, some
of which may be degenerated (vacuolar) ; sometimes they are

1 Dehio, Deutsche Arch. f. klin. Med. Bd. Ixii., 21 Dec. 1899 ; also an extract
from Dehio, Petersb. med. Wochenschr. in Epit. Brit. Med. Journ. No. 9, 1901.

10 " CARDIOSCLEROSIS " part i

patchy in distribution, around the insertions of the valves, in
the papillary processes, about the twigs of the myocardial
vessels ; sometimes diffuse, sometimes in well-defined strands.
The diffuse and the patchy forms seem to be of somewhat different
nature and origin ; but neither of them, unless very extensive, or
invading cardinal parts such as valves or conductive bundles,
is of much practical importance. It must be difficult in a syn-
cytium such as the myocardium to follow these interlacing
strands in their early development ; but Fahr, the Prosector of
the Hamburg Hospital, in a very interesting paper x argues that,
as age advances, the muscle of the heart becomes more and more
unready to open quickly, and that for this purpose a diffusely
arranged elastic network is developed (" die Muskelfibrillen zu
umspinnen ") as auxiliary in the expansion of the heart in
diastole, as in elderly persons the arteries begin to stand open ;
this material, he says, is largely increased, for the same reason,
when the heart is under stress, "as in arteriosclerosis." Jores
also says that it is a structural support. However this may
be, as Krause says,2 " In children's (hearts) fibrous tissue is
scanty, but increases extraordinarily in adults." This we have
seen in the homologous arterial tree ; not till about the age of
30 is connective tissue apparent, with Van Giesen's stain, in
the intima, and it reaches no considerable development until
the decade 40-50. Hirschfelder again (2nd ed. p. 313) regards
the gradual increase of connective fibre as a strengthening
rather than a weakening of the chambers of the heart. This
fibrosis may lie on the marches between physiology and patho-
logy ; but Fahr also points out that only in the new-born
infant does the myocardium consist of pure unsupported muscular
fibres ; that then a fine connective network begins to embrace
the muscular fibres, and increases as the heart has more and
more to do. Thus it lies parallel, as it were, with Thoma's and
Jores' regenerative fibrosis, and such a name as " endocardia's
fibrosa " is inapplicable. Tripier,3 in refinements which are
beyond me, still regards these fibrous changes as "inflammatory,"
but he seems to observe no distinction between inflammation and

1 Fahr, Virch. Arch., 1906.

2 Krause, Normale Histologic, 1911, p. 208.

3 Tripier, Etudes anat.-clin., 1909.

chap, viii MYOCARDIAL FIBROSIS 11

active hypertrophy. I still hold to my postulate of fifty years
ago, that inflammation implies lesion and repair of lesion ;
arteriosclerosis is lesion, but the repair is insignificant. How
again are we to accept the statement of a distinguished recent
French author who says that a " sclerous myocarditis " is
one of the manifestations of arteriosclerosis ? In England,1
France, and Germany the best observers nearly all agree that
the process, if a proliferative reaction, is not inflammatory ;
often it starts not around the interstitial vessels but remotely
from them, whither nutrition has less instant access. Marks
of old infection, such as the rheumatic or the diphtheritic,
have other characters ; the fibrosis is perivasal, the vessels
themselves are thickened at the foci, and small scars testify
to the bygone mischief. From the present category then
chronic myocarditis is excluded. Krehl and other pathologists
tell us that elastic fibre also begins to appear in the maturing
heart, and increases up to old age ; but connective fibre has
about 100 times the resistance to stretch of elastic fibre.

Once more, Aschofi says decisively (he. cit. ii. 37) that it is
false to regard the so-called " myofibrosis " as inflammatory or a
sign of weakening of muscular energy ("Muskelkraft"). He
calls it "compensatory " ; and if it be so, or at any rate
auxiliary, the process must be distinguished in reason from an
irritative or atrophic fibrosis (p. 15). If this argument be sound,
and the facts verified, to name this change " Chronic sclerous
myocarditis " is as wrong as Cardiosclerosis is misleading.
Dr. Cowan 2 however describes three kinds of cardiac
fibrosis : (1) Periarterial fibrosis, never extensive ; (2) fibrosis
in much larger patches, remote from vessels (dystrophic) ;
(3) large fibrous lumps (callus). The first kind he attributes
to a reaction to various causes, such as infections. Hyper-
trophied hearts, he says, are not necessarily fibrous but
frequently are so, more or less. In the periarterial form
Dr. Aldren Wright (he. cit.) found about the small twigs
fine fibrillary connective tissue in a ground substance, and
numerous connective corpuscles, flat spindle or irregular nucle-
ated branching cells, with long axes parallel to the vessel.

1 Cf. Mackenzie, Brit. Med. Journ., Oct. 20, 1906.

2 Cowan, J., Journ. of Path, and Bad., Dec. 1903.

VOL. II B

12 " CARDIOSCLEROSIS " part i

Dr. J. Mackenzie takes a different view, saying that myo-
cardial fibrosis is in inverse proportion to the heart's capacity ;
but he gives no histological proofs of this. I have some-
times guessed that, old hearts being drier, their electro-con-
ductivity may be less. The arteriosclerotic kidney gets on well
enough (p. 371), but in each and every part, whatever the
reason and however normal the myocardium may seem, an
old man has a narrower reserve. Brault, when he con-
sidered the nodes and trabecule of connective fibre in these
hearts as insignificant, as mere curiosities, went perhaps to the
opposite extreme. However, his testimony may be added to
mine, that in not a few hypertrophied hearts, even of Bright's
Disease, the myocardium — unless at a few small points of stress —
is histologically normal ; the striations- are clear and the nuclei
well stained. But in the later stages, if no nodules be present,
streaks of connective fibre traverse and interpenetrate the
myocardium. These changes, and the nodules also, are com-
monly found in the hearts of aortic regurgitation ; and again of
atherosclerosis without high pressures.

In many fibrotic hearts the muscular fibres, although em-
bedded in this fibre, are often demonstrably quite healthy,
even in the papillary muscles. On the other hand they may be
as distinctly diseased, and heart failure on the way. Thus in
the heart of an old man, the subject of arteriosclerosis, recently
examined in our laboratories by Dr. Haynes, although the
ample coronary trunks admitted a large probe freely (and we
know from Jores that in these cases of coronary atheroma
the interstitial vascular network is usually intact), with some
myocardial fibrosis the muscular fibres were widely degener-
ated. In some hearts of long and good service there is plenty
of fibrosis ; in others, which had proved rather decrepit, and
prematurely so, whatever the other marks of muscular decay
fibrosis is scanty.

For a considerable degree of interstitial fibrosis a long time
seems necessary ; it signifies a heart long under some disadvan-
tage ; we find it not in old hearts only but in younger hearts
if crippled by old-standing valvular defect. It seems propor-
tional to strain, and apparently offers resistance to it.1 In
1 See Stadler, Deutsche Arch. /. hlin. Med., 1907.

chap, vni MYOCAEDIAL FIBROSIS 13

the auricles fibrosis is often almost complete, although the auri-
cular branches of the coronaries may be but little diseased.

As in the arteries then so in the myocardium, the effect
of laying down this inferior fibre serves in part to support
the muscle by a tougher tissue, but at the expense of the limits
of elasticity ; resistance is gained at the price of less resilience ;
once overstretched, the contractile organ will be the less able to
return to its normal diameter. The auricles, when so converted,
may almost cease to be contractile sacs. It is not impossible
however that by its native tendency to contract it may have
some bracing effect upon the fabric.

In some paragraphs on cardiosclerosis in his work on the
Heart (pp. 237-8), Dr. James Mackenzie identifies this term with
fibroid heart, but he scarcely distinguishes between interstitial
fibrosis, which proceeds from childhood to old age, and " replace-
ment fibrosis " ; indeed, he rather assumes that all cardiac-
fibrosis is substitutive. He then marvels, as well he may, on
the diversity of symptoms in patients in whom this alteration
is found after death. In many cases the alteration of the
heart had little or nothing to do with the symptoms — as e.g.
his cases of angina pectoris ; in others the relation was but corre-
lation, was but the fibrosis which in advancing years is general
in man, and throughout the bodily tissues. The cardiac fibrosis
may have had as little to do with the symptoms of a particular
case as the fibrosis of the skin or of the pancreas. Dr. Mackenzie
dwells with much valuable exposition on limited cardiac response,
but here again one desiderates more distinction between the direct
cardiac lability of disease and that lessened cardiovascular
capacity which, waning as " The Strong Hours work their Will,"
is still compatible with longevity. And in high blood pressure,
on the other hand, the so-called " degenerate sclerotic heart " is
often sustaining a blood pressure, of systole and diastole, of 20
per cent or more above normal.

Dr. Mackenzie says, after Huchard, that persistently excessive
pressures are " necessary " for the production of well-marked
" cardiosclerosis." If so, we must contrast this cardiac fibrosis
of high pressures (" high tension ") — a fibrosis of defence — with
another fibrosis, more dystrophic in nature, of decrescent arterio-
sclerosis ; though the difference may be rather inferential than

14 " CARDIOSCLEROSIS " part i

histological. The first would be the " compensatory " process ;
the others degradations, gradual or static, cheaper products or
remnants, or disseminate sequels of toxins such as those of
diphtheria or rheumatic fever. If then the name cardio-
sclerosis is to be used at all, it must be given to fibrosis the
result of coronary atheroma or senile withering, without high
pressures or other stress upon the heart.

Dilatation is at least of two hinds : that which is an adapta-
tion for a larger mass of blood (contraction-volume) — whether
relatively to the other chambers or absolutely in respect of
the whole system — and the yielding under distention, due to
disease or only to loss of tone. We cannot admit with certain
Leipzig pathologists that a dilated heart always signifies failure
— failure by loss of nutrition, or by myocardial infection,
or even by loss of tone ; clinical experience is against this
assumption : we meet with many a heart both hypertrophied
and dilated yet in functional equilibrium ; and conversely
we can rely on no direct relation between dilatation and
morbid histology.1 Myofibrosis and hypertrophied muscular
fibres may be co-ordinate. AschofE and Tawara examined
150 hearts consecutively, on Krehl's method, and found no
correlation between excess of connective tissue and failing
hypertrophy (p. 11). Indeed we have no anatomical facts
to show where and how in these cases dynamic default
becomes manifest statically as structural change. Aschofi and
Tawara think that, apart from increasing valvular incom-
petency, hypertrophied hearts fail because of minute scattered
" Schwiele " diffused under the endocardium by thrombo-
endocarditis. The "Schwiele," in its mature and permanent
state a scar, consists at first in a focus of congestion in which
grow fibroblasts and phagocytes ; this focus quickly becomes
ansemic, or, if in a district of coronary circulation without
ready anastomosis, is from the outset anaemic, and a white
scar or callus, consisting of fibrous tissue, is formed (Cicatrix
myocardii). These bodies may, as we know, reach very large
dimensions. Generally speaking, they are of thrombotic or
embolic origin ; and if they form, as often they do, in the
columnar part of the ventricle the apex contraction is impaired

1 See Myocardial Values, p. 32.

chap, viii CARDIAC CALLOSITIES 15

and the mitral flaps are slackened or, ultimately, distorted.1
Baumler 2 states that when in lumps they are due to coronary
disease or chronic nephritis, but when in broader and flatter
breadths they are old masses of toxic origin.

To turn to my own experience, this kind of fibrosis, unless
in considerable quantity, is not directly related to heart failure
(p. 11). In its beginning it is most easily found about the
apex and the columnar region, and in the septum. In its
earlier stages it appears as yellowish moist streaks — Ziegler's
" soft sclerosis " — then, as it contracts and withers, it becomes
the more or less pearly scar with raylike extensions into the
neighbouring myocardium. If these coalesce, large callus is
formed, with strands of muscle relics lying between the several
primary spots. Cohnheim's well-known experiment may here
be recalled to mind in which he clamped out portions of the
ventricular wall without any consequent fall of arterial pressure.
The heart of a healthy old man may be larger and seem stronger
than that of a weedy youth ; whether under various kinds of
stress it is essentially more enduring is another matter. With
increasing years the heart often increases a little in bulk ; and,
as we know, the systolic pressures gradually rise to a moderate
excess — say to 140, or even 150. The diffuse form of fibrosis,
in fine lines or patches, often first laid down in the mitral
columns, is in these larger hearts more abundant, and the
walls are rather thicker and a little harder to the knife ; but this,
as we have seen at length, is not " myocarditis." Indeed
this kind of change, even if widespread, " is usually a post-mortem
finding " (Josue) ; it gives rise to no symptoms, nor does the patient
die of it. Josue says truly that by this fibrosis, so long as
it does not affect the valve mechanism or conductive tracts,
cardiac f miction is little impaired. There is no consistency
in its degree, nor even in its concurrence, with symptoms of
failure. This fibrosis is often a part of a universal change which
age brings with it, not only throughout the arterial tree, but
also throughout all senile structures. We have followed this
fibrosis in deteriorating arteries and seen that it may lie
between normal elastic layers. The elastica may, of course, split

1 Aschoff, Lehrbuch P.A., 1909, Bd. ii. pp. 18 and 35.

2 Baumler, Deutsche Arch. J. klin. Med. Bd. ciii., 1911.

16 " CAKDIOSCLEROSIS " part i

independently, and nodular atheroma is prone to impose itself
upon the diffuser product and, becoming confluent, to involve the
whole vessel in decay. But, atheroma apart, we have no evid-
ence that the change in later life, whether in heart or vessel, is
one of much gravity. The whole tree is, of course, less resilient,
with the consequences we have discussed.

A little cardiac enlargement then may be a character of
decrescent arteriosclerosis, though in this condition, if uncom-
plicated, the heart never attains anything like the dimensions of
that of hyperpiesia or of chronic renal disease. To the eye and
hand the organ is solid rather than big. Charcot, in 36 cases of
arteriosclerosis without valvular disease, found the heart some-
what enlarged in 36 per cent ; and in the Salpetriere it is
probable that the large majority of cases were of the
decrescent kind.

We have dealt with the assumption in current writing, though
particular writers may here or there modify their statements, that
arteriosclerosis of whatsoever kind, or of whatsoever clinical
process, is the cause of cardiac hypertrophy. Bourguignon 1
wonders how "old sclerosed" hearts can stand for years excesses
of blood pressure, sometimes double the normal. They don't. The
heart of high pressure may be sound till near the end. Because
arteriosclerosis is found it does not follow that the pressures
had been high. For the heart to grow under high pressures
is one thing ; to be reduced in quality by sclerosing coronaries
is another. This Huchard and his pupils did not see. But we
have seen that in hyperpiesia the cardiac hypertrophy is not a
result of the arteriosclerosis, which is a subsequent event, but of
the peripheral resistance ; yet the assumption still prevails that
in all and any arteriosclerosis it is this change which augments,
directly, the dimensions of the heart, an inveterate opinion
which has been fully criticised in preceding pages. If in a body
presenting senile arteriosclerosis, even to grotesque degrees, the
heart be increased at all, the increase is quite moderate, such as
during life could not be detected by physical diagnosis. Here
again we are beset by the notion of " provisions of nature " ;
because more work might be expedient to overcome failing storage
of energy in the vessels, therefore such more work is provided.
1 Bourguignon, French Congress of Med., Geneva, Sept. 1908.

chap, viii NATURE OF THE FIBROSIS 17

If provided at all, it is in quite subordinate measure ; indeed
if considerable it might force the failing vessels. The consequence
in elderly arteriosclerotics is not so much a circulation compen-
sated up to or near the normal values of younger and sounder
persons, as in a moderate aortic regurgitation for instance, but
a narrower range of effort and perseverance. Elderly persons
live the quieter life that their age and their languor dictate ;
their blood runs more slowly. An attempt, if foolishly made,
to vie with the livelier habits of youth, would lead not to the
accelerative elastic capacity and output possible to the younger
heart, but to arhythmia and incomplete emptying of the chambers.
The heart of the old man cannot do it. Whatsoever dissipation
of energy there may be is not compensated, neither persistently
nor temporarily ; the automatic energy of the myocardium is
less ; moreover if its own arteries are implicated in the same
degeneration, they are worse carriers, and the functions of each
and every organ and part are less exacting.

We have seen then that, histologically speaking, fibrosis and
inefficiency are by no means parallel ; we are not at all sure that
some diffuse fibrosis is a change of much gravity (p. 49) ; it may
indeed be conservative. We have found it difficult to discrimin-
ate between such a fibrosis, apparently conservative, and a mere
dystrophic sclerosis such as may be found more or less throughout
the structures of an old man. This general sclerosis can
scarcely be conservative, it is simply cheap. To talk of a
" fibroid diathesis " is mere verbiage. In the heart, as else-
where, dystrophic sclerosis usually depends on defect of the
nutrient vessels ; it is a " substitution fibrosis," not dependent
on any exudative or periarteritic irritation.1 Very slow deteriora-
tion of the coronary branches, if protracted over years, may
lead to a substitution fibrosis, as on the other hand prolonged
stretching, within limits, leads to the conservative fibrosis :
a fibrosis, as Councilman and others have demonstrated, in hearts
whose coronary arteries were not only efficient, but, as is common
in hypertrophy, themselves also enlarged. Dr. Shinglewood
Taylor, in a thesis on Aortic Stenosis for our M.D. degree
(1914), was " surprised in many cases to find extensive

1 For a discussion of this kind of fibrosis see Adami's Pathology, vol. i.
(2nd ed. 1910).

18 " CAKDIOSCLEKOSIS " part i

fibrosis of the left ventricle with no apparent loss of efficiency."
With increasing work the coronaries frequently enlarge. With
the sustenance of the heart after closure of the coronary arteries,
or their mouths, I shall deal later (pp. 23 and 363).

Gennari 1 set himself to compare the somewhat contradictory
statements of Krehl and of Dehio, on the one hand, that myo-
fibrosis is constant in hypertrophic states of the myocardium
and may be one cause of its ultimate default, and on the other,
of Aschofi and Bollinger, and I may add of Kanthack
and myself, that, on the contrary, this alteration is often
absent. Gennari took nine hypertrophied hearts, selecting such
as to the naked eye presented no lesion. Of these he
made many and various sections, and in two of them, after
the most prolonged search, no fibrotic invasion could be
detected. In the remaining cases fibrosis was found, but
very irregularly ; sometimes only in a small proportion of
the sections examined. Moreover, in apparent date, the
fibrotic areas bore no relation to the phases of the clinical
symptoms. Indeed, in perusing his paper, I inferred that in
some of them the fibrotic areas described were evidently relics
of some long-past infection. On the whole Gennari concluded
that the secret of myocardial failure did not lie in fibrosis, whether
inflammatory, compensatory, or substitutive. Bradycardia,
which formerly was attributed to the kind of this ventricular
deterioration, is now explained by the seat of it.

I suggest then, if conjecture in pathology may be forgiven,
that a distinction should be made between auxiliary and
substitutive fibrosis, and that the distinction may be this :
that whereas in substitutive fibrosis the genuine muscular fibres
are supplanted by the fibrous, in the auxiliary mode a sub-
stantial proportion of the fibrous tissue may be laid down in
support of the muscular. If we may suppose, on the com-
parison I have made more than once, that by arduous work juices
are squeezed out into the myocardium after the manner of the
juices on the lee-side of a tree, so in the myocardium, expressed
juices may be converted into, or feed, either a larger bulk of
muscle or of muscle and connective fibre, as the result may
be. The one issue is muscular hypertrophy ; the other is a myo-

1 Gennari, Arch, per le sci. med., Dec. 1905.

chap, viii NATURE OF THE FIBROSIS 19

fibrosis, yet still of a conservative mode, of a mode auxiliary
to, if not the full equivalent of, the " nobler " fibre. It is the
second best. The third best or substitutive mode arises, probably,
out of failing capacity of the nutritive factors to sustain the
" nobler " standard ; muscle gives way to a cheaper and in-
ferior kind of fibre. I have seen it stated in works on gynaecology
that if a fibroid tumour pull upon a long stalk, or if its vessels are
interfered with by the pressure of surrounding parts, its muscular
fibre is so far supplanted by connective tissue. Thus,
if a ventricle of the heart be submitted to dilating stresses,
the extra juices thrown out may make more muscle or, under
less favourable conditions whether of stress or of nutrition,
muscle with a buttress of connective fibre ; both processes being
conservative. If however dilating stresses be excessive and
nutrition fall short of the best, then no addition may be
made to the muscle, but the normal scaffolding of connective
fibre may be fortified ; if nutritive capacity be still more in
default, connective fibre will be the utmost that the impaired
capacity of the self - regulating machine can produce, the
muscle itself will be supplanted by the lower fibre. If so,
the distinction between supplementary and substitutive myo-
fibrosis is real. The one, let us say, in a ventricle submitted to
dilating stresses, is an adaptation and relatively an advantage ;
the other is simply tissue degradation in a ventricle perhaps
exposed to no excessive stress, presenting it may be no dilatation,
but falling short of its own proper structure. Such a conjecture
would, I think, reconcile the diverse opinions of sundry
writers, such as of Krehl and Dehio of the one part, and of
AschofE and Bollinger, Kanthack and myself, of the other.
It is almost needless to add that in the same heart both kinds of
fibrosis — the protective and the substitutive — may be mingled
in incalculable degrees ; as, for instance, in an old and slow case
of aortic regurgitation with hypertrophy, dilatation, and athero-
matous coronary arteries. In an extremer degradation of the
myocardium, not even connective fibre can be kept up, and the
muscle falls into granular or vacuolar demolition. Cardiosclerosis
then, unless used simply and clearly to mean myofibrosis, is
but a vague term, and in any case is not wanted.

To go back to the beginning ; these considerations emphasise

20 " CARDIOSCLEROSIS " part i

the fallacy of the confusion of hyperpietic and decrescent arterio-
sclerosis, as in Huchard's (passim) three stages of " cardio-
sclerosis"; firstly, the "presclerotic," with high tension; secondly,
the stage of cardiac degeneration (cardiosclerosis proper) ; thirdly,
the " mitro-arterial." In the first stage, he said, " arterial lesions
are a minimum," and are curable ; in my interpretation arterial
lesions in this stage have not begun, or are only nominal,
they are consequential, and often tardy ; the third stage he
regarded, not as one of a defeated heart, frequently hyper-
trophied and with patent coronaries, and presenting only
auxiliary fibrosis, but as one of an intrinsic decay, not conse-
quential but primary ; a part of a general toxic cardioarterial
deterioration. Such a series we may find in my Decrescent
mode; but in Hyperpiesia, or chronic renal disease, there is no
such intrinsic decay, but a perpetual mechanical strain
resisted better or worse according to the original quality of the
individual system and its reciprocating organs.

Again, in respect of the third or " mitro-arterial " stage,
Huchard and his school fail to draw the intimate distinction
between the mitral insufficiency caused mechanically by high
tension with dilatation of the wall of the chamber, and athero-
sclerotic decay advancing from the aortic area to the anterior
curtain of the mitral valve. The former series — in Hyperpiesia
or Renal disease — usually issues in the ordinary course of " big
dilated heart," with scanty lateritious urine, tender liver, cardiac
dyspnea, and dropsy ; the latter series in gradual decay —
" cardiac failure," without these overt and unequivocal
symptoms and signs of rising venous pressures and cardiac
conflict.

We have to consider further the kind of so-called " cardio-
sclerosis " which I postponed (p. 15) ; namely, the formation of
callosities or nodules in the heart, masses regarded by many
writers as fraught with grave mischief as impediments to the
ventricular contractions. To the minuter and more gritty form
of these nodules and the remnants of old infections I have already
alluded. On the larger masses an important early essay was
written by Thiele more than twenty years ago ; x but many years

1 Thiele, Uber Herzschwielen mit Veranderungen der Coronararterien, I.D.,
Gottingen, 1892.

chap, vin FIBROSIS AND CORONARY ARTERIES 21

before that Hilton Fagge,1 and after him Gowers,2 and Charlwood
Turner,3 had led the way ; and six years after them the late
Lindsay Steven 4 followed up the enquiry. Dr. Turner attributed
the nodules to defects of the coronary arteries. Karl Huber 5 had
detected the part of the coronaries in what he called erroneously
— as we now know (p. 11) — "chronic myocarditis," and de-
monstrated these changes in 18 cases. In the early papers callus
formation was not clearly distinguished from the diffused forms
of myofibrosis, auxiliary or atrophic, which we have discussed
already; but Lindsay Steven rightly argued that these callosities,
often as large as a split pea or an almond, or still larger, should
not be classed either with chronic myocarditis or diffuse fibrosis.

The coronary artery leading to the patch may however be
healthy; in this case the callus may be attributable to infarction ;
embolus being far less frequent than thrombus. An infarct may
be followed by a hgemorrhagic exudation, and this, " becoming
organised," may contribute its part to the mass. Or smaller
patches may coalesce to make up a large callus. If a coronary
plug be very big and sudden, more grievous symptoms or death
may ensue : these cases I shall deal with in my chapter on
Angina Pectoris, p. 450. Masses thus produced may lie deep in
the heart substance, or may be subendocardial or subpericardial ;
they are most frequent in the left ventricle, and towards
the apex, where the well-known ectasy and rupture may occur
(aneurysma cordis).

As regards the dependence of fibrosis, nodular or diffuse, upon
the coronary circulation, there are many facts to check too
ready assumptions on the subject. Among the hearts which
Kanthack examined with me, I remember one in particular
which was notable in this respect, that not only were the
coronary arteries calcified, but their orifices also were so utterly
obliterated that the very seat of them was indefinable ; yet in
this heart, so far as the microscope could tell us, the myocardium
was normal. And this experience is far from singular ; a greater
or less abatement of the coronary circulation with, or even with-
out, comparatively slight degrees of fibrosis is not uncommon

1 Fagge, H., Trans. Path. Soc, London, vol. xxv. 1874.

2 Gowers, W. R., Reynolds'1 System, 1877, vol. iv.

3 Charlwood Turner, Trans. Med. Congress, London, 1881.

4 Steven, L., Lancet, Dec. 1887. 6 Huber, K., Virch. Arch., 1882.

22 " CAKDIOSCLEKOSIS " part i

(p. 267). Letulle, by two examples especially, enforced the maxim
that coronary occlusion need not imply myocardial decay, but
that " even considerable hypertrophy of the heart may coexist
with coronaries obliterated by atheroma." Baumler,1 in a careful
study of the subject, questions the invariable dependence of
callus upon coronary disease or infarction ; he believes that in
many an instance he has demonstrated these knots in parts of
the myocardium where the respective coronary branch was
pervious, and he quotes Gierke and Ziegler to the same effect.
Most pathologists indeed, as Fahr of Hamburg 2 for instance,
now admit that, often as callus and coronary stenosis or
occlusion are associated, yet they stand in no direct propor-
tion one to another — in no parallel. If with extreme coronary
disease some hearts present much callus, others show but little ;
and conversely some with much callus show little coronary
obsolescence. Baumler throws the scars of bygone infective
foci into the same class, where they seem to me rather out of
place ; if within themselves they may pursue a similar histological
course, their history and significance are otherwise.

It may not be altogether out of place to quote here Baumler's
corresponding notes on the clinical signs, and the symptoms by
which he thinks the presence of these knots may be betrayed :
these are, a feeble first sound and a loss of the apex beat, inde-
pendently established; for instance, that digitalis may bring back
the apex beat without restoring the quality of the first sound. If,
however, he adds, the fibroid thickening is much towards the apex
and the heart is slack, the blood charge (contraction volume) may
force itself against the chest wall ; especially if a cardiac aneurysm
be forming there. Sir William Gowers, in a pioneer article on
Fibroid Heart (loc. ciL), had previously pointed out the signs of
defective apex beat and impaired first sound ; but it seems to
me that these signs, however truly a result of callus formation
in the ventricle, are too universal in enfeebled hearts to be
admitted as criterions of callus formation, corroborative as they
may be in conjunction with other indications.

One important factor in the comparative immunity of the
myocardium under deprivation of coronary circulation is time ;

1 Baumler, Deutsche Arch. /. klin. Med., 1911.
2 Fahr, Virch. Arch., Feb. 1906.

chap, viii FIBROSIS AND CORONARY ARTERIES 23

if the process of obliteration be very gradual, alternative supplies
of nutriment can somehow be contributed (vide Angina Pect.,
pp. 363 et seq.). Every one who has worked with the perfused
heart knows upon how little — a few calcium ions, etc. — it can
live and work for a while. One alternative access may be by
the veins of Thebesius ; by their subsidiary aid, in spite of
coronary sclerosis, nutrition may be kept up ; so that it will not
do from the state of these vessels to infer a decayed myocardium
(see Morison, p. 362). Coronary sclerosis and myofibrosis do
not run parallel. On the surrogation of the veins of Thebesius
some interesting researches were made by Porter,1 and by
Pratt 2 of Harvard. Pratt found that if in the excised heart (of
the cat or dog), while the heart is kept beating with defibrinated
blood (in this experiment Ringer's solution is not sufficient),
the coronary arteries be closed, and then one of the coronary
veins incised, a slight but continuous stream of blood will
flow from the interior of the ventricle through the foramina
of Thebesius into the coronary veins, and out at the artificial
opening ; moreover, in its course through the heart walls it
becomes venous (see Redwitz, p. 364). Wardrop 3 had made some
interesting remarks to the same effect ; and he in his turn
quoted some corroboration from Abernethy.4 Jores' recent
demonstration that atherosclerosis, which so readily attacks the
coronary trunks and branches, does not readily invade their
finer ramifications,5 and the free inosculations demonstrated by
West and by Spalteholz (p. 363) make this alternative irrigation,
both in experiment and in clinical medicine, more intelligible.

Now let us turn from the myocardium to the inside of the
heart, and especially to the valves ; there sclerosis — cardio-
sclerosis if you please — may be conspicuous. Of sclerotic disease
in and about the aortic valve we are abundantly informed, but
a part of this information is that even the extremer degrees of
this lesion are associated not infrequently with a very fair myo-

1 Porter, Brit. Assoc, Toronto, 1897.

2 Pratt, Amer. Journ. Physiol., Jan. 1898. See also note p. 49.

3 Wardrop, Diseases of Heart, 1859.

4 Abernethy, Philosophical Transactions, 1798.

6 See e.g. in Jores' 1904 paper in Virch. Arch. ; the old woman of 71 ; senile
dementia and advanced general arteriosclerosis ; the coronary twigs within the
heart's muscle, as likewise the twigs in the skeletal muscles, were unaffected.

24 " CARDIOSCLEROSIS " part i

cardium. Now and again in old atheromatous patients I have
seen, on the establishment of aortic regurgitation, the left ventricle,
in spite of supposed sclerosis, hypertrophy not a little to meet
the new conditions {e.g. Vol. I. p. 453). We know also how by
the ear in the living patient, and by the eye in the necropsy,
the mitral valve is liable, whether of its own frailty under normal
or abnormal stress, or by extension from the aortic area, to suffer
sclerosis ; and indeed that under these conditions a corresponding
systolic murmur during life is no very grave item in prognosis.

The common experience that, as years are added to years,
the pressure in the arteries normally rises somewhat, must
signify fair cardiac efficiency ; were the heart, by whatsoever
common " sclerotic " or other change, to lose contractile value,
the disadvantage would be so multiplied that few of us would
cross the threshold of old age. My own impression, a superficial
one I admit, is that in such later periods the heart rather
waxes than wanes ; but to determine this question difficult
comparisons both of weight and quality would have to be made.

Finally, in some few cases we may see a very severe and
extreme change of the whole heart's muscle, chiefly of the left
ventricle, in which the part is almost wholly converted into dense
harsh fibrous structure, diffuse knotty and nodular, without any
notable dilatation or disease of the coronary vessels. The con-
dition is an obscure one, and in nature different ; I note it here
only to distinguish it from Dehio's alteration which we find
first in the auricles, and from callosities.

Cardiosclerosis, then, is a name signifying no definite con-
ception ; on analysis its meanings prove to be divers and
confused. Huchard applied it not to the heart of decrescent
arteriosclerosis, of which he had no discernment, though to
this it might have been given with less ambiguity, but to
the heart of hyperpiesis, the big dilated heart overstretched
by high tensions (the " Hochdruckstauung " of the Germans),
and defeated at length by them ; ultimately with a mitral
insufficiency, due rather to forcing of the mitral orifice than
to sclerosis of the valve. If the name cardiosclerosis be applicable
at all, it should denote aortic decay with cognate atheroma of
its whole area, of the aortic valve and ring, the aortic cusp of
the mitral, and the coronaries ; for in the hyperpietic series the

chap, viii MYOCARDIAL VALUES 25

scleroses, if any, are a secondary, a late, and not an essential,
feature ; indeed the whole heart differs but little from that of
chronic renal disease.

Myocardial Values. — In my youth it was a common jest
to ask what N. or M. died of, the witty answer being
" shortness of breath, of course." The jest has vanished, but
the platitude remains, with some alteration of the formula, which,
instead of " shortness of breath," now runs " of heart failure."
In the obituary notices of our current journals we read daily of
these deaths by the half-dozen, that N. or M. died of " heart
failure " ; and the vogue of appendicitis is threatened. Now, do
we owe this new fashion to the physician or to the pathologist ?
for it is often worth while to observe the straws floating in the
wind ; we may learn something from some of them. Is this
a parrot phrase put up as a kind of shorthand between the
doctor and the registrar of deaths ? or does it, like appendicitis,
signify a fresh point in pathology, claiming its catchword ?
Does the phrase mean that a snap of the heart stopped the
whole machine, otherwise capable of working on, as a snap of
a connecting rod may stop the engines of the Majestic ? or does
it mean that the heart was the ultimum moriens, and that, so
long as this central organ held to it, death was kept at bay ? In
this case to say that one died of " heart failure " is surely as
empty a truism as to say that he died of " shortness of breath."
On the other hand, as it is true that we have of late years learned
more — much more — of the heart's work and of its diseases, both
on the clinical side and on the side of pathology, so the new phrase
may be a shadow thrown by some shift of position — whether
clinical or pathological — in our view of the heart and its functions.
Four or five years ago, when engaged on an article on the treat-
ment of heart disease for Musser and Kelly's System of Thera-
peutics, I was brought closer to this problem and found the
answer so difficult that it has occupied much of my attention
since, and I have sought the opinions of my friends upon it.

Now, if I appeal to a clinical physician, asking him what
he knows about " heart failure," I get a ready answer : I
hear of many a case of sudden and mortal stoppage of the
heart ; of heart failure in infections ; of cardiac dilatation and

26 MYOCARDIAL VALUES part i

defeat under high pressures, venous or arterial ; of senile decay,
so undermining the heart that it can work no more ; of angina
pectoris ; of aortic regurgitation, and so on — his data are
in plenty, his opinions decisive. And likewise, when I betake
myself to the pathologist, I find him no less ready for me : from
him I hear of fatty degeneration ; of " cardiosclerosis " — what-
soever this may mean ; of rheumatic, diphtheritic, and such-like
myocarditis ; of fibroid disease of the ventricular walls ; of sap-
ping of the a-v bundle, and so forth ; data again in plenty,
opinions decisive. But when I desire to link up the two classes
of information, when I confront the physician with the patho-
logist and seek to correlate these times, periods, and modes of
disease and death the one with the other, I find myself but little
nearer to practical guidance than I was before. Of course, we
all know that a " fatty " heart is not so good as a sound one ;
we all know that a senile heart will not sustain an attack of
influenza like a young one ; we all know now that damage of the
a-v bundle may disconcert the rhythms : but when we ask the
physician to draw a parallel in the living patient between the
formidable modes of decay described by the pathologist, how
and when these degradations are manifested, how, in the long
course of cardiac decay, the imminence of sudden death is to be
foreseen and provided against ; how indeed we are to know
that any such process is at work at all ; or, lastly, how in a case
of known heart disease the degrees of its advancement and of the
cardiac reserves are to be noted and tested — then the physician
retires from the argument. And so with the pathologist : when
we show him a heart from a case of sudden death he will con-
fidently demonstrate to us on the specimen why a heart so diseased
could not have gone on ; but if beside this one we place another
heart — still more diseased, it may be — and tell him that the
possessor of this heart lived for long enough, and perhaps in the
end died of something else ; or if we show him yet another in
which, by the poison of rheumatic fever, the tract of Tawara was
attacked, and yet, notwithstanding, there was during life no
considerable divorce of auricle and ventricle, he in his turn retires
from the argument, saying that he is not concerned with clinical
conundrums. Thus we have the physician and the pathologist
trotting each on his own side of the hedge, each intent upon his

chap, viii THEIR UNCERTAINTY 27

own scouting and his own bearings, and neither able as yet to
reconcile his own observations with those of his comrade ; both of
them being perhaps a little too indifferent to the need of mutual
counsel and comparison.

Both Vaquez and Wenkebach at the London International
Congress asked (as I had done) how it was that prognosis or even
diagnosis in myocardial disease was so unsatisfactory, or even
totally erroneous, that we had no measure of cardiac in-
sufficiency. The difficulty lies of course in the complexity of
the circulatory coefficients and the academic character of the
means of diagnosis of cardiac reserve, means admittedly as
yet of little clinical service. Professor Thayer went so far as to
say that diagnosis of heart weakness was almost always wrong ;
and other speakers of experience agreed with him. One of us
remarked that the best notion to be got was " the poor one of
watching the case throughout " — if there be any " case."

Whether it be then for lack of mutual co-operation, or because
of the perplexities of the subject, the interpretation of cardiac
pathology in terms of clinical medicine, so far from becoming
clearer, has darkened, and the intricacies of the path have become
more baffling. Our fathers, knowing less of the entanglements
of the subject, and newly provided with a collection of the blunter
facts of morbid anatomy, took the matter more easily. That
people died suddenly of heart disease was for them an old story ;
when therefore they were introduced to diseases of the valves
of the organ, and to coarse lesions of its substance, their diffi-
culties were almost solved. The patient is dead, here is the lesion
which caused his death ; what more does one want ? But, as
pathology became more and more curious, these simple solutions
became less and less acceptable. Kirkes, Bence Jones, Wilks,
Fagge, T. H. Green, and many others with them, began to demur.
In the dead man lesions may have been discovered enough, and
apparently fully enough, to cause his death ; but the man
had died suddenly, and the lesions under demonstration were
of long standing, or, in a series of such cases, were very various in
seat and nature. Again, in a series of such cases valves were
diseased and not diseased ; kidneys were diseased and not
diseased ; atheroma was considerable and inconsiderable ; the
ventricles were dilated or were not dilated ; the myocardium

VOL. II c

28 MYOCAKDIAL VALUES part i

was in extreme decay or virtually normal ; its lesions were
now focal, now diffused. Thus gradually it dawned upon the
pathologist that the problems of cardiac failure were not so
simple as in the rise of morbid anatomy had been supposed ;
and upon the physician, that his clinical methods were fallible
indeed, far more so than had been supposed during the rise of
stethoscopy. By what system of compensations was it that the
same heart could be at once fairly competent clinically and yet
pathologically the seat of old and intimate decay ? By what
system of compensations could a heart go on fairly well, or indeed
without suspicion, while its structure was being undermined ?
Surely, before the sudden collapse, there ought to have been
some stage of manifest incompetency, or at least of falter ?

In no organ is this lack of concord between the signals of life
and death so disconcerting as in the heart. As Dr. Hector
Mackenzie has said,1 " the heart that failed had sometimes been
passed sound in a searching examination for life insurance only
a short time before." In all living structures there is a factor of
safety, that potential which in the heart we call reserve ; but
in none perhaps is it so large as in the heart. Moreover this
reserve is not wholly muscular ; there is the coefficient of arterial
elasticity also, and an unknown coefficient of nervous reinforce-
ment. And we may confuse cause and effect ; thus excess of
blood pressure may not be, as ordinarily, mere constriction, but
a lack of depressor response. Hasebroek looks to the degree
of arteriolar propulsion, which he says can be exhibited in the
rabbit's ear ; Broadbent and Rosenbach looked rather to the
rhythmical activity of the tissues. Yet of this reserve, of what
the heart, in case of need, can do for output, for strength and
velocity of systole, we have no scientific measure; the microscopist
cannot detect it, the clinician has no valid tests for it. At one
time it maintains a defective heart ; at another time it betrays
a heart which, to all appearance, if not impeccable was at any
rate not plainly corrupt. So more thoughtful observers began to
put the matter more cautiously, and to say that " when a patient
succumbs to heart failure certain degenerative changes are
usually found in the myocardium and vessels, and these are
supposed to account for the heart failure." Evidently even yet
1 Mackenzie, H., Lancet, March 23, 1912.

chap, viii CLINICAL EVIDENCE 29

some more refined investigation into the phases and intricacies
of cardiac qualities must be instituted if these apparent caprices,
clinically speaking, of the heart of man are to be explained,
computed, and foreseen. " Heart failure " is evidently a very
composite notion — one which must be submitted to a no less pene-
trating analysis. We are beginning to learn in the heart, as
we learn in less striking ways in other forms of organised matter,
that complexity of structure and conditions mean not less but
more stability ; that equilibrium endangered in one direction,
or in more than one, may be supported by readaptations of other
factors of the concert ; so that the organ, if it may not be
restored to its pristine capacities, may be kept in some
tolerable adequacy, such as, under favourable circumstances and
within limits not too wide, to preserve it from default. The heart
of an active undergraduate, if slightly and temporarily impaired
by a " bad cold," may by the stresses of rowing become gravely
harmed, and give rise to unmistakable clinical symptoms ; while
a senile heart, far more radically vitiated, may for years amble
comfortably along the serener paths of old age. Non intelligitur
quando obrepit senectus.

To pass from these general reflections into more concrete
observations, we may begin either with the clinical or the patho-
logical side : as the clinical side is the field of practice, let us begin
there ; remembering how Goethe taught us that the general is
always to be found in the particular. In the clinical field we shall
first be impressed by the part of the heart in almost all diseases,
and under conditions such as anaesthesia. In infections we know
that the heart is concerned in three ways : in some of them it is
directly attacked ; in others it seems to suffer rather from a
general depreciation in common with other parts and tissues,
an impairment due apparently to pyrexia or to some diffuse
effect of the specific poison ; in others, again, from a dissociation
from its peripheral complement, from a loss of tone in the " peri-
pheral heart," so that it beats the air in vain. Now, for these
different conditions have we any crucial symptoms by which to
distinguish them ? Have we in a particular case any criterion by
which, in an infectious disease for instance, we can discriminate
myocardial lesion, myocardial sympathy with a more general
and temporary debility, and slackening of the peripheral circula-

30 MYOCAKDIAL VALUES part i

tion 1 These several factors may overlap each other, cross each
other, and supplement each other inconstantly, and in degrees
of which appreciation seems very difficult. Nay, we are well
aware that in infections — as in diphtheria, scarlet fever, rheu-
matic fever, pneumonia, etc. — a diagnosis of direct attack upon
the myocardium, unless it occupy the conductive tracts, is,
perhaps usually, beyond our methods ; if in rheumatic fever
dilatation is no infrequent accompaniment of it, in other infec-
tions, as in diphtheria, it is at least frequently absent. And in
chronic myocardial deteriorations is it too much to say that in
the majority of cases of sudden or rapid death the underlying
condition is not detected till once for all it is revealed on the
post-mortem table ? We have seen that many an ill-looking
heart, especially of the fibrous kind, may have worked even against
atheromatous stenosis for many a year, and death after all not
been directly due to its default. Soft "rotten" hearts are much
more apt to " shut up," but how are they manifested?

During and since my student days attention to cardiac disease
has taken various directions, dependent on the various improve-
ments of our means of diagnosis. As a student I witnessed the
developments of auditory diagnosis — methods which certainly
served to detect many cardiac diseases, such as pericarditis and
mitral stenosis, not decisively demonstrable before. Then, by
the efforts of Sansom, Ewart, Lees, and many others, especial
emphasis was laid on percussion as a means of measuring the
dimensions of this chamber or of that — a method by later dis-
ciples pushed to extravagant lengths, or used with indiscriminate
assurance. The sphygmograph came next, and from it more
was expected than it could give ; though twenty years later it
was restored to practice by James Mackenzie with largely de-
veloped powers ; still, even thus improved, the instrument could
tell us only certain things, chiefly facts about rhythm — facts
important enough, but, excepting occasionally in respect of
pulsus alternans or dissociatus, throwing little light upon myo-
cardial values. Then pressure gauges were to open out the
way for us. Inventors made and improved these instruments,
and much was attained in measurement of maximal pressures
and even of pulse amplitudes ; but after a while we found
that we were as far perhaps as ever from appreciating the

chap, viii METHODS OF ESTIMATION 31

values of cardiac reserve ; as much as ever in cardiac disease we
were taken in surprise by sudden deaths. Now, again, the
X-ray method, and the method of the electrocardiograph, are
to place in our hands tests of myocardial dynamics ; but
hitherto we have had to be content with records which, however
interesting otherwise, do not give us the intimate criterions which
we seek ; for cardiac potential we are still without a gauge.

From these introductory remarks it will be apparent that I
do not intend to dwell upon what we call broadly the valvular
diseases of the heart. In the valvular diseases we can often,
generally perhaps, form some approximate forecast ; the con-
ditions are more frankly and audibly mechanical : in these cases
the myocardium may count for much, but, generally speaking,
it is the static structures rather than the dynamical potentials
which take the crooked way. If in a few instances, as in
aortic regurgitation, the heart may drop without warning, yet,
as a rule, valvular diseases of the heart do not end suddenly ;
as a rule we may rely on it that a comparatively intact muscle
will fight with fairly good reserve energy till defeated by accumu-
lating venous stresses, and by those regional falls in velocity
often known by the inept term of " backward pressure." Now
of these shortcomings we have for the most part in symptoms
and signs no insufficient indications.

From what I have said then it will appear that in the class
of cases to be discussed I cannot dwell upon symptoms ; for
the point is that, even in the gravest cases of myocardial lesion,
symptoms may be none ; still, there are a few remarks of a
critical kind to be made concerning alleged or occasional symp-
toms. Moreover the problem of sudden death — that is, of
absence of symptoms during the main run of a myocardial lesion,
even to an extreme period — is not materially altered, if we include
certain other cases in which indeed some symptoms do precede
death, but do not put in an appearance till the lesion is far
advanced. Dyspnea for instance, or falterings in the pulse, or
again syncopic phenomena, if they appear at all, may not, and
often do not, appear until the malady has entered upon its final
stage ; so that the issue is removed by but one step from death,
and the problem little varied.

But, before considering these admittedly late and almost

32 MYOCABDIAL VALUES part i

irremediable symptoms, let us dwell for a few minutes upon any
symptoms or signs from which more timely warning may be
obtainable, such as dislocation or readaptation of the chambers ;
murmurs, unless as superfluous signs of demolition, we may
disregard. Fluctuations in the intensity of a murmur depend
on so many conditions that, unless other evidences of asystole
be present, no reliance can be placed upon such differences,
even if referable to any standard. Hypertrophy of the ven-
tricles is so alien to intrinsic degeneration of the myocardium
that we may pass it over ; but in passing I would remark that,
from our present point of view, the alleged intrinsic instability
of hypertrophy — say of the left ventricle — apart from the general
instability of the diseased individual so affected, seems to me to
lack any serious proof. Apart from the causes and conditions
of the hypertrophy in the particular case, I know of no evidence
that the mere hypertrophy depends upon any encroachment on
the normal reserve of the heart, or is taken out of it. So far as
evidence yet goes, a soundly hypertrophied myocardium is as
good as a normal muscle ; a persistently hypertrophied myo-
cardium, as such, does not stand at any intrinsic disadvantage ;
if the need for it be temporary, the part will recede to its normal
dimensions as if no such change had ever taken place. Whatever
we may guess, we do not know that it is more easily fatigued, or
more liable to degenerative disease ; it stands in the disadvantages
in which all parts of an embarrassed organ are involved, it is
involved in a growing default not its own, and no more.

The heart beat, the impulse against the chest wall, is not a
cardinal point, either way. The subcostal impulse is not a
simple function of the ventricular contraction ; the blood
propulsion impulse is not precisely the same contractile
movement as the wall shock. It is common knowledge that a
well-marked chest impulse may be coincident with a small and
bad radial pulse ; and conversely.

Dilatation we cannot dismiss so readily (p. 14). It is true
that there is nothing very stealthy about a dilatation which is
an accommodation for an excessive output or residuum ; indeed
we need not take alarm at a dilatation suggestive of a loss
of tone, if we have reason to believe that it depends on this only,
and not upon a textural dissolution. If however it be a result

chap, viii HYPERTROPHY AND DILATATION 33

of myocardial disintegration — as for instance in a heart of fatty
infiltration in an obese person, a state which is nearly always
associated with an unknown amount, often considerable; of
intrinsic degeneration also — then we may well be anxious. Un-
fortunately, in these persons, with their brawny chests, an
accurate delineation is not often practicable. But here we have
to halt, or even to return upon our steps ; the wall of an en-
feebled heart, so the unwary would say, must yield, and yielding
signify to the careful observer an increasing dilatation. So it
would seem, no doubt ; but so it is not — -not as a rule. It is a
strange thing, but one too generally acknowledged to need
arguing here, that frequently a degenerate ventricle does not
dilate ; indeed it may diminish in bulk. There is no direct
or known relation between dilatation and tissue impairment
(p. 14). As Lubarsch says, the mere size of the heart goes for
little ; a small and even somewhat atrophied heart may outbeat
a large one. Dr. Mackenzie J says, " Dilatation is merely
evidence of exhaustion of one function, namely, tonicity," and
" many severe cases of heart failure show no signs of dilatation."
Heart failure, as he well observes, depends upon many coefficients
which need analysis ; such as blood quantum, diastolic pressure
at moment of systole, friction, vessel tonus, and so forth. Even
were this not so. by the close attention recently given to per-
cussion in respect of bath treatment, we have learned that,
when controlled by orthodiagraphy, its many fallacies become
only too apparent.2 No experienced physician can doubt, it
is true, that percussion, taken with other information, may
be of great service as a corroboration, but its direct indica-
tions are to be accepted very cautiously. Again, we have no
definite means of distributing enlargement, say of the left
ventricle, between hypertrophy and dilatation, or between the
several chambers, if by other considerations we may guess at it.
Of the absence of dilatation in some such cases, even in many
of them, there is no doubt ; of the explanation there is much
doubt. We may wonder how a decaying muscle can keep its
tone ; for my part I suspect that dilatation depends upon the

1 Mackenzie, Jas., Brit. Med. Journ., Oct. 20, 1906.

2 See Weber u. Allendorf, Deutsche Arch. f. klin. Med. Bd. civ., 1912.
Vaquez's urinary volumes are, I think, open to the same fallacies.

34 MYOCARDIAL VALUES paet i

distribution of blood pressures. In any case, we cannot too care-
fully remember that there are two modes of dilatation, that of
yielding, and that of readjustment which essentially is not morbid.
Differences may lie in a contrast between focal lesions and
diffuse. In any case then dilatation is no gauge of the histological
condition of the myocardium ; we have admitted that in some
maladies, as in rheumatic fever, an impaired ventricle may be
attended with dilatation ; while in others, as in diphtheria, no
such correlation may be found, usually is not. I am disposed
to mistrust too ready a resort to logical explanations by
severance of one cardiac quality, such as tone, from another ; but
the endowment of tonicity may perhaps maintain in position
a decayed — even an extremely decayed — ventricle. And if a
wider percussion area after exertion be a test full of fallacies we
are still without a criterion. We cannot agree with the Leipzig
school that dilatation is any exact measure of the quality of
the myocardium. On the other hand, a temporary over-
distension of the left auricle may deceive us by setting up
an arrhythmia resembling for the time the perpetual mode.

If then the delineations of the heart's dimensions which
we obtain by percussion, or even by X-rays, give us no constant
or trustworthy criterion, what of auscultation % Well, we are
but little better off. It was in the discussion at Chelsea which
followed the reading of this paper that Dr. Hector Mackenzie
spoke of the cases of heart failure in persons who, a short time
before, after a searching examination, had been passed as sound
for life assurance. Yet the text-books complacently repeat that
feebleness of the apex beat, falling off in the tone and quality
of the first sound, and prevalence in a larger area of a thin acute
second sound, often signify myocardial degeneration. They
may ; but they are neither obligatory nor conclusive ; they
depend on transitory causes, and cannot be trusted as warrants.
Baumler repeatedly laid stress upon a weak first sound as thus
significant, even though the apex beat were undiminished and
quite palpable. The apex beat may be reinforced by recoil
from the aorta, but surely a weakness of the first sound is often
transient. As to defect of impulse, and defect of sound quality,
let any experienced auscultator ask himself how often he has found
himself misled by ill-definition of an apex beat, by a poor first

chap, viii EQUIVOCAL SIGNS 35

sound and a thin second — severally or even together — in patients
who proved in the end to be little or none the worse for the
variation. Among scores of such instances I will recall two,
both in men approaching threescore and ten. One of them had
been reduced in health by business mishaps and by a gall-stone
abscess ; the other after many years of keen and arduous
work was out of heart and anaemic. Neither was obviously
emphysematous ; yet in both the caridac impulse and area were
but feebly appreciable, if at all ; the first sound was poor,
the second thin and extensive. In both cases consultations
were held with " cardiac experts," and in both a diagnosis of
cardiac degeneration was pronounced, with little hesitation.
The one lived fourteen years afterwards, and died at the age of
83 of an incidental illness ; the other ten years later, at an
age nearly of fourscore, is still giving his distinguished services
to his country. In the first case the heart was examined after
death and found free even from atheroma. A fagged or anaemic
patient may, without any grave affection of the heart, present
for a while the defects of impulse and the quality of sounds
which in another might truly signify such a flaw. These
equivocal signs then are not criterions. In cases of athero-
sclerosis, with considerable myocardial deterioration, the impulse
usually is not reduced, it may be increased. Patients in
whom the sounds are good, or in whom a snappy second may
suggest no more than a stiffened aortic limb, a condition of
no great relative importance, often die suddenly, and at the
necropsy the left ventricle may appear stuffed with callosities,
and the muscular largely supplanted by connective fibre. Again,
the contrast of small pulse and full apex beat need mean no
more than a large area of vasoconstriction, as a soft and full
pulse may mean peripheral expansion.

There are other signs which are grave enough, if present,
but which are not constants, and so not warrants. One of
those is " the paradoxal diminution of ventricular pause (instead
of prolongation) after an extrasystole " (Hering, he. cit.). This
is not a matter of the vagus. Again Volhard states that in myo-
cardial weakness the prosphygmic interval ("Anspannungszeit")
is prolonged. He finds this the rule in pulsus alternans, but I
am not at all sure about this rule. The records of Mackenzie

36 MYOCARDIAL VALUES part i

and of Lewis do not seem to show it, and by expert sphygmo-
graphers it should be verifiable. If it be true, the rule would
be of considerable value in several directions. What, I think,
might be fruitfully worked at in chronic heart depreciation, by
the auscultatory or Pachon's method, is the curve of diastolic
pressures.

To turn from signs to symptoms. Syncopic or vertiginous
phenomena often accompany cardiac default ; but, whether
from dyspepsia, slight labyrinthine disturbance, vasomotor
atony, or other obscure cause, we are too familiar with this sub-
jective symptom to rely upon it as crucial in the diagnosis of
failing heart. If it be an item amid other signs and symptoms
of heart disease, it may indeed enter, and enter gravely, into a
diagnosis, as cumulative evidence ; but, taken alone, or indeed
without strong corroboration, it is very equivocal.

Yet surely by the pulse we ought to be able to make a fair
inference concerning the state of the heart. Nay, even here again
we are baffled. It has often been asserted that the profounder
changes in the myocardium are betrayed by an irregular pulse ;
but as our experience of cardiac disease has widened, we
have learnt that in the rhythms we have no constant or
regular criterion of cardiac values. Impairment of certain tracts
should, so we think, be surely betrayed by altered rhythms, but
we have no criterion even here ; we have learnt by autopsy
that even the tracts of Tawara may be seriously undermined
by disease without derangement of rhythm (p. 50) ; so likewise
may the nervous masses in the coronary sulcus. Lubarsch x
insists, that in old persons with coronary sclerosis, callus, and
fibrosis, fatty degeneration of the a-v bundle may prove to
have been extensive without the least functional disturbance.
On the other hand, in old hearts there are subtle and perilous
changes below the microscopic horizon, as revealed by the
experiments on the stabilities of old hearts as compared with
young ones (p. 475). I think then I shall meet with a general
agreement in an opinion explicitly given by von Leyden,
Baumler, Ebstein, and many others, that in the pulse we have
no guide to myocardial damage, acute or chronic. Under the
cover of normal rates, rhythms, and pressures, decay may pro-

1 Lubarsch, Herzpathol. Jahreskurse f. drtzl. Fortbildung, January 1911.

chap, viii EQUIVOCAL SYMPTOMS 37

gress nearly to the utmost ; while positive variations of the
pulse may mean little.

Notwithstanding, two variations of the pulse are there,
which, when present, are ominous ; these are a persistent rise of
rate and the pulsus alternans. On pulsus alternans I will not dwell,
for Traube, and of late Professor Wenckebach, Dr. Mackenzie,
and Dr. Lewis, have urged, a little too positively, that this
change — the true as contrasted with the pseudo-alternans — is
invariably a herald of heart failure (see refs. p. 58). How-
ever, as the sign is no common feature of such default, but a
somewhat rare one — one more often absent in failing myocardium
than present (Gallivardin found ten cases in twelve months) —
it is as a clinical criterion inconstant. Dr. Mackenzie warns
us that, if imperceptible to the ringer, pulsus alternans may
be revealed nevertheless in a sphygmographic tracing. It is
to be found in the falling blood pressures of hypertrophy with
dilatation of the left ventricle. Prolongation of the pause after
an extra-systole — extra-pulse delay — which may be measured
on the sphygmogram, is a phenomenon of the same order. The
only exception to its significance, as a note of disease, is an occa-
sional appearance of it under the action of some poisons. The
researches of H. E. Hering x on the causes of pulsus alternans,
if not strictly relevant, are so interesting that one is tempted to
mention them here. The phenomenon depends, so it appears,
on variable refractory periods of the fibres, some fibres being
late in response, so that partial asystoles are summed up in rhyth-
mical recurrence. Thus vagus stimulation, by slowing beats,
though occasionally reinforcing pulsus alternans, may reduce it,
and substitute a continuous hyposystole. Such interferences
suggest that between the myocardial fibres there are some obscure
differences in value — at any rate in certain hearts ; or that the
vascular supply may be unequal. The accelerans, on the other
hand, as it quickens the rate, may increase the alternation, or
by modulation of the refractory discords make it manifest. Thus
the cardiac nerves can influence the systolic volume not only
directly, but, by modulating the refractory phases, indirectly also.

The other way in which the pulse may suggest decay of
the myocardium is by a persistent change of rate, whether of
1 H. E. Hering, Zeitschr. f. exp. Path. u. Therap., 1908-1909.

38 MYOCARDIAL VALUES part i

acceleration or of retardation ; though here again we have not
a constant but an inconstant criterion. We shall see (p. 50)
that the tract of Tawara may be destroyed, or profoundly marred,
without perceptible effect on the pulse ; and it is common ex-
perience that a normal rate of pulsation is consistent with deprava-
tion of the left myocardium at large. Notwithstanding, it has been
strongly impressed upon me that a permanent change of rate, either
way, is ominous of failing heart. On bradycardia, or again on tachy-
cardia, I need not insist — these conditions are better and better
recognised every day ; I will insist rather on the less familiar
sign of simple acceleration. Let the pulse of a certain man be
known as habitually 70, at rest 65-70 ; and let this pulse rate be
found to have become habitually ten more — that is, 80-85, on
slight movements rising to 90-100 or over ; and let this change
show no substantial alteration under prolonged rest, let it fall,
that is, under whatsoever rules of tranquillity of mind and body,
never below 80-85 ; then heart failure is in the offing. If, more-
over, with this acceleration there be attacks of faintness, or of
slight dyspnea or vertigo on moderate effort, the failure of the
heart's muscle is at hand ; and in elderly persons but little
amendment can be promised. Of course, before a final opinion
is given, any possible nervous influence, or the influence of coffee,
tea, tobacco, which in later life often become less well tolerated,
or the passage of an infection, such even as a catarrh, will be
reckoned with. Two or three cases of this significance have im-
pressed themselves on my memory : one of them in a patient
of Dr. George Johnston, of Ambleside, a country gentleman
of advanced years, but for his years of great activity, both
of mind and body. In climbing over a stone wall into his
own park he was aware of some little faintness, which might well
have been a transient affair of little importance. However he
was persuaded to send for Dr. Johnston, who found his pulse then
at a continuing rate of 100-110. There was little or no evidence
of general arteriosclerosis, and arterial pressures were normal.
It seemed to the patient and his friends that to keep a vigor-
ous man, with all the appearance of health, permanently
at rest, or only to allow him to drive out in his carriage,
was a serious decision. I saw him with Dr. Johnston twice
at an interval of twelve months ; and in spite of the demurs

chap, viii EQUIVOCAL SYMPTOMS 39

of his friends, who hinted at hypochondriasis or neurasthenia —
neurasthenia does not often come on unaccountably in the later
life of persons previously healthy — I could not but support Dr.
Johnston's injunctions ; for if during complete rest the pulse rate
were reduced under 100, or sometimes even to 80, on effort it
returned at once to the higher numbers. Gradually, in the course
of the next eighteen months, syncopic sensations at stool or under
any considerable effort, increased upon him ; further and more
ordinary symptoms of cardiac failure set in, and he succumbed
without any abiding amendment. But here again, as with
pulsus alternans, we have no criterion ; acceleration of rate
in myocardial breakdown is an inconstant phenomenon, and
indeed in certain peripheral relaxations may continue for some
while without any myocardial disease.

We approach a little nearer to a criterion by calculating the
amplitude-frequency product, taken in the several positions of the
body, lying and standing ; and also after certain measures of
effort ; in a degenerate heart the pulse, instead of quickening,
may be retarded. This test merits a more careful trial than it
has received. A fall of maximum pressure may in some cases be
favourable, if the minimum fall also ; but if with fall of maximum
the minimum rises we fear lest the heart be yielding. Martinet
(loc. cit.) urges that the urine also should be valued at the same
time ; and, as we have seen again and again in these arguments,
unless a very broad basis of comparisons be made, variations
in other conditions — in the peripheral circulation for instance —
may fog our picture. Core puts it (loc. cit.) that when between
blood pressure, pulse rate, and clinical symptoms there is no
correspondence, the fault lies with the heart; but one of my points
is that for a long period clinical symptoms may be equivocal or
none ; and we have seen, earlier in this work, that the relations
between pressures and rates are very variable (Vol. I. p. 43, etc.).

Although the familiar test of recovery of pulse rate after
exertion is not without value, we see in convalescents,
even from non- infectious illness, that recovery rate depends
largely upon peripheral tone and other coefficients of stability.
In unaccustomed persons subsidence of effort-acceleration is more
protracted than in the accustomed. Ergostat and other effort
tests (see e.g. Sternberg u. Schmidt, Munch, med. Wochenschr.,

40 MYOCAKDIAL VALUES part i

Jan. 28, 1913) are of little use ; the psychical factor (boredom,
or expectant attention) is large, and the adjustments difficult.
Janowski, after long and various effort tests, was surprised to
find, as I had found, how fallacious they are. (See Vol. II. p. 43.)
Of the many other and more familiar symptoms of heart
failure, such as dyspnea, slight oedema, albuminuria, cyanosis
of ears and lips, fulness and tenderness of the liver, pulmonary
crepitations, arrhythmia perpetua, etc., I need not speak ;
more or less sudden heart failure is too frequent without
any of these features ; in any case they usually signify late
phases of the malady, speaking only too plainly ; but too late.
Of the many symptoms to be discounted, I will refer only to
arrhythmias pertaining to the extrasystolic kind, which in some
cases are, to the inexperienced observer, terrific. One of the
worst of these clumsy, bustling hearts I examined three or four
years ago with Dr. Davies of Histon, in an elderly gentleman, who,
after a little treatment, was safely permitted to go about his
business ; and now I often see him engaged, apparently without
disablement, in public or social occupations. Another case, almost
as troublesome, I witnessed about ten years ago in a gentleman,
now living, then some 78 years of age ; at Homburg he made a
good recovery from some " gouty " conditions, and his heart
practically recovered its steadiness. Almost as I write these words
(1912), he has, on the borders of fourscore and ten, successfully
weathered an attack of genuine influenza. In these and such
cases of this kind of disorder, even if the heart never wholly re-
covers a normal rhythm, no harm may come. The symptom group
of every such case must, of course, be sifted, for, on the other
hand, in pneumonia or diphtheria, or aortic regurgitation, even
a mere extrasystole with prolonged pause may be the first
presage of heart or peripheral failure. Some recent teaching
about the comparative innocence of " extrasystolic arrhythmia "
must be taken with salt. Again and again in cases of chronic
and apparently stable valvular lesion have I found this
phenomenon to be a harbinger of evil ; especially in aortic
regurgitation. Not at once, not perhaps for many months,
or even a year or more, yet sooner rather than later,
too often it proves to be a sign of breakdown. If a sub-
stantially healthy heart may be, and often is, disturbed in

chap, vni THE ELECTROCARDIOGRAM 41

this way by some extrinsic cause, in a faulty heart a new
irritability may be a sign of fatigue. In such cases the inter-
mittency does not vanish, or but for a while ; it hangs about and
never quite takes its leave. If an intermittent heart be throbbing
and uneasy, or even painful, there is the less reason to be afraid
of it ; harmless extrasystoles may pass imperceptibly, but the
intermittences of a failing heart are often also unfelt.

Sphygmomanometrical observations have proved, hitherto, to
be of no use in the detection of myocardial disease. That under
prolonged high arterial pressures the heart may be defeated is
true enough ; but this is not a primary myocardial decay. A
test of blood velocity, which is probably always reduced, would be
more trustworthy, but it is reduced in atherosclerosis, and in
persons who live, notwithstanding, to advanced ages.

For the electrocardiograph claims in this direction have
been extravagant ; in time we may get some definite or even
decisive signals from it ; but the F(T) wave is at best only the
electric expression of the systolic act ; it gives the duration
of reaction, not the outflow nor the energy. The F(T) wave of
a heart proved after death to be depraved may be good
enough. Einthoven himself is of more chastened temper ;
but he is still hoping thus to calculate the weights of
the right and left ventricles. And there is another possible
opening : in general as age advances, the ordinary height
of the F(T) wave diminishes in relation to J(R), and in
the dying heart it disappears altogether. Dr. Scales in our
laboratories thinks that splintering of the curve suggests senile
cardiac decay ; but one such case at least I remember in a
man who some time later was in good health. Again Eiger 1 states
that, in dogs, on chloroform or ether inhalation the F(T) wave
flattens out, and even may become negative ; cardiac metabolism
being profoundly altered. Strubell 2 states that up to the age
of 50 this after limb of the curve is well marked, and if with in-
creasing years it becomes gradually less, it does not quite die out.
If under the age of 50 it wanes, the muscle is somehow not up
to standard ; the normal proportions of the healthy adult being

1 Eiger, Prager med. Wochenschr., 1911, Nos. 23-24 ; quoted Arch, des mal.
du caur, avril 1912.

2 Strubell, "Kl. d. Electrocardiogram," Deutsche med. Wochenschr., 1912,
No. 21. (Doubt has since been thrown on these opinions.)

42 MYOCARDIAL VALUES parti

J : F : A as 100 : 25 : 10. On the A wave age, pressure, and
heart size have little or no effect. In young people with moderate
pressures the J peak is said to be relatively lower, F relatively
higher ; in old people the reverse. Thus the ventricular coeffi-
cient y may wax with age, pressures, and size of heart. But these
rules are open at least to much exception ; e.g. in diphtheritic
myocardium the electrograph shows no great variation.1 Stru-
bell advises, if an estimate of myocardial value is to be obtained,
that records of manometer, X-rays and electrograph should be
compared, on which comparison he formulates for persistent high
pressures four rules, as follows : (a) high final wave, with
auricular wave unaltered, signifies high pressure with good
heart ; (b) the same with a higher auricular wave suggests a
further stage of the condition, with growing stress upon the lesser
circulation ; (c) the same with a waning final and large auricular
wave, a failing ventricular muscle ; (d) the same with a
negative F, myocardial failure. By ray method a dilated aorta
would often then be seen. Kahn of Prague,2 by obtaining
parallel curves of electrocardiographic and heart sounds, found
some interesting relations between heart tones and heart work ;
such relations, as I have said, so long as merely subjective, are
not trustworthy nor recordable, but if traced on paper they may
give us useful aid. For the present of course such methods are
out of the reach of ordinary clinical work. Vaquez,3 with whom
I have had some conversation, contests Nicolai's opinion that the
electric curve can indicate the size, if not the value of the heart's
contractions. Professor Mines agrees with Burdon Sanderson
that the final wave F(T) is not crucial ; it signifies the passing off
of the process with a difference of potential in several parcels
of the cardiac complex towards diminution of the excited state.
It is not likely that it would pass off symmetrically or simul-
taneously in all regions of the muscle.4 It is in nature accidental,
and can be no sign of failing cardiac value. Indeed it can be
varied under experiment. For instance, in a typical case of

1 Rohmer, F., " Electrokardiogr. u. anat. Untersuch. Diphth'herztod,"
Zeitschr. f. exp. Path. u. Ther. Bd. xi., 1912.

2 Quoted in various journals.

3 Vaquez, " Sur la signification de 1' electrocardiogram," Soc. de Biol., juillet
1911.

4 Mines, Journ. of Physiol, vol. xxvi. No. 3, June 19, 1913.

chap, viii THE ELECTROCARDIOGRAM 43

pulsus alternans, although the unequal values of the two diastolic
pauses were seen on the sphygmogram, the electrocardiogram
betrayed no difference in amplitude of contraction ; no variation
of ventricular energy was apparent. In this conclusion Mines
supports the previous opinions of Hoffmann and of W. E. Hering
to the same effect. Hering has shown x how far stimulus and
reaction capacity are not directly proportionate ; and that
electrical stimulus is no complete test. As I have urged on
former occasions, this is the curve not of the contraction, but of
the quantity of the electrochemical changes which determine a
contraction. Chemical stimulus, which is not identical with an
electrical stimulus, might, if measurable, tell us more, especially in
pathological states ; still it would not indicate reaction capacity.
As we have to consider heart nerve tones against heart muscle
tone, so Hering, Monckeberg, Aschoff and others point out a
distinction between the contractile power of the heart, and the
formation of stimulus ; infirmity or even death might be due not
to waning contractile power, but to failure of stimulus. Hering 2
says that stimulus (Reizbildung) has also its reserves, its potential.

So far then the polygraph and electrocardiograph have
done us invaluable service by revealing laws of centres of
stimulation and dissociation, but so far have done little for the
estimation of capacities, of intrinsic values. Vaquez warns
the electrocardiographer not to exaggerate the value of his
records, for in his opinion these are of less value than X-ray
observations taken daily.

I have alluded to the method of measuring ventricular
contraction before and after measured efforts, a method of
which the difficulties, complexities, and possible fallacies,
psychical and otherwise, are only too plain. It is indeed
premature to say, as some are saying, that even from this
variation a criterion of the state of the myocardium can be
obtained ; we have for instance to make sure of the inclination
of the heart's vertical axis (Waller) ; still a waning of this wave,
and yet more a negative oscillation, may prove, under due con-
trols, to have a definite pathological significance, especially if the
pauses are protracted. On the other hand, a persistence or

1 Hering, W. E., Pflvger's Archiv, cxliii., 1912.
2 Hering, W. E., Deutsche med. Wochenschr., Sept. 11, 1913.

VOL. II D

44 MYOCAKDIAL VALUES part i

recurrence of the juvenile type in adult life may signify a nervous
factor.

When fibrillation of the auricle has set in, with arrhythmia
perpetua, we have before us no doubt a grave degeneration of
one limb of the organ ; for the cases in which it occurs, and at
the comparatively advanced stage when it occurs, it is ominous
enough ; though as a signal belated. And it seems still neces-
sary to state clearly that auricular fibrillation is not a cause of
cardiac failure but one mode of it. Fibrillation of the ventricle
indeed is one of the modes of sudden death ; it is hardly con-
sistent with survival.

Two other tests of cardiac values have been suggested ;
Abram's reflex and Livierato's reflex. By the first we chafe
the cardiac area with a towel or india-rubber glove, then, if the
heart be active, the percussion area should diminish ; if it be
weak there is no recession, or but little. By the second we
make a number of short, deep, sudden strokes in the middle
vertical line, xyphoid to navel ; the heart's area should move
inversely as the cardiac capacity. Surely these methods are
open to much fallacy. Etienne 1 however reports a case of a
gouty man with poor irregular pulse, dyspnea, and some
pulmonary oedema, in whom, to both these reflexes, the heart
responded well ; he underwent the Roy at cure and did well ;
and continued well, being able to climb hills, and so on.

I must not tarry to discuss the various devices for testing
cardiac reserve proposed by Katzenstein, Graupner and others ;
suffice it to say that, while some of them are inconvenient,
none is effectual or even approximately indicative of the avail-
able capacity of the heart under observation. The fallacies of
unstable peripheral tone, especially under tests more or less
vexatious, are alone enough to confuse the results.

It is said that the rise of venous pressure due to effort is
greater in cases of cardiac insufficiency ; but what standards
have we 1 Such verifications are very difficult, and, when done,
we have no analysis of the many coefficients concerned.

How little we can read cardiac capacity from blood pressure
records we have seen abundantly in the chapters on Arterio-
sclerosis. It may be true, as Sir L. Brunton suggests, that in

1 Etienne, Paris mid. t. 46, 1912.

chap, vni MANOMETRIC RECORDS 45

old people a slackening of arterial pressures may signify a
gradually failing heart, if, that is, the patient be watched over a
long period, and the readings are consistent. Max Bruckner x has
studied these indications in about 200 cases of diphtheria in the
Children's Hospital at Dresden. The results were, so to speak,
quite capricious ; out of them emerged no trustworthy rules of
diagnosis or prognosis. Drops of pressure, perhaps vaso-
motor, passed off harmlessly, while cardiac failures were not
definitely thus foretold. In grave myocardial infection a drop
of 50 mm. might occur with the heart failure, but of such
defaults there were no premonitions ; that is to say, clinical was
not preceded by manometric evidence, or not with any regularity.
The opinion that in acute infections the failure is often
peripheral and vasomotor rather than primarily cardiac, has been
gaining ground ; as for instance in the late Professor Curschmann's
clinic.2 This alternative, or supplement, attributed by some to
poisoning of the adrenal bodies with suspense of their function,
must not be forgotten ; but it would be a dangerous confidence
to take such a view of the majority of these cases. In no circum-
stances is our lack of any clinical warrant of cardiac capacity,
and of cardiac stability, more painfully manifest than in the acute
infections. Again and again, in such diseases as diphtheria and
scarlet fever, young lives are maimed or cut short by heart
failure without more definite warning than the vague fore-
bodings cast by the shadows of like cases gone before. The
young man or young woman may, so far as clinical observation
can tell us, be going on well, and yet be within a few minutes of
eternity. A persistent increase or decrease of pulse rate may
hint at the danger ; but more often there is no such sign of peril.
Now, to drop out in this way, a heart must have been gravely
affected for some little while before. Again, after an infection as
mild as a " common cold," more commonly after an influenza,
the patient has no warning that his convalescence is incomplete
until he engages in some effort, such as a game of football, and
then finds himself invalided for many a month to come. Without
any clinical manifestation his heart had become the seat of occult
disease. Here again our only guide is crude experience ; we

1 Bruckner, M., Deutsche med. Wochenschr., 1909, No. 14.
2 See also Passler and Roily, Munch, med. Wochenschr., Oct. 1902, p. 1737.

46 MYOCAKDIAL VALUES part i

have no criterion. Tanaka 1 declares how remarkable it is that
a " heart often functions well up to the moment of sudden
death," yet after death the myocardium reveals disease both
extensive and profound. The ventricle may or may not be
dilated. It is a little out of my subject, but I am tempted here
to say how marvellously the myocardium recovers after infections
in young people. I remember a paper read last year (1912)
by Heffter, at the Minister Meeting of the Deutsche Naturforscher
u. Artze, in which a very competent histological report was
given of the heart of a boy who, while recovering from diphtheritic
heart, died of cerebral embolism. The regenerative process was
very evident, and included a new development of muscular fibres.
The paper seemed to me to be one of much interest and
importance, for the author followed up the report with more
evidence of the same kind.

Thus baldly I have tried, from the point of view of the
physician, to show how indefinite, inconstant, and obscure
are the symptoms and signs of myocardial insufficiency ; let us
see then what the pathologist has to say — if with his scalpel and
probe he can offer us more definite measures of cardiac capacity.
We shall say to him, surely you ought to discover why the patient
died 1 why his heart, or the other man's heart, broke down
without warning ? or in any case what was the critical point at
which its resources could no more avail ? But too often in his
turn the pathologist gives the same uncertain sound. In this
heart he found too little to account for death, in that too much —
the patient had no business to have lived so long. On grounds
as insecure as those of the physician, he finds one heart which,
with comparatively little or even no evidence of decay (Cabot),
surrendered at the first summons, or became suddenly in-
sufficient ; and, conversely, another which by the very extent
and chronicity of decay testified to the long period during which
it had managed to wage an unequal fight with silent tenacity.
From the side of morbid anatomy then the want of parallel,
of apparent correlation, between the physician and the pathologist
lacks nothing of its emphasis.

But, at the outset of this side of the matter, I would with

1 Tanaka (of the Gottingen Pathological Laboratory), Virchow's Archiv,
vol. ccvii., 1912.

chap, viii FATTY DEGENERATION 47

all due deference suggest that in many a report to the physician
from the post-mortem chamber, the histological changes described
are consistent with, or even declare, rather the effects of the
decomposition of death than of disease during life. I have had
to discard many a note recording blurred striation, nuclear
alterations, " hyaline " change, etc., when recorded without any
note of date after death, or of the state of the atmosphere.
Indeed so common is the tendency in the viscera to a focal
distribution of their lesions that one may wisely, I will not
say reject, but regard with suspicion, reports of diffuse and
uniform myocardial disintegration, as possibly due to mere post-
mortem decomposition.

Of the kind of detriment called " fatty degeneration "
opinions of late have undergone some fluctuation ; the term,
for a while discarded, seems to be returning into use, though
with some difference of interpretation (p. 58). The distinction
between fatty degeneration and fatty infiltration, though the
extremes are rare, still holds its ground, and between them lies
every grade of transition. If in the obese heart much of the fat
is to be traced to an interfibrous penetration, yet on the other
hand in very few such hearts is this penetration unaccompanied
with some deterioration of the muscular fibres themselves. And
if in "fatty degeneration" the droplets of fat may be but particles
of unassimilated nutriment rather than a disintegration of muscle
cell, or a metamorphosis of albuminous structures into fat,
and if indeed we cannot say that simple fatty accumulation
is a myocardial regression, yet even delay of absorption and
assimilation seems to signify some alteration of chemical change,
if in rate only ; and if so to signify some modification of
muscular energy. Aschoff however goes so far as to suggest that
this fatty manifestation may signify an excess of physiological
activity. It is certain at any rate that, in the midst of it, the
fibres and their striations may still be well defined (Aschoff,
Lubarsch, and many others). In old hearts with coronary
sclerosis Kent's bundle itself may be thoroughly " fatty," yet
with no apparent conductive decay. Fatty content must
be contrasted with fatty decay ; it may be due to a passing
torpor of function, or to slow arterial and lymphatic circulation ;
or occasionally to the arrest of death. The vacuoles we

48 MYOCARDIAL VALUES paet i

read of are probably artefacts. The nuclear reactions should
of course be tested. In diphtheria, beside the fatty deposits,
the muscle fibres also are obviously diseased. In some toxic
cases it would seem that the " fatty " state may be established
in twenty-four to thirty-six hours. However, what I have
to emphasise is the agreement that even well-marked fatty
deposits, severe and diffused, may appear without any clinical
evidence of heart failure ; so that in this context pathology can
provide us with no criterion. That, as I have recently seen
stated, the " fatty heart " is to be known by dilatation or by
irregularity of rhythm cannot be maintained (p. 34) ; these
coincidences are quite inconstant.

In rheumatic myocarditis (Romberg, Cowan, Carey Coombs)
sudden heart failure is less common ; usually it is so combined
with dilatation and valvular disorders that clinical symptoms are
not wanting. Interesting as the changes are from a histological
point of view, I must not in this context dwell longer upon them.
Nor do the distinctions, definite or transitional, demonstrated
by Dr. Carey Coombs and others, between acute interstitial
and parenchymatous myocarditis much concern us here. We
will pass on to chronic myocarditis.

In so-called " chronic myocarditis " again, probably not
strictly an inflammation but partaking rather of an atrophic
or degenerative nature, we find no closer correlation between the
clinical and the pathological series. Cabot, in a very search-
ing report * — one in which he compared clinical and patho-
logical notes taken independently — says that he has quite given
up attempting to diagnose " chronic myocarditis " ; "in it
diagnosis is a mere matter of luck. It has no clinical symptoms,
no characteristic physical signs." So this point needs no further
pathological discussion.

But from the clinical point of view I must return for a
moment to fibrosis of the myocardium, a change which an
eminent student of heart disease but a short time ago assured
me was of great clinical importance. To this I demurred, for,
as I have said (pp. 11-18), this fibrous invasion may be wholly
without clinical correlations. Many years' experience has
convinced me of the truth which Cabot again (loc. cit.) has
1 Cabot, Massachusetts Gen. Hosp. Reports, October 1911.

chap, viii CARDIAC FIBROSIS 49

lately emphasised ; namely, that " not infrequently gross fibrosis
of the myocardium is found in hearts which had been perfectly
efficient during life." Dr. Hale White x also says of a fibroid
heart that it is practically undetectable. This paradox is true
of both the forms of cardiac fibrosis of which I have spoken — of
the diffuse form described by Dehio 2 in 1899, and the focal form,
in which the wall of the heart, especially of the left ventricle, is
beset with callosities ; though this, if extensive, is by far the
graver lesion. These callous nodules or lumps were at one time
attributed only to local ischsemia due to a closure of a coronary
branch, by infarct or by sclerosis. Histologically however they
do not essentially differ from " myocarditic " effects of other
origin ; moreover, recent research has demonstrated many a callus
towards which its particular coronary twig was open (pp.21-23).3
But these nodules, often old foci of toxic myocarditis, are not
always to be found by simply slicing the ventricular wall with
a knife ; sections must be made and stained. Conversely,
Kanthack and I, in investigating the effects of coronary disease
on the heart, demonstrated repeatedly that these arteries might
both be very gradually blocked by atherosclerosis, and yet the
myocardium keep normal enough for the age of the patient.
Clinically speaking, with such hearts patients may, as Dr. Hale
White says, die suddenly ; but we have no criterion of the
change, nor can the pathologist tell us how or when it causes
death, if indeed it does directly cause it ; which is doubtful.

Diffuse or dystrophic myocardial fibrosis is a different condi-
tion. Dehio attributed it to venous stagnation, comparing such
hearts with "cardiac kidneys" and the like ; and it is true that
dilated ventricles are often fibroid. Still, I have examined
many hearts presenting this fibrosis in which evidence of venous
congestion was not obvious. However, I must not leave signs
for points of pathology which from that point of view I have
dealt with already (p. 9 et seq.) ; in respect of symptoms suffice
it to say that cardiac fibrosis, so far from being a cause of

1 Hale White, Clin. Journ., November 29, 1911.

2 Dehio, Deutsche Arch. f. klin. Med. vol. lxii.

3 Ebstein, " Schwielenbildung im Herzen," Zeitschr. f. klin. Med. Bd. ii.
S. 97 ; Fahr, Vir chow's A rchiv, February 1909 (and Baumler, Gierke, and Ziegler
agree). For presence of fibrosis in hearts which probably were efficient see
(p. 18) Gennari, Arch, per sci. med., December 1905.

50 MYOCARDIAL VALUES pakt i

cardiac failure, seems not infrequently, as in hypertrophy with
dilatation, to have some conservative value. We have seen that
connective fibre is a less resilient tissue, and its elastic limit
narrower, so that once overstretched it cannot well recover ; but
it is tougher. Syphilitic fibrosis is, of course, another matter ;
any effect this variety may have on the cardiac function depends
on its site. "Cardiosclerosis" then, whatever its propriety as a
name for this condition, — one however to which it has not been
definitely attached: I have said that we never succeeded in
ascertaining precisely from Huchard, or from his disciples, what
they meant by the name, — has in this sense no clinical con-
notation. It was adopted for logical symmetry rather than
to express the complexities and elusiveness of nature.

Let us now pass on from the histological nature to the seats
of lesion. Is it less the nature than the position of lesion
or decay which determines the mortality ? Here again I
fear the answer of the pathologist is still equivocal, though it is
true that closer methods of observation may prove more en-
lightening. The lesion, or the critical lesion, may be overlooked ;
for instance, Falconer and Duncan,1 beside valvular lesions in
a certain heart, found diffuse lesions in the right auricle (less in
the left), while, save for a slight perivascular lymphocytosis,
the ventricular muscle was normal.

In respect of site our thoughts turn promptly to the tract of
Tawara, and perhaps to Wenckebach's area about the superior
vena cava, for we must not be content to say that lesions in this
area set up disorders of rhythm only. We readily suspect, in
such a concert as the function of the circulation, that rhythmical
discord may abut upon and issue in defective work. At first
sight it seems that even if scattered focal lesions — such as
those described by Carey Coombs, Poynton, and others — come
short of gravely disturbing conduction, yet such a check must
follow a more diffuse and general invasion of these structures ;
for ventricular automaty, detached from the cardiac system, is
certainly less effectual. Many cases are published in which
cardiac function persisted normally in spite of what appeared to
be (as in Dr. Raw's sarcoma case and many others) complete
destruction of the conductive tracts (p. 36). But to say in a
1 Falconer and Duncan, Heart, vol. iii. Part II. para. Tachycardia.

CHAP. VIII

KENT'S BUNDLE

51

particular case that the destruction was complete is to beg the
question ; only a jury of experts could come to this decision (see
note 3). Syphilis, by its proclivity for the septum, especially
menaces Tawara's tract. Now some observers are of opinion that
this tract, whether by its looser texture or by its peculiar blood
supply by a branch from the right coronary artery, has in its
disease some independence, be it more or less, of the rest of
the heart.1 Spots of hseniorrhagic and leukemic exudation,
aortic rheumatic foci, and the like are found not infrequently
in this tract, especially in the left limb of it, when absent in
other quarters of the heart. Tanaka insists, as I have done, on
the curious maintenances of heart function and of medical con-
fidence in not a few cases in which the myocardium and conductive
tract proved to be in extremes of fatty degeneration, until in a
moment death brought all to an end.2 This, he says, as Dr.
Hugh Anderson had illustrated in the cat (Vol. II. p. 475), is
especially characteristic of old as contrasted with young hearts.
But we must not, I think, make too much of this alleged
independence ; decay proceeds as often from the myocardium
to the bundle and knot, and again, as Dr. Coombs has shown,
both tracts and myocardium, if unequally affected, are often
attacked simultaneously. Saigo 3 examined 100 hearts from
this point of view, and concluded that rheumatic nodules do
often arise in the bundle ; that regressive processes also —
such as fatty vacuoles — come early in it ; but that in brown
atrophy and fibrotic hypertrophy the bundle may be involved,
or may be free, or nearly free. Lewis, Coombs, and others
have shown by careful methods that transient ventricular lag
may be revealed in such infections as rheumatic fever, diphtheria,
or influenza ; yet they will probably agree that such clinical
phenomena are rare, and when present indicate the seat rather
than the degree of the lesions. A block of slight degree may
coexist with widespread myocardial injury ; and conversely.
Frequent as are dots and foci of toxic lesion in and around
the conductive strands, alterations in the auriculo-ventricular
sequence are surely exceptional (Poynton, Coombs). And in

1 See Tanaka ; loc. cit.

2 These anomalies Prof. Kent has since explained, B. M. J., July 19, 1914.

3 Saigo, Ziegler's Beitr. Bd. xliv.

52 MYOCARDIAL VALUES part i

young hearts, under proper treatment, happily they are usually
transient, and are completely repaired with the formation of tiny
scars, and even some redintegration of nobler tissue (p. 46). In
old hearts of course the mischief may be irremediable, but on this
well-worn subject I need not dwell. A patient of Dr. Canney of
Cambridge, aged about 65, whom I also saw repeatedly, seemed
to recover from a grave attack of scarlatinal myocarditis. For
some months his state was perilous, but he got actively about
again, and after six months' absence from work and change
of scene, he returned to his usual exercise, bicycling quietly up
and down hill, and the like. Some months thus passed with
no sign of ailment or of morbid cardiac action ; but one evening
after complaining for an hour or two of feeling very cold, he went
out to certain duties, and in the midst of them turned faint,
rose to leave the room, and died in a few minutes.

Lubarsch x on this complicated problem investigated 500
hearts ; in many he found changes, such as acute rheumatic
nodules, predominant in and about the tract, especially the left
limb of it. Brown atrophy he found to occur in both myo-
cardium and tract. His observations may be summed up thus :
in moderate focal fatty myocardium the limb of Tawara's
tract may be quite free ; or in extreme and widespread focal fatty
myocardium the a-v bundle may be very slightly affected ; or
fatty change may be quite isolated in it, even the papillary
muscles being free (but this is rare) ; or fatty change may be
marked and extreme in the a-v tract, with very slight myocardial
affection, say slightly in the papillary muscles only ; or fatty
change, moderate or much, may be practically alike and equal in
both myocardium and bundle ; finally, Lubarsch thinks these
variations are dependent upon vascular conditions, such as local
retardations of blood velocity.

In Tanaka's cases of diphtheria affection of the bundle was
five times more, three times less than the rest of the musculature,
and four times the incidence was equal. " Only once was an
almost isolated bundle-affection found." In the bundle the
changes are more diffuse. " But," he concludes, " a sudden
failure of the heart can also come about without essential lesion

1 Lubarsch, Jahresb. arzt. Fortb., 1911. See also Amer. Journ. Med. Sci.,
1912.

CHAP. VIII

KENT'S BUNDLE

53

of the bundle ; occasionally indeed arrhythmia appears without
any marked degeneration of the bundle."

In one of Lubarsch's cases, in which dissociation was complete,
while in the myocardium were found after death large focal
callosities, in the bundle were only small ones, with some fresher
spots of exudation and minute hemorrhagic points ; none ex-
tensive enough to rupture continuity. On the other hand, many
cases are published (by Reinecke and others J) in which, under
what seemed distinctly to be complete demolition of the bundle,
there was during life no dissociation. In one case 2 the whole
bundle was calcified ; in others in which the tract seemed broken
up dissociation was often incomplete ; sometimes there was
only slight retardation. Dr. Coombs' researches again make it
probable that acute rheumatic or septic toxins may far invade
the tract without any characteristic symptoms during life. Con-
versely, cases of heart-block occur in which expert pathologists
discover no disease in the bundle.3 If one limb of it is affected
there may be incomplete dissociation. In a few cases tachy-
cardia has been observed ; I have seen two such instances. I
will consider presently how far intrinsic and extrinsic causes
(bundle, vagus, bulb) must co-operate ; or again how far
chemical perversions may be concerned in arrests of the heart.

I make no excuse for dwelling at this length on the patho-
logical relations of the bundle and the myocardium, for in them
we may find some explanation of the obscurity of the causes
of continued cardiac function on the one hand and of sudden
cessation of it on the other. In some bundle cases, probably
in most, the proper symptoms of dissociation are present, but
in some they are absent ; and as yet we have no histological
elucidation of this inconstancy (see however p. 51, note 2).

Attempts have been made to test myocardial values by
drugs, but with little that is promising. A drug may affect the
heart muscle directly or through its nervous machinery, motor
or afferent ; it does not seem probable that we shall make much
out of this kind of test. We cannot establish controls.

I have alluded more than once to the part of the nerves

1 See Deutsche Arch. f. klin. Med., 1908.

2 Nagayo-Aschoff, "Adams -Stokes Sympt. -komplex," Zeitschr. f. klin.
Med. Bd. lxvii.

3 E.g. Fahr, Virchow's Archiv, 1907, vol. 188.

54 MYOCARDIAL VALUES part i

in cardiac function, and so in the clinical surprises which we are
discussing ; but the nervous coefficients in these functions are
very dark. Is it by means of nervous influence that a heart
which is the seat of advanced disease may be carried along so
far and so efficiently as again and again to deceive the clinical
observer outright ? We know that the heart is thickly beset
with nervous ganglia and plexuses, that these are motor in
function, and that much, if not all, of the harmony of the circula-
tion must depend, and intimately depend, on their integrity ; but
our new interest in Kent's and Tawara's tracts has diverted
research from these nervous governors. We may destroy aortic
cusps without immediate heart failure, we may poison the
myocardium into extreme fatty change without immediate
heart failure ; but if with the soundest myocardium we cut the
vagi, or even cut one only, the organ may promptly stop — at any
rate in dogs and cats.1 Kronecker's experimental determination
of a nervous co-ordinating centre in the upper third of the inter-
ventricular septum is well known ; a needle puncture here (in
the dog) produces fatal delirium cordis, a result not to be
obtained by puncture anywhere else. The morbid histology
of the nervous cells and afferent and other fibres of the heart
is little understood ; even their normal anatomy is vague, and
the pathological records are dubious. Our methods may be
inadequate, but hitherto the allegations of morbid changes in
the nerves do not amount to proof. Vagus alterations have been
reported, but on scanty evidence ; yet if the nervous strands
and centres deteriorate, and we cannot suppose them to be
immune to the lot of all organised structures, their irritation or
decay may account for a waning cardiac reserve, and for un-
expected heart failure, even in cases in which muscular degenera-
tion may be inconsiderable. In degenerate hearts Romberg,
Krehl, Rosenbach, all turn for explanation of the paradox of
endurance, and of deferred crisis, not exclusively to the " im-
manent properties " of the organ, but also to its nervous endow-
ments, and especially to its ganglionic integrity. Whatsoever
our opinions on the rather academic controversy between the
neurogenists and the myogenists, we shall not forget that the

1 Among many such records see, for example, Balint, Deutsche med.
Wochenschr., January 6 and 13, 1898, and Vol. II. p. 475 of this book.

chap, viii THE NERVES OF THE HEART 55

nervous system of an organ, such as the heart, is not only the
conductor of its numerous and harmonious concert, but also
an instrument of its development. To Gaskell and Professor
Langley we are chiefly indebted for the knowledge we possess
of the sympathetic system, and Langley tells us that although
the ganglionic cells of the heart comport themselves differently
from sympathetic cells, yet that if deprived of nutriment these
ganglia die rapidly ; as for example in animals bled to death.
They have, it is true, a greater resistance to deprivations of
oxygen than has the central nervous system, yet oxygen may be
more important to them than to nervo-muscular tissue.

And, beside the intracardial nervous structures, we have
mentioned the extracardial, the vagus and the bulb ; and, above
these, the psychical influences which on the heart are supposed to
have a peculiar potency. One would guess that a heart failure
attributable to these influences might be due to a cortical dis-
turbance propagated through the vagus (Vol. I. p. 70).

Furthermore, the vasomotor system has reinforcements and
defaults of which we have little comprehension. Many a
syncope, or death, attributed to the heart is due to a failure
of the " peripheral heart," to a relaxation in large vasomotor
areas. For such cases a clinical test for adrenin is wanted.
The " weak heart " of women is often thus to be explained ;
their peripheral vessels are labile and slack. Here again one
is tempted to dally with the hypothesis suggested by Henle,
and ingeniously advocated by Hasebroek and Griitzman 1 (see
Vol.1, p. 51), that the peripheral heart — the muscular arterial net
— acts, not only as a break on the central propeller, but also as
forwarding machinery, a subsidiary means of propulsion.

Another side of vascular dynamics is not fully seen, namely,
the reciprocation of the several areas ; yet these mutual tides are
ubiquitous and incessant. I have often observed that if the
warm hand be placed between the thighs, and the pulsations
in it felt for a few minutes, oscillations of vascular volumes,
independent of respiration, will become clearly perceptible.
And Miiller 2 and Weber 3 have shown that areas are very

1 Griitzman, Deutsche Arch. f. klin. Med., 1906.

2 Miiller and Weber, Arch. f. Anal. u. Physiol., 1905.

3 Weber, ibid., 1906. References to well-known English writers are not
necessary.

56 MYOCAEDIAL VALUES part i

independent, often indeed in conflict, and that such pressure
interferences have their echo in the heart ; if in an area
dilated for work velocity is not to fall, there must be an
equivalent and harmonious constriction elsewhere, or the heart
will have to make up the difference (p. 30). The mere move-
ment of a limb determines at once an afflux of blood thither.

Furthermore, we must not forget the chances of sudden
death by fat embolism, nerve toxins, pulmonary embolisms,
and so forth ; or possibly, as suggested by Dr. Hawkins- Ambler,
by increases of the specific gravity of the red corpuscles. There
are probably many subtle agents, of which we have little notion,
which enter, alone or together, into these nice poises of life
(see chap. Viscosity, Vol. I. p. 112) ; and likewise alterations in
molecular constitution invisible even to the " ultramicroscope."
An old rubber band may to the eye show no change, but on
use its molecular change will become apparent ; it will die
suddenly. The heart of Dr. Hugh Anderson's elderly cat
could not withstand vagus inhibitions to which the young cat
reacted indeed plainly, but which it withstood with security
(p. 475). Beyond our reckonings, within the visible features,
there is a world — a world of surface tensions, osmoses, reaction
potentials, viscosities, differential pressures, and the like.
If we apply cold to the sinus area, we retard the rate of the
whole heart ; if heat, we accelerate it, as in fever ; yet to the
eye there is no tissue change ; and to other parts of the heart
such applications of heat or cold are relatively indifferent.

Still, if sound and not too old, the heart, as Sir James Good-
hart declares, will stand almost anything ; no combination of
stresses seems too much for it. The distinctions urged by
Merklen, Hoffmann, Rosenbach and others between anatomi-
cal and functional cardiac integrity are pushed too far ; there can
be no function without correlative molecular motions, and if the
function continues irregular, well, the corresponding molecules
have not returned to their normal pattern ; there must be some
dislocation, and this may be permanent — a " new set." I am
told that if by repeated blows a piece of steel be fatigued,
although to the microscope no molecular alteration may be
visible, yet nevertheless, by a change in its electric conduc-
tivity, a permanent molecular dislocation may be detected.

chap, viii CHEMISTRY OF THE HEART 57

Perhaps some day we also may be enabled by the test of
electric conductivity to gauge an old, a fatigued, or a
poisoned heart. If the texture of a heart has got a perma-
nently new set, whether the intimate alterations be visible or
invisible, it is no longer sound.

Another curious point about cardiac reserve, or what we
think to be such, is that it is trainable. A man in training
seems to have many times the reserve, the cardiac reserve,
of one out of training. In athletic training the heart probably
grows larger with its skeletal kindred, and therewith no doubt
the tone of its motor ganglia and of the peripheral vascular
system ; and the capacity of the lungs is developed also. In
Cambridge an old boatman used to test an oarsman for staleness
by drawing a finger down his cheek and noting the persistence of
the ruddy line. However athletic training is not a mere matter
of heart and lung endurance ; the acquired economies of the
skeletal muscular groups count for much. We cannot yet
analyse all these manifold factors. In some elderly persons
the skeletal muscles seem to have kept their vigour almost
too well ; the heart was not able quite to keep up with them.

Then there is the world of chemical reactions in the heart ;
the ionic motions and substitutional interchanges of which we
know little : but, from the known behaviour of salt perfusions,
they must be of the most intimate kind. Such researches as
those of Dr. Walter Fletcher and Mr. Barcroft are bringing some
lio-ht into this subject. Dr. Gaskell showed years ago that to
perfuse the heart with even a very weak solution of lactic acid
is to stop it in diastole ; a reaction due to mere acidity, to
the positive ion H. Stronger solutions drive it into rigor. And
Dr. Fletcher has shown how by a previous application of oxygen
these effects can be prevented.1 The mammalian heart lying
after death in an atmosphere of oxygen, " so long as the
normal architecture of the muscle is maintained," does not
become acid, or but slightly so ; and after perfusion with
oxygenised Ringer's solution, and even some hours' pulsation,
no trace of lactic acid appears. In the fatigued but normal
heart on the access of oxygen the lactic acid promptly dis-
appears. Dr. Fletcher has shown me how many occult flaws there
1 See Fletcher and Hopkins, Journ. of Physiol, March 27, 1907.

58 MYOCAKDIAL VALUES paet i

may possibly be in the balance of colloidal mechanisms in the
cardiac muscle ; and more than this — that the heart may have
abundant fatty deposit in it, and yet the muscle cell on the
motor side be, as we have said (p. 47), intrinsically intact, and
prove no more vulnerable than one histologically normal. This
he illustrated by the figure of an engine clogged with dirt and
grease, which, notwithstanding, may do better work than another
engine bright and clean, but with tight bearings or an unseen
crack in its cylinder. I repeat, as Welch and others have shown,
that moderate degrees of grey and fatty change are compatible
with fair heart work. But when, beyond perverse metabolisms,
we pass into the region of toxic influences we recognise again
how near the edge our gyroscope may revolve.

Finally, we know that the heart's balance depends on that
of many other parts also ; the gaseous exchanges are not in the
myocardium only, not even in the lungs only — they are burning
in every muscular area, in every viscus. Thus, even if the
haemoglobin be constant in quality and quantity, if velocity
begins to fall we are in a vicious circle ; velocity — which means
oxygen exchange — slows down in every organ, especially in those
which, beside the lungs, have a double capillary system,
such as the liver and the kidneys ; in these areas we very soon
find evidences of stasis. And retardation in the lymph system
also is not to be forgotten. Such defaults as these may for whiles
miss or neutralise each other, but when at an unhappy moment
a summation of alternating conditions comes about — capillary
retardations in the viscera, tissue calls, lymph pressures,
vagus and vasomotor waves, psychic thrills — in such cases as
these, cases not without their forebodings, we may not be
at a loss to comprehend the suddenness of death. But
the riddle, which I have done so little to read, is the frequent
suddenness of death in one who, scarcely having known illness,
expires under no extraordinary effort ; or in the peace of his own
bed or chair passes silently away. The reading of this riddle is
not yet.

P.S. to p. 37. Further, on pulsus alternans and extrasystole, and on
the forecast, see two papers by V. Hoeslin and O. Roth, Deutsche Arch,
f. Bin. Med. 114, 1914 ; also Gravier's treatise, 1914.

CHAPTER IX

DIAGNOSIS AND PROGNOSIS OF ARTERIOSCLEROSIS

Diagnosis. — The bent of mankind to deal with things not as
facts and experiences, but in an abstract, logical, and even fanciful
fashion, is very curious ; passing over a transitory feeling for
reality in ancient Greek lands, and again in the thirteenth century,
it was not until the sixteenth that any systematic and persistent
attempt was made to observe things as they are. Curiously
ingenious as have been the logical and speculative categories of
the pulse in ancient and even in comparatively modern times,
many of them indeed being based on more or less accurate clinical
perceptions, yet >ur remoter forefathers took little heed of what
seems to us so plain, the various thicknesses and resistances
of the arterial tunics (see Vol. I. p. 3). An appreciation of such
changes, coinciding more or less with the experiments of Hales,
Chauveau, and their disciples on arterial pressures, somewhat
suddenly created a new field of diagnosis. But in the pre-
ceding pages I have implied, or even directly indicated, so
much in comparison of symptoms that I need make no long
repetition of such matter. Concerning diagnosis then I will
confine myself to a few brief and desultory remarks on certain
points of emphasis or of application.

The first broad distinction to be made is between the hyper-
pietic, the toxic and the senile or decrescent sclerosis. The different
issues of these three kinds I hope I have made clear. The
toxic modes are often so closely associated with an infectious or
poisonous cause as to carry their diagnosis with them ; as in
the cases of typhoid fever, syphilis, or lead. In these cases, as a
rule, the blood pressures do not rise. As regards the toxic varieties,
I may urge the reader once more not to forget the wide prevalence

vol. n 59 E

60 DIAGNOSIS OF ARTERIOSCLEROSIS part i

of syphilis, and the value in any doubtful case of the
Wassermann test. He will not forget, for instance, that a
virgin may unhappily become infected ; by fondling a syphilitic
baby for example, or by some other chance, as in medical or
nursing duty. We must not take any person to be outside
the possibility of syphilis. Many persons so infected are
wholly ignorant of it ; many indeed who have incurred the
disease by their own fault are unaware of their punishment,
and from some of these the truth must be concealed. And as
Dr. Mitchell Bruce says,1 even in a case where a past syphilitic
infection is known, we may have to unravel a complexity
with metabolic or other perversions of function.

The so-called " neurotic " or " functional " cases of high
pressure are only high systolic pressure ; the diastolic is un-
changed, or lowered. The level fluctuates widely.

Gibson used to demur that my divisions of hyperpietic
and decrescent disease were wanting in sharp boundary lines.
Well, where in animated nature are such lines to be found ?
Between these two chief classes indeed the divisions are rather
sharper than is common in nosological classification. But it
may not always be easy to discriminate between hyperpietic
and decrescent arteriosclerosis in the cases where these two
processes co-operate. However, the mixed or intermediate cases
are rare : the following seemed to be a case of mixed senile
and hyperpietic disease :

Rev. C, set. 68. Patient of Dr. Ealand of Farnham. For a
year or more had found his mental powers failing ; became depressed
in a morning, better towards evening. Cannot pursue his thought ;
e.g. he can preach an old sermon well enough, but cannot write a
new one. Also cannot walk so far ; fatigues in a mile or so. Wakes
too early (4-5 a.m.). Andrew Clark had told him ten years ago that
he suffered from suppressed gout. Spare and rather pallid man.
Gait quite normal to all tests. I saw this gentleman several times,
and, to sum up the conclusion in a few words, — the blood pressures
ranged, both systolic and diastolic, above normal, say to 180 as
highest systolic. But his heart was obviously yielding ; it was
widely dilated to the left, and murmurs (systolic) were audible at
both orifices. The second aortic sound was ringing, over a large
area. The accessible arteries were large and leathery, contained

1 Bruce, M., Second Luml. Led., July 15, 1911.

chap, ix OF HYPERPIESIA 61

calcified dots, and, to toinh, suggested Broadbent's " virtual
tension." At first sight I regarded this case as simply de-
crescent ; but on consideration I felt sure that it was in the
first instance one of hyperpiesis, on which the decrescent series
had engrafted itself : or the two processes may have been
practically concurrent. How far the heart failure was dependent
on coronary disease, how far on the stresses of high pressures,
probably never extreme, could not be decided. The large left
ventricle pointed at least to no inconsiderable coefficient of blood
pressure (see also Episodic Hyperpiesis, Vol. I. p. 453).

In diagnosis of Hyperpiesia it seems paradoxical to say
that a disease of high blood pressure and hypertrophied heart
is often mistaken for neurasthenia ; yet such is not rarely the
case. As it happens that my attention has been given to both
these maladies my opportunities of observing this confusion
have been many. And the dilemma is by no means always one
of confusion of terms. To distinguish in a particular case
between hyperpiesia in its earlier stages and neurasthenia may be a
matter of some difficulty ; in an impressionable subject it may
be almost impossible to secure a pressure record free from the
fallacy of nervous exaltation, and to discriminate in their early
stages between cardiac enlargement and irritable heart, especially
in women with large breasts. Moreover in such persons the
aortic second sound, on account of some laxity and larger
diameter of the vessel, is frequently accentuated. Dr. Theodore
Jane way, in his well-known work, rightly criticises " the
reported high readings in neurasthenia " ; and points out that
these may on the one hand be due to transient nervous im-
pressions, or on the other to vascular or renal disease. In
neurasthenia, he says quite truly, the blood pressures, if they
can be taken in tranquillity, run rather under than over the
normal values. One criterion is that if in neurotic persons the
systolic pressures are apt to run high, especially under examina-
tion, the diastolic are unchanged. Dr. Eric Macnamara,1 in
an article chiefly devoted to therapeutical means, comes to similar
conclusions. His pressure records in neurasthenia were often
minus, but sometimes plus ; and were very variously affected
by treatment (chiefly electric). In reading his paper I could

1 Macnamara, E., Lancet, July 18, 1908.

62 DIAGNOSIS OF ARTERIOSCLEROSIS part i

not avoid suspecting that some of the cases regarded as
neurasthenic were in fact early stages of hyperpiesia ; in
these high frequency currents are often followed by a reduc-
of the arterial pressure (see Vol. I. p. 441). By precise ortho-
diascopy enlargement of the heart may be ascertainable before
it becomes manifest by ordinary physical signs. We must
remember also that hyperpietics are themselves prone to
nervous exaggerations of systolic blood pressure, so that
for sure diagnosis the records must be patiently verified.
Von Jaksch also reminds us that these patients are often
" nervous " ; they may apprehend ill - health, or interference
with their work in life ; in such conditions after the patient
has become more used to these investigations the excessive
pressures slowly fall, and under treatment the instability
may prove to have been temporary. Notwithstanding, I do not
feel sure that von Jaksch fully discerned the differences between
hyperpiesia and neurasthenia ; for in another place he speaks of
"neurasthenia" as one of the first symptoms of arteriosclerosis ;
thus using the term not in its technical sense, but too literally
as mere debility or weariness. In this sense " neurasthenia "
becomes one of the first, or last, symptoms of any malady
whatsoever — a futile proposition. Dr. Stengel scarcely avoids
ambiguity in this respect. Occasionally then one sees false
diagnosis of hyperpiesia in cases which are really but
neurasthenia with unsteady cardio-vascular conditions and high
systolic pressures. When a well-known foreign physician writes
that neurasthenia is a consequence of sclerosis of the cerebral
arteries, he throws all nomenclature on the scrap heap. Mere
local vasomotor tides, such as cold hands and feet, flushes of
the face and the like, are of course independent of the general
arterial pressure. Paresthesias of the legs often occur in both
maladies. As an instance of the dilemma we are discussing,
I may allude to a case which I saw some years ago with Mr.
Winwood Smith of Torquay :

Mr. , about middle life, a gifted man of a very highly

strung temperament, and of a very " nervous " family, had been
" neurotic and dyspeptic all his life." So far the diagnosis lay in
little obscurity. But recently Mr. Winwood Smith had found his
arterial pressures ruling high — 170-180 ; I verified these readings,

chap, ix FROM NERVOUS MALADIES 63

taking such imperfect precautions against artificial exaltation as in a
consultation were practicable. And these observations were reinforced
by an unquestionable increase of the heart to the left. The aortic
second sound was ringing ; the rhythm was rather laboured, with an
occasional extrasystole, and a disposition to reduplication of the
first sound. To the touch, the arteries were in fair condition. Under
diet and other remedies these symptoms were ameliorated, and
indeed disappeared. A few years later this gentleman, previously
unknown to me, became a friend and neighbour, so that I had many
opportunities of determining his condition ; and although he had
now and then to seek for medical advice, the hyperpietic condition
did not return.

AnaBinia is not, as a rule, a feature of hyperpiesis ; there
are, as I have said, sallow hyperpietics, but speaking generally
anaemia would rather suggest renal disease (see Vol. I. p. 452).

We shall not forget the possible influence of variations in
glandular activity in some cases. The records of blood pressures
in Graves' disease are inconsistent ; some observers postulate
in this disease a definite and persistent rise of pressure, others
deny it.1 That in particular cases of Graves' disease the systolic
blood pressures are often exalted is certain, but this is rather a
frequent incident of the disease than a character of it. The
diastolic and mean pressures are usually moderate, or even low.

If neurasthenia may be confused with hyperpiesia, or con-
versely, and if again even worse diseases, such as General Paralysis
of the Insane, diffuse cerebral syphilis, or incipient dementia,
may at their beginning be confounded with neurasthenia, we
perceive that in particular cases some nicety may be required
in deciding on the diagnosis. It would be out of place here to
enter upon the large field into which these distinctions would
carry us, and happily I can refer the reader to a far better apprecia-
tion of these complex factors in Dr. Mott's article on the subject.2
In some of these cases the Wassermann test may be required,
and possibly an examination of the cerebro-spinal fluid. Of
course the pupillary reactions, and the state of the back of the
eye will not be overlooked. Some writers say that knee-jerks are
inversely as blood pressure, but this is a very fallible maxim.

1 See also Spiethoff, Zentralbl. /. inn. Med., 1902.

2 Mott, F., " Diagnosis of Syphilitic Disease of the Nervous System," Lancet,
June 12, 1909 ; and other articles.

64 DIAGNOSIS OF ARTERIOSCLEROSIS part i

Hypochondria, a definite but somewhat rare disease, may
present some difficulty ; especially if it be associated with de-
fective elimination, and blood pressures instable under nervous,
or katabolic disorder.

Hysterical dyspnea. — We are consulted occasionally in cases of
dyspnea, really " neurotic," but simulating organic disease ; and
often in cases of organic dyspnea not due to hyperpiesis, but
pulmonary or cardiac in origin. We have seen that in many
cases of cardiac disease, in the adjustment of balances, the arterial
pressures are raised (see Vol. I. p. 393) ; in cases of asthma asphyxia
may raise blood pressures, as we know (p. 129), and in hysterical
or excited panting women the pressures and the heart's action
are often exasperated. There ought not to be much difficulty
in disentangling such cases as these, but it seems that not infre-
quently the distinction is missed, even by experienced physicians,
and the case interpreted as hyperpiesia, or incipient Bright's
disease. The pressure increases are almost wholly systolic.
But for fuller discussion of cases of this kind I may venture to
refer to my article on Neurasthenia in the second edition of
Allbutt and Rolleston's System.

The lungs must be watched for any sign of oedema, and
suspicions of tissue hydrsemia tested by comparisons of the
bodily weight. Chronic oedema, gradual in final stages, must be
distinguished from acute suffocative oedema.

In some cases it may be difficult to disentangle signs of hyper-
piesia from the effects of other heart disease, definite or indefinite.
The following case is an example of such a doubt : —

Male, set. 62. Seen with Dr. Lloyd Jones. Fifteen years before
had rheumatic fever, which did some damage to the mitral valve ;
at any rate there was a mitral murmur ; but for some years he had
suffered no inconvenience from this defect. Shortly before our
consultation, in May 1911, he had been falling off in health, not with
cardiac symptoms but with depression of spirits of a morning,
irritability, feeling unequal to business, and so forth. He was a
very large meat-eater, but said to be temperate in alcohol ; however,
in answer to closer question, he admitted that he was wont to take
a glass of whiskey in a forenoon, as a pick-me-up, though after that
he took alcohol with his meals only. No doubt he had lived
generously. Dr. Lloyd Jones was called in urgently because of the
sudden occurrence of an attack of dyspnea, followed by a persistent

chap, ix DYSPNEA— THE HEART 65

shortness of breath on moving about. Dr. Jones was puzzled at
first to find symptoms and signs not consistent with the history of
rheumatic mitral disease. From the symptoms and signs indeed
it seemed that this defect was slight, and had but little to do
with the instant distress. For now the left ventricle was largely
hypertrophied, and the arterial pressures very high. The radial
artery was thickened and rather tortuous. There was no oedema,
no enlargement of the liver, no sign of renal affection, primary
or " cardiac."

Of episodes of high pressures in persons affected with the
decrescent kind of arteriosclerosis I have spoken elsewhere
(Vol. I. p. 452) ; in these cases, if the vessels be thickened, we
have to decide whether the state under observation may be one
of persistent hyperpiesia with secondary arterial lesion, or of the
"senile" form with intercurrent hyperpiesia. Generally speaking,
if the previous history be unknown, the results of treatment only
will solve this problem : but this test usually suffices : these
episodes are remarkably tractable. But cases of high pressures
occur every now and then in which the observer catches them
in a falling phase, say at 140-150, and assumes them to be about
normal ; whereas this may be but a temporary phase. Only
continued observation can decide upon the course and nature
of such a case. The consultant, if he has not the assistance of
a family physician who has watched some length of it, may be
unable on the data of one visit to give a final opinion.

As concerns the heart itself we must guard against a false
interpretation of its embarrassments ; and in cases of high pressure
we shall not assent to a diagnosis of cardiac inadequacy without
asking ourselves — If inadequate, then inadequate to what con-
ditions ? Is the organ simply failing in its ordinary duty, or is
it succumbing under some abnormal stresses ? Is the fault in
itself, or in its circumstances ? That a heart overburdened by
high arterial pressures should fall under the sentence of inherent
frailty I have deprecated again and again. For instance,
not long ago as I write, I saw an elderly lady with alleged cardiac
degeneration ; the arterial pressures were high, and the heart
was in fact big and labouring on gamely. But the pulse rate
was rising to 85-90, a bad sign ; and acute oedema was beginning
at the base of the right lung, with crepitations nearly as fine as

66 DIAGNOSIS OF ARTERIOSCLEROSIS part i

in pneumonia. This flood continued to rise, and in three more
days caused her death. Yet from the beginning the case had
been regarded as an intrinsic " heart failure," and treated as
such. Such a heart however, if we come to its aid, has a
substantial reserve capacity, and often, after the burden is in
some measure lightened, responds to digitalis ; whereas a heart
primarily degenerate does not make much out under any succour.
Concerning " cardiosclerosis " we saw that, unless the case
were known to us in its previous course, doubt might arise
whether a mitral murmur were due to a primary valvular
disease, to a forcing of the valve in a strained ventricle ; or
again to an atheromatous cusp no longer adapted to its bed.
In a middle-aged patient a history of rheumatic fever may be a
will-o'-the-wisp. In such a case, one which arises rather in
decrescent sclerosis, the murmur is ordinarily not attended with
heart symptoms of importance ; it does not signify a grave
disorder of its functions : more noisy the action may be, but
not much less efficient than in atheromatous hearts without
murmur. The distinction between a forced leak and a mitral
sclerosis must depend much on the history of the case ; usually
in mitral lesion enlarged the left ventricle is not much altered,
and there is no history nor sign of past high pressures. In
high pressure cases the aorta is more dilated, and the second
sound on the right louder than on the left, whereas in primary
mitral disease the converse is the case. Strasburger's method —
rate of blood stream, etc. — which is an aid in aortic disease or
nephritis, cannot, as he suggests it should, be relied upon in the
problem now under discussion. Indeed diagnosis between the
big heart of chronic nephritis and that of hyperpiesia cannot be
made upon the organ itself ; it must be inferred from the other
signs and symptoms of the case — the albumin, the persistently
low specific gravity of the whole day's urine, the casts, and the
ursemic symptoms. It is remarkable that in these big hearts
aortic regurgitation is rare, as it is also in the senile disease;
though an episode of high pressures may force an atheromatous
aortic cusp (see p. 453). While distention of the right heart
shifts the " apex " to the left, dilatation of the left ventricle
without notable hypertrophy may not materially alter the point
of this maximum impulse ; the position of the apex may also be

chap, ix THE HEART— THE KIDNEYS 67

affected by dilatation of the auricles (see also " Heart-swing "
Vol. I. p. 396). Professor Waller's estimation by the electro-
cardiogram of the obliquity of the heart's axis may help us in
these distinctions. " Functional " cardiac disturbances are more
frequent in hyperpiesia than in mitral disease.

Stenocardial conditions are fully considered in the essays on
Aortitis and Angina Pectoris.

Some indecision of diagnosis might arise in certain alcoholic
hearts. Of the alcoholic heart Dr. Mitchell Bruce says x it is
always enlarged, say to about 17 oz.,and the mitral valve is usually
leaky, though there may be no disease of the flaps.2 There
is radial sclerosis in about one - third. The myocardium is
degenerate (Mott, Bruce, Maguire). Death is often sudden.
Alcoholic nephritis might be confused with arteriosclerosis.
However, in my experience there is no difficulty in distinguish-
ing these flabby hearts, really feeble even if they be enlarged,
from the fundamentally efficient heart of hyperpiesia, fagged
under the strain of inordinate labours. Albuminuria and all
degrees of anasarca may be seen in either disease ; and in
the extremity of either the complete picture of cardiac dropsy,
though less commonly in hyperpiesia.

The sometimes difficult diagnosis between hyperpiesia and
chronic renal disease has been considered at length in more than
one chapter of this book. However the difficulty of interpret-
ing some of these cases is well illustrated by this one, which I
saw with Dr. Maund of Newmarket :

Male, set. 61. Is not grey, and looks younger. Made no com-
plaint till four months ago (seen in December 1906), then complained
of a vague debility. No headache, no vomiting. Blood pressures
not increased, but sclerosis of accessible arteries extraordinarily
great. Expression a little blank, and rather staring, but no sugar in
the urine. There is a slight cloud of albumin. Heart in normal
position and within ordinary limits. No sign of hypertrophy ;
possibly some diminution, or some emphysema. The arteries were
so extraordinarily diseased that one could hardly detect the blood
current within. Aortic second sound altered in quality, but not loud.
No murmurs. Shortly after our consultation he was seized with con-
vulsions, in which he died. (Uraemic ?)

1 Bruce, M., Lettsomian LecL, 1901.
2 See also Maguire, Trans. Clin. Soc. vol. xx. p. 235, 1888.

68 DIAGNOSIS OF AKTEEIOSCLEEOSIS part i

Now what was the diagnosis ? Cystic kidney with rapid and
premature decrescent arteriosclerosis occurred to us, but no
necropsy was obtained.

In these diseases it may not always be easy to be sure of
early degrees of arterial thickening, as the sustained wave,
and perchance contracted artery, interfere a little with a due
emptying and rolling under the finger ; yet the coats may prove
for some time to keep fairly normal. As I have said, in
comparatively young persons high pressure may exist for some
time without palpable injury to the arterial wall. In Dr.
Humphry's case of diseased hypophysis (Vol. I. p. 271) the heart
weighed 45 oz., but the aorta appeared to the eye but little
altered. The patient's age was 39. The length of the illness
was unknown ; he did not seek advice, and was at work up
till three weeks before his death. Moreover, as we have seen, a
contracted artery is so far a protected artery.

The rule that in renal disease, and in gout, the excretion of
purins is delayed, is used by Professor Hopkins as a diagnostic
method : all purins are cut out of the diet for three or four days,
and then restored ; when, if the kidneys are normal, purins should
appear in the urine freely and at once.

Latent oedema may be detected at a very early stage by a rise
in weight, when the urine should be tested for salt content ; thus
an improving patient may lose weight (see Salt in Diet, p. 93).
It is desirable therefore to keep a careful register of the weight
of hyperpietic, as of other cardiac and renal patients. In
decrescent arteriosclerosis there is not quite the same need for
this record.

Epistaxis is no infrequent diagnostic signal of hyperpiesis, as
it is of renal disease ; the immediate cause in both being the
high arterial pressure. For the same reason it appears not
rarely in aortic regurgitation. I have mentioned also that
hgemoptysis may have a similar origin.

Healthy persons can generally bear compression of both
carotids behind the jaw, the vertebrals being of course open, for
a few (say ten) seconds ; it has been said that in high arterial
pressure this toleration is much reduced, so that in three seconds
giddiness and bewilderment appear, and the patientmust sit down.
I am not sure that the experiment is quite justifiable ; and other

chap, ix THE DECKESCENT KIND 69

less dubious methods are open to us. In one instance, of a healthy
undergraduate, a compression of both carotids produced an
epileptic fit ; the duration of the compression was brief — how
brief I cannot say. The garotte was put on during some
jujitsu scuffle. Furthermore, I think that a praeternatural
susceptibility to this compression exists in other conditions —
as for example in neurasthenia.

I have mentioned (Vol. I. p. 162) Dr. MacPhedran's test of
the degree of conservation of muscular efficiency in the arteries
by the reaction time under nitrites ; if the reaction is slight and
delayed it is presumed that the quality of this tunic is falling.

Vertigo may be mesophalic, cerebellar, labyrinthine, gastric,
anaemic, neurasthenic ; Cheyne-Stokes respiration may arise from
cardiac, renal, or bulbar disorder ; but this last may arise from
high pressures. Attacks of spasmodic dyspnea may be due to
asthma, hysteria, renal, or cardiac disorder. Hysterical pantings
ought not to be misapprehended ; they are inconsistent with the
other symptoms and with themselves ; for instance, the alae
nasi are often at rest. In all cases the pupillary reactions and
other reflexes will be ascertained, and search made for patches
of anaesthesia (hysteria, tabes, etc.).

In diagnosis of decrescent arteriosclerosis the outward
vessels may be distorted without such disease of the inward vessels
as to shorten life, or even to diminish the faculties beyond
what is usual in advancing years. And it does not follow that
whatsoever maladies may dog the steps of age are due to the
vascular decay. Nervous symptoms, such as tinglings, darting
pains, numbnesses, cold tricklings, dead fingers, may be simply
" functional " and transient ; or they may signify arterial
obsolescence, or neuritis. For diagnosis then we shall test,
so far as we can, the functions of the several organs of the
body ; searching for traces of albumin or sugar in the urine,
for increasing emphysema, latent carcinoma, a growing intolerance
of tea, coffee, or tobacco, fatigue on moderate exertion, slurring
gait, failing sleep, drowsiness, inability of attention, loss of
memory, irritability, depression of spirits, or perchance delusions.
Such symptoms, whether directly due to vascular occlusions or
to the general drying up of the dews of life — a change cognate
with arterial decay — point to biochemical ebbs which, if not

70 DIAGNOSIS OF ARTERIOSCLEROSIS part i

wholly unmanageable, are essentially irremediable. A hsema-
temesis (p. 448) may raise an anxious doubt of ulcer, simple
or malignant.

An allusion must be made to that terrible disease, as
yet wrapped in obscurity, in which arterial trunks are seized
by an acute arteritis with agonising pains and gangrene ;
this " thrombangitis " is not to be confounded with the
arteriosclerosis either of hyperpiesis or of decrescence. The
senile gangrene of decrescent arteriosclerosis is on the whole
painless and belongs to a different series of events. Of this
result I have nothing to say which is not well known.
Syphilitic arteritis, or chronic meningitis, may be distinguished
by headache, vertigo, local nerve lesions — -especially about the
orbits and face — sluggishness, convulsive phenomena, transient
aphasia or other palsies cerebral or spinal, aneurysm, and so
forth. Here the Wassermann test, of course, may come to
our assistance.

How far is it possible to discern arterial disease in the inward
arteries ? Aortic patches, without giving rise to symptoms,
may reach large dimensions, and give warning in the manage-
ment of life ; if, as is asserted, these can be revealed by the
X-rays our gain would be considerable. Dilatation of the aorta
may be measurable by the same means. Haenisch,1 in noting this
revelation of calcareous patches in the aorta by X-rays, pursued
certain experiments which have been made with the rays on the
corpse, in the hope of ascertaining the state of the coronary
arteries (Simmons 2 and others). So far, they have been
unsuccessful ; in any case, as Haenisch truly remarks, the
practical advantage would be slight, as the existence of calcareous
patches in a vessel would not tell us much concerning its
permeability. Arnsperger 3 gives a plate significant, as he
interprets it, of a calcareous deposit in the aorta ; a dark spot
is certainly visible at the point signified. The Grodels of
Nauheim have given much attention to the indications of the

1 Haenisch, Deutsche med. Wochenschr., 1912.

2 Simmons, Fortschritte d. Rontgenstrahlen, Bd. xii. Heft 6, S. 371. I have
not seen this paper, but quotations from it.

3 Arnsperger, Die Rontgen-untersuchungen d. Brustorgane, 1909. He gives
many interesting plates of diseased aortas. See also Williams, New York,
Rontgen Rays in Med., 1901.

chap, ix PROGNOSIS OF ARTERIOSCLEROSIS 71

X-rays in the detection of disease of the walls of the aorta, and
with some measure of success. A difference in the two radial
pulses would suggest deposit at the forks of the arteries of the neck;
on the other hand, a downward swing of the cardiac apex, even to
the axillary line, must not be taken too confidently as indicating
hypertrophy ; we have seen that this may be, and often is, due
to a lengthening of the aorta ; this in its turn may be due to
deterioration of structure, or to the slackness of some kind of
atony (Traube). A few records have been published of more
superficial trunks thus made visible in sclerosis ; but in arteries
of the limbs the touch needs no assistance. In so far as
thickening of the arteries of the limbs may be any guide to the
state of the inner vessels we may detect it early in such vessels
as the tibials. Alterations of the temporals seem to have but
little significance.1

The rate of wave propagation increases as the vessel, whether
stiffened by degeneration or made taut and inelastic by sustained
blood pressure within, becomes more rigid. I have alluded to
this method of measurement, as yet inchoate, in a preceding
section (p. 84).

Strubell is of opinion that the electro-cardiogram will prove to
be a useful means of diagnosis in arteriosclerosis. His interpre-
tations are formulated in a somewhat too categorical way,2 and
for the present are, in my opinion, in advance of their proofs.
It may well be that, with a larger experience of this method,
some diagnostic advantages will be obtained. As yet these
curves serve best to interpret rhythms ; and signify rather the
moments and degrees of chemical excitation than those of work
done. There is no direct relation between the amount of the
excitatory process and that of the correlated work.

Prognosis. — -In what has gone before, the principles of
prognosis in these diseases, if not formally expressed, are implied.
But a few maxims may be emphasised.

In hyperpiesia, when dyspnea has occurred the malady has
entered into its last stage, it is hardly remediable, and quite

1 As regards X-rays in Phlebosclerosis, see Carl Beck, New York Med. Joum.,
April 23, 1904.

2 Strubell, " Therap. d. Arteriosclerose," Deut. med. Wochenschr., Nov. 7,
1912.

72 PROGNOSIS OF ARTERIOSCLEROSIS part i

incurable. The case will travel from bad to worse ; the heart
dilates, it is strung up with digitalis, it gets along again for a
while, then relapses, is again perhaps pulled up, and so on ;
but it is a losing fight. Pulmonary oedema is menacing, and a
whiff of it means imminent peril.

In a case of hyperpiesia, of which the symptoms have been
dispelled three times only to return, the prospect of substantial
amendment is dim.

Hyperpiesis occurring as an episode in elderly persons (p.
453), when it is of course often associated with senile athero-
sclerosis, is generally curable, and with care to be banished and
prevented. Still, when it overrides, however temporarily, a
body already frail, we have seen that some harm may be done ;
an aortic cusp may be forced, an enfeebled heart put to strain,
or a corroded cerebral artery burst. It is important therefore
to dispel it as soon as possible.

In the earlier stages of hyperpiesia, before the vessels are in-
jured, we may hope to clear the distemper away. What Huchard
called " the stage of presclerosis " is, as he said, " very amenable
to cure " ; the difficulty is to catch the malady in this incipient
stage. The French School of to-day speaks hopefully of cure
in " hypertendus purs," " sans lesion renale " ; if caught in
time, that is, before the arterial tree is injured. By one chance
or another many patients do present themselves early enough for
efficacious treatment, yet too often for their malady only to be
still overlooked. It sounds paradoxical to say that the prospect
is no better for younger patients than for the older, but one is
driven to this opinion. Perhaps, as we see in renal and other
diseases, the longer the body remains free from the proclivity
the better the resistance to it when it appears ; the original
bias is less. But the following exemplary case of recovery in
youth has been published by Dr. William Russell : x

Male, set. 25. Blood pressure, 220. Although no renal symptom
could be elicited, yet the prognosis seemed gloomy. He was put to
bed for four weeks on low diet and appropriate remedies. At the
end of this time the pressure was down to 135, and after some further
courses of treatment it was brought down to the normal. The
patient, I gather, did well.

1 Russell, Win., Lancet, Feb. 13, 1909.

chap, ix ILLUSTRATIVE CASES 73

I may add, not of course as proofs, but as illustrative
instances, the four cases which follow :

Male, set. 51. Kather burly, high-coloured man. Health always
good, unless " rather gouty " — no podagra. A hearty appetite but
no gourmand. Moderate in stimulants. Smokes one cigar a day,
and two ounces of tobacco in the week. Heart's apex not much out,
but beat hard, and second aortic loud. Arteries normal ; and to
the finger nothing notable. But the pulse was barely arrested
at 200 (Martin's machine). If 10-15 were taken off for attention the
pressure remained far too high. Pulse wave sustained. I prescribed
the usual diet and regime with calomel, etc. So far as the next few
months went he recovered quickly ; but one loses sight of people.

Reported by Dr. Edgecombe of Harrogate. Male, set. 40.
Sedentary and a high feeder. Complained of malaise ; pulse not
obviously tense. Arterial pressures — systolic 190, diastolic 145 ;
apex an inch outside nipple. No murmur. Liver rather full. No
symptoms nor signs of renal disease. After a course of diet and spa
treatment the pressures had fallen to 170 and 130 respectively. A
careful regimen was advised and a return to Harrogate every year.
The patient did well, and in four years a permanent cure was
established, the pressures remaining at 130 and 100 respectively.
The accessible arteries were never thickened.

Eeported by Dr. L. Willianis.1 (Rather worse than the preced-
ing.) Male, set. 60. Diagnosed by an eminent physician as Bright's
Disease. Some albumin in urine, but " on repeated examination
no casts found, or but a few hyalines. Arterial pressure 200. Heart
enlarged. After three months' treatment, including a spa course,
the pressures had fallen to 150, and the heart had receded within
normal dimensions. No relapse occurred, and he continued to
report himself as in good health. A good cure, for that age and
with such symptoms. Probably a case in which the causes had been
recently active, and the consequences, if acute, yet also recent.

Mrs. B., seen with Dr. Bulmore of Wisbech, January 27, 1909.
Female (set. 60 ?) Depression, fatigue, and broken sleep. Mother
died of apoplexy. The pulse had become " extremely tense " ;
and a rough systolic murmur had appeared over the base of the
enlarged heart. Loud ringing second aortic sound. A London
consultant of standing had assured her there was no renal disease,
confirming Dr. Bulmore's opinion. A few days later I saw her and
verified all these points. Apoplexy was feared. It was difficult
to stop the radial pulse with the finger, but the arterial wall did not
seem much the worse. She was on strict diet and Vichy water, to

1 Williams, L., Clin. Journ., April 22, 1908.

74 PROGNOSIS OF ARTERIOSCLEROSIS part i

which we added courses of blue pill. She made a progressive amend-
ment to complete recovery, the pulse becoming soft and normal.
I learn that she has continued in good health.

But here we have to formulate the maxim that if the patient
can be prevailed upon to obey certain rather rigid rules he may
be cured ; if not, not. Dr. Mantle x speaks of the many patients
who present themselves at Harrogate with high pressures, some
cardiac hypertrophy and abdominal disorder, but with no
clinical evidence of nephritis. For these he has accepted my
name of Hyperpiesia, and urges that, if caught early, the condi-
tion is curable ; if not, it ends in apoplexy or cardiac defeat.
He reports instances.

When the malady has gone so far as to have enlarged the heart
conspicuously, and impaired the arteries, the outlook is of course
so much the worse ; indeed complete restitutio ad integrum is out
of the question. Nevertheless, if dyspnea on exertion has not
appeared, something, much perhaps, may be hoped for ; the
arterial pressures may be mitigated, and the heart may recede
even within normal limits. If this can be achieved the impair-
ment of the elasticity of these vessels may not have any very
grave consequences ; it may mean nothing worse than some
circumscription of the sphere of bodily work. Dr. Mantle 2
records a remarkable example of arrest of such a severe case of
hyperpiesis. But at this stage the prognosis is far from bright ;
the arterial system has probably got a new set, and one out of
proportion to moderate blood pressures. A radical cure is
impossible, and a certain individual standard of high pressure
must be accepted ; but of course this means a shorter life for
the machinery. Notwithstanding, much may be done to alleviate
the patient's conditions, so that he may be brought back to a
fair semblance of health, and his liability to apoplexy or heart
defeat withstood.

The cases of worst prospect are those, at whatever age of
adult life, in which vasoconstriction extends far inwards. If not
only the radial, but also the brachial and other larger vessels be
obstinately tight the prognosis is grave ; the mortal issue, whether

1 Mantle, A., Lancet, May 3, 1913.
2 Mantle, A., Clin. Journ., June 18, 1913.

chap, ix THE PATIENT'S POINT OF VIEW 75

by the heart or by apoplexy, can hardly be staved off. This
condition is most stubborn to treatment ; hyperpiesia with
radials of normal or expanded diameter — " large leathery vessels "
— is more manageable. We shall see that the best course
in these cases of extensive constriction is to bleed from the
beginning, and to repeat the venesection at proper intervals.
Unfortunately, the public prejudices are for the present against
this measure, and to persist against a general prejudice may
bring other troubles with it ; the alarm of the patient and his
circle may lead to evasions, and in various ways defeat or
hinder our purposes, yet notwithstanding, all these circumstances
enter into our prognosis.

One very important consideration I would reiterate, this
is, not to rely too much in prognosis upon the range of
systolic pressures (Vol. I. p. 90). Besides the emotional and other
contingent causes of temporarily exalted pressures, it is possible
that normally individuals differ in their blood pressures. I
have watched with some anxiety not a few friends or patients
whose health is as yet unbroken, but whose blood pressures un-
doubtedly seemed, all deductions made, to have rmi high, to 170,
or possibly more, even before middle life ; and von Basch has
alluded to such cases. These persons are of energetic tempera-
ment, work hard, and, for many years, with apparent impunity.
It is only by chance one happens to discover such subjects. Von
Basch had watched one such patient for ten years (up to date of
writing), and he had continued in good health. On the other
hand, two healthy-looking men, both of whom for many years
had worked hard and successfully, but always — as I happened
to know — with high blood pressures, both in their seventh decade
were smitten with apoplexy. Still to give an anxious prognosis
on so chance a discovery would plant an arrow in the heart of an
earnest hard-working man, or sensitive woman, and might spoil
a life. We fear, but we do not know, that a vascular system
working at such pressures must wear out prematurely, and to
harass and thwart a life's work on speculative gromids would be
very unwise. A man of spirit, were the conditions known to him,
would no doubt decide to fulfil the ends of his life in unselfish faith
rather than nurse it on terms which would hamper or defeat
them ; and it seems to me that the physician's place is, after

VOL. II F

76 PEOGNOSIS OF AKTEKIOSCLEROSIS part i

some cheerful but decisive counsel, to let him live his life as free
as possible from apprehensions. Nay, I will go a step farther :
let us assume that such early symptoms of high pressures do
signify something worse than a quasi-normal idiosyncrasy with
perhaps a vascular system of corresponding tenacity ; let us
suppose that by a free-living or a sedentary life the malady is
really on foot ; well, it may be, it often is, curable. But in
any case, let us not overshadow the man's life by forebodings ;
let us encourage such an one to rule himself and his condi-
tions in hope and fortitude ; for

If man could see
The perils and diseases that he elbows,
Each day he walks a mile ; which catch at him,
Which fall behind and graze him as he passes ;
Then would he know that Life's a single pilgrim
Fighting unarmed amongst a thousand soldiers.
It is this infinite invisible
Which we must learn to know, and yet to scorn.1

Bbddoes.

On the other hand, much in prognosis depends upon the
amenability and habits of the patient. In some cases we may
say, paradoxically, the worse the patient's past habits the better
the prognosis ; a constitution not yet wrecked may be staggering
under folly and error : then, if the patient will be wise and
obedient, restoration is often within reach.

In older persons, and in irremediable stages, we shall bear
in mind the remarkable insusceptibility of the old to general
symptoms, to the acuter general constitutional reactions, so that
in old persons especially local signs must be sought and weighed
continually and carefully. Of these, I may allude again to any
sign of oedema at either pulmonary base ; or to a pneumonic
consolidation which, even within narrow limits, and unaccom-
panied by general reaction, may nevertheless prove rapidly
mortal. In children, of course, the contrary is the case ; in them

1 Quid tarn sollicitis vitam consumimus annis,
Torquemurque metu caecaque cupidine rerum ?
Aeternisque senes curis, dum quaerimus aevum
Perdimus, et nullo votorum fine beati
Victuri agimus semper, nee vivimus unquam ?

Manhjus (quoted Mackail, Lat. Lit.).

chap, ix ITS KINDS AND DISTRIBUTION 77

turbulent general symptoms may have less sinister meaning, and
local disorder be transient.

The chances of lifting on a dilated heart for a while may be
estimated by the clearness of the lungs, and by the response to
alteratives and digitalis.

At the risk of being tedious, I must here again insist that
in making a forecast of the issue of a case of arteriosclerosis,
my distinction between the hyperpietic and the decrescent mode
must be borne continually in mind, as must also any suspicion
of renal or other toxic condition. Persistently low diurnal
specific gravity of the urine is of ill omen. Under what
circumstances hyperpiesia may be curable or incurable we have
discussed already at length ; it is a serious malady. Decrescent
arteriosclerosis is variable in its incidence ; in some cases it
is associated with only too evident signs of the graver
atrophies, with loss of facial expression, shuffling gait, lapses
of memory, and so forth. In other cases the vascular decay
seems to pursue the visceral arteries ; the aortic and mitral
valves degenerate, and the great vessels decay, while the mental
functions are but little, and the muscular not gravely, impaired.
These patients may die of asystole, the hyperpietic of dropsy.
In others again the decrescent disease proves consistent with
length of years and a persistence of no inconsiderable abilities,
whether of mind or body. One guesses that in these cases
the incidence is chiefly upon the long arteries of the limbs,
but, if so, these decay in the easy classes as in labourers.
I have still many a friend whose vessels, so far as they are
in touch, are, and for many a year have been, grotesquely
deformed ; yet who still turn out as fair a day's work as
most of their contemporaries, if with a slower recovery from
fatigue. The limitation of powers in such persons often lies less
in the quality of the work than in endurance, and more and more
in fatigue after effort. The labourer is incapable of a full day's
labour every day, and so is liable to dismissal ; but, in shorter
hours and without bodily exertion, the parson, or the judge,
may still turn out excellent work. Dr. Mitchell Bruce has said
(loc. cit.), " I have known a man live from the age of 73, when I
first saw him, and then found his radials sclerosed, and a systolic
murmur in the aortic area and albumin in his urine, to the age of

78 PROGNOSIS OF ARTERIOSCLEROSIS part i

93, enjoying reasonably good health." (This was, no doubt, a
case of my decrescent sclerosis ; no hyperpietic could show such a
history.) Dr. George Oliver writes i1 " Hypertonus is a frequent
and menacing concomitant of arteriosclerosis. . . . Arteriosclerosis
without high pressures (i.e. my decrescent form) is consistent
with length of days and a vigorous and active old age, pro-
viding that the blood pressures are moderate." They are
moderate ; the truth is, the cases are of different nature from
first to last, and the prognosis depends upon whether the patient
has the one disease or the other. Sir Thistle ton Dyer once told
me that Sir Joseph Hooker, at least thirty years before our con-
versation, had presented atheroma of the radial arteries, and
evidence of vascular disease elsewhere ; he ceased all exacting
work and retired to the country, and was then in good health,
with all his faculties unimpaired, at the age of 91, " though his
arteries were worse than ever." I do not feel by any means sure
that in these cases we are to assume too readily that the sclerosis
is wholly peripheral, and that the visceral vessels are intact. The
post-mortem revelations are by no means consistently to this
effect ; hearts and brains which during life had shown
little sign of failure, have after death exhibited vessels in states
even of well-marked decay. Happily the vessels of the base
and the great ganglia of the mid-brain usually harden before
those of the cortex ; when those of the cortex suffer, the
mind must sink in dilapidation.

Concerning Life Assurance, I have collected some materials
but find myself unable from them to formulate any maxims of
service. The tables furnished fail to discriminate between the
sclerosis of high pressures and the decrescent mode.2 So long as
Arteriosclerosis is accepted as a " disease," statistics are im-
possible ; the tables are compiled on heterogeneous materials ;
or, if blood pressures are taken, only the systolic are recorded.3

1 Oliver, G., Clin. Journ., 1908.

2 E.g. Burwinkel, Zeitschr. f. Versich. Med., 1909, Nos. 6 and 7. Dr. Jane-
way's laborious survey (Arch, of Int. Med. vol. xii., 1913) of many cases of
high blood pressure labours under another confusion, a confusion of all kinds
of morbid processes attended with such pressures. He was well aware of it,
but did not see his way to disentangle the coil.

3 E.g. the returns of the North Western Mutual Company of the United
States from 500 districts, city and rural, in which their referees are using the
sphygmomanometer. Under tests for life insurance few systolic pressures
would represent the mean condition.

chap, ix LIFE INSURANCE 79

No doubt a rule to reject all persons of 40 years and upwards,
whose blood pressure (systolic) ranges above a certain figure,
will exclude many persons unfit for insurance ; but, on the other
hand, it would exclude many more whose claim to insurance
would be unjustly denied. So long as systolic pressures only are
registered, the fallacies, as we have seen at length, are manifold ;
but, unless it be by the auscultatory method, which unfortunately
is a subjective record, we are not yet ready, either with instru-
ments efficient enough, or knowledge mature enough, to under-
take the test of blood pressures as a condition of insurability.

CHAPTER X

TREATMENT OP ARTERIAL DISEASE

Arteriosclerosis then, Bright's Disease apart, is, as we have
seen, not a clinical but a pathological name. The arterial tree, as
a whole or in parts, may undergo injury or deterioration in the
course of more than one series of morbid events ; we have seen
that however closely in the advanced stages all sclerosed vessels
may resemble each other in their superficial, or even in their histo-
logical aspects, the systemic disorders on which they ensue may
be several. If, towards the end of their life, the arteries abut
upon a common form of decay, the processes of initiation are
nevertheless various, each with its own primary pathological
features. For arteriosclerosis itself there can scarcely be any
treatment ; but as the modes of disorder leading to such damage
or decay of the arteries are several, each must have its own way,
and its own means, of therapeutical aid. It is in default of this
discernment that many careful and serious chapters on the thera-
peutics are in confusion ; 1 arteriosclerosis and high blood pressure
are taken as convertible terms, and as constituting a single
malady. But, as I must pursue that discrimination of the kinds
of arterial disease which I have adopted, let us consider the
treatment of :

(1) Arteriosclerosis, the effect of persistently high blood
pressures (Hyperpiesia).

(2) Arteriosclerosis (Toxic), the effect of certain poisons or

toxins as of syphilis, typhoid fever, lead, diabetes, etc., in many

of which the blood pressure is not necessarily, or usually, much

increased, if at all ; although in others, such as plumbism, it

may be raised throughout.

1 E.g. Strubell, Deutsche med. Wochenschr., Nov. 7, 1912, who classifies on
superficial, not radical, features.

80

chap, x OF HYPERPIESIA 81

(3) Arteriosclerosis (Decrescent), the effect of "senile" in-
volutionary changes, in which form again the arterial pressures,
if increased, do not exceed the quasi-normal increase which is
general in later life ; unless indeed hyperpiesis intervene, as not
infrequently it does (Vol. I. p. 452).

It is evident, then, that if these several processes arise
in different ways, they must be counteracted on different
methods.

In the first variety (Hyperpiesia) the increase of peripheral
resistance, upon which the rise of pressure may depend, is of
obscure origin. " The immediate cause is increased friction,
which must depend either on a narrowing of the arterial bed,
or on an increase of viscosity of the blood ; or, of course, upon a
combination of these factors." x How the viscosity of the blood
varies we have seen ; on the other hand, we have seen also that
the arteries may contract persistently over areas large enough to
maintain a considerable rise in the general pressure. The com-
pensatory mechanisms may be liable to get out of gear, or become
" labile." The proximate cause of such arterial constriction may
come from without, may be a product of distempered meta-
bolism, or may be an intoxication by refluent waste ; we have
seen that some such poisons exist, poisons which may act upon
the vasomotor centre, or widely upon the vessels themselves.
Until we understand these conditions rational treatment must
be retarded.

If we can catch hyperpiesia early, and keep at work against
it, it can be cured more often than not. " Malum nascens
facile opprimitur ; inveteratum fit robustius." Before, then, a
systematic treatment of hyperpiesia is commenced, we must
ascertain what, in the individual case, it is possible to
achieve. When the system has taken a new set, the whole
has readjusted itself -to the altered conditions, and the new
attitude is more or less permanent. Therefore, to bring back
the old equilibrium, of pressures by active treatment is out
of the question ; and diligently to attempt it is to do more
harm than good. Our first business must be to satisfy
ourselves, as far as may be, of the stage at which the patient

1 I am quoting my own paper of 1894. See recently Martinet, A., Pressions
art. et viscosite sanguine, Paris, 1912.

82 TREATMENT OF ARTERIAL DISEASE part i

has arrived. If, in a comparatively young man, say of 45-50,
after a period of bed and simple treatment, the heart has receded
within its normal dimensions, if the pulse has softened, and the
aortic second sound is abated, we may suppose that the dis-
order had not been long agate, and that the system may not yet
have suffered strain, that it may not yet have got that new
set. In such persons again and again we see that restitutio ad
integrum is quite possible. But if the vessels have begun to show
signs of strain, and the heart remains persistently out of bounds,
a bias has arisen which thenceforward may have, more or less, to
be accepted. If the morbid stresses could be removed altogether,
the altered bent of the arterial tree might never be rectified ;
strained vessels cannot be made anew. Notwithstanding, some
compromise may still be practicable ; if return to the normal
form be unattainable, by gradually modifying the stresses the
system may have so much resilience left as to find an inter-
mediate resolution. These conditions cannot be apprehended
all at once ; for a while our observations must be vigilant and
continuous, and therapeutic measures kept below the activity
which makes the patient feel uncomfortable. Here the sub-
jective sensations of the patient are a useful guide.

Furthermore, I must reiterate (see Prognosis, p. 76) the
precaution pertaining to all therapeutical methods, but which
bears with peculiar weight upon Hyperpiesia, lest by our diligence
and counsels we awaken apprehensions and meticulous self-
examinations of a kind and degree injurious to the patient's
equanimity. We should be slow therefore to order any long
stoppage or suspension of business, lest he " sicken of his
vacuity," which Milton said was Hobson's fate when his business
was broken up by the plague of 1630-31. We have seen that a
vigorous middle-aged man, when told that in spite of a seeming
of health he is the subject of abnormally high arterial pressures,
due probably in their turn to some perverted state of his nutri-
tion, may fall into a dread of an apoplexy, or of heart defeat.
He will be watching himself, wondering how his pressures are
running, touching his pulse every hour or two, deliberating on
his diet, fearing to walk up hill or stairs, until he becomes
hypochondriacal. In many cases, much, even to the goal of re-
covery, may be done, and a forecast of favourable issue given in

chap, x OF HYPERPIESIA 83

a cheerful and hopeful spirit. And I repeat that, in spite of our
reasonable desire to trace the periods of the arterial tides, we may
have to deny ourselves the advantage of frequent observations
and, when made, we shall be wise to keep the records to our-
selves. By the finger and the stethoscope a fair notion of
the patient's phases can be got : and if we are always silent
about figures, whether good or bad, the patient ceases to ask
about them, and abides content with general appreciations. We
shall tell him truly that as the arterial pressures are very un-
stable, and our instruments rough, we are guided, not by the
gauge only, but by broader views of his conditions as a whole.
I have learned that, fallacious as under the patient's anxiety
they are, to make incessant pressure observations as tests of
progress is unwise. Having got a grip of the case and of its
principles, we shall pursue our reasonable methods with as little
fidget over details as possible ; so long, that is, as the patient
is in no instant peril.

Nevertheless the proper preaching has to be done ; it is
idle to begin a course of treatment so prolonged and systematic
as these maladies require unless the patient has will enough
and perseverance enough to submit to tiresome rules, and to
methods which will make no little claim on his faith, so long may
it be before their good effects become plainly manifest and abiding.
Let him retire from posts of vexation and fatigue, whether in
business or in society ; and let us impress upon him the usual
if rather futile advice about " not worrying " ; but let us not
all at once knock a man off all his duties, either temporarily or
permanently. However for most patients, it is true, we have to
establish new habits ; to persuade the man to relinquish the
customs and manners of a lifetime. Some tractable persons
accept our counsels kindly, and pursue them methodically ; but
unfortunately the majority of our patients are of other temper :
some are impulsive, wilful, intolerant of discipline, especially of
self-discipline ; others, if more reasonable, are of ardent, untam-
able natures, admirable, it may be, in all relations of life except
those of the invalid ; others again imperiously demand at the
hands of the physician a cure they will not try patiently to
compass for themselves. Patience, gentle persuasion, sympathy,
a sense of humour and knowledge of men may do much, and

84 TREATMENT OF AETERIAL DISEASE part i

convert even the rebel and the faithless. For, as Huchard
well said, the question is one not of a drug but of a regime.

The foundation of all treatment must lie in the resetting of the
natural conditions of the patient, and in " Naturheilkunde " diet
(Vol. I. p. 238) comes first. In the cases of children (p. 172) the
rules of treatment, empirical as they are, are promptly efficacious.
The diet must be restricted, particularly in respect of fats, sugars,
meat, and strong broths. In these cases even milk may be
given too liberally, especially in its natural state ; for a child of 10
years of age, thus disordered, one pint of milk, prepared in one way
or another, may be sufficient for the twenty-four hours. Indeed
the quantities of food must be moderated in all directions, for the
mother is too apt to stuff the child, or the school-boy to stuff
himself. During the ailment, three or four rusks and a cup of
milk are enough for breakfast ; a little fight broth, with a biscuit,
may be given in the forenoon, and at dinner some plain white
fish, or chicken, with but little potato, and a light pudding.
Full plates of farinaceous or stodgy puddings, flatulent and
clogging to the digestion, are to be forbidden ; light steamed bread
puddings, a little blancmange, junket, and the like, will be
preferred. Tea to be as breakfast, rusks or dry toast being
better than thick slices of bread. Butter is to be given scantily ;
fruit, raisins, currants, jam, cakes, not at all. Some milk food
will make a sufficient supper. The temperature in these cases
sometimes rises a little in an irregular way ; when this is so, the
food should be even more sparing for the time, and but little of
it solid. If feverish the patient must stop in bed ; otherwise he
is better about, gentle exercise out of doors being encouraged.

Of medicines, mercury is the chief. It may be administered
as calomel or as grey powder. Grey powder is the form of which
in children I have most experience. Under the use of fractional
doses the breath sweetens, the actions of the bowels become more
normal, and the stools less offensive. For a child of 10, a quarter
of a grain of grey powder thrice daily may be ordered, and this
in repeated courses of four or five days at a time. The mouth
must be closely watched, and kept very clean. If the drug pro-
duces two motions a day, we need not hold our hand ; but if
mucus becomes evident in them, the remedy should be reduced
or suspended. As the tongue cleans, and the other symptoms

chap, x HYPERPIESIA IN CHILDREN 85

are mitigated, a bitter stomachic mixture may be administered.
Children dislike bitters, but they are efficacious, and if
pleasantly flavoured will be taken by well-disciplined children.
They should be given before the meals. The diet may now be
cautiously enlarged, but fats, sweets, and even starches are to
be given with a sparing hand. These children are often of
nervous stock, and their ailments may be coloured by whims
and ill-humours ; still, the disorder seems substantially to be one
of the jprimae viae.1 When thoroughly clear of the disorder, it
is helpful to give these patients cod-liver oil ; during the colder
months of the year this fat is so well digested by the young that
it may displace with advantage some of the other " rich "
elements of the dietary. Under this kind of management the
full sustained pulse and obtrusive artery gradually subside.
When the vessel returns to its normal tenuity I cannot tell, as
before this comes about one loses sight of the patient ; but, if some
years later an opportunity arises for a re-examination, it may
be found, should the amendment have been maintained, that
the walls of the vessels have returned to their normal state (Vol. I.
p. 178). The variation may lie in an increase of the muscular
tissue only. Whether these children are more apt than others
to fall into the hyperpietic disorders of later life, I am not yet
able to say. This is one variety of arterial disorder ; there are
others for which we have as yet no explanation, and therefore no
rule of treatment. Latent infections may be concerned in them.
In hyperpiesia of the adult, the symptoms may be not unlike.
Unfortunately, as we have seen, hyperpiesis often establishes
itself in the adult without betraying its presence, so apt is the
bodily system in adjusting itself to abnormal conditions. Indeed
high pressure in the cerebral vessels may give rise, for a time, to
a sense of well-being. A man of middle life may report himself
to be in excellent health, when, for a skin eruption perhaps, or
for life insurance, he comes to a physician, who may discover a
systolic pressure of 160-190 mm. Hg. The radial artery may be
already a little thickened, and the left heart moderately enlarged,
yet it may still be possible to restore the health more or less
completely if the man, who had regarded himself as healthy, will

1 Some recent observers have made the interesting suggestion that these
cases may prove to be mild degrees of acidosis.

86 TREATMENT OF ARTERIAL DISEASE part i

submit on trust to the long, close, and vexatious medical treat-
ment, and the irksome management of his diet and habits,
of which I have spoken. Diet is the foundation of all treat-
ment ; Hecht 1 says definitely that by diet hyperpiesis is reduced,
" in vielen Fallen bis zur Norm," in many cases cured. Strauss,
Hoffmann, and our own physicians give the same testimony.
On the other hand, to continue in this disorder for a few years
more will lead to death by apoplexy or by heart failure, even if
life be not cut short sooner by an acute pneumonia.

The patient then may get rid of his plethora and his cardio-
arterial strain, if he will pay the price. But I cannot help re-
peating that at a somewhat later stage the outlook is not so
hopeful ; the circulatory tree — heart and vessels — is now per-
manently altered, and a restoration of the normal balance may
be no longer practicable. In such a state to try to reduce the
arterial pressures to the normal disturbs the artificial balance
without re-establishing the original mean, and the dietetic and
other treatment is not completely successful ; at best it is a
compromise ; yet the compromise, in moderate cases, may
suffice to keep the disorder at bay, to postpone or prevent
an apoplexy, and to husband the resources of the heart.

Happily, if my argument is sound, the heart in these cases is
usually of good quality ; its coronary circulation, till checked
by atheroma, is at high pressure ; and even in atheroma, if
the progress of the disease be gradual, the nourishment of the
heart, stretched and strained as the organ may be, is kept up,
somehow or other, with a wonderful steadfastness (p. 542). The
so-called " weak " heart is often staggering under systolic
pressures of 200 mm. Hg, and great bulks of blood ! As an old
writer says, " After a plentiful supper, and his usual load of
liquor, he complained ; etc. etc." Our treatment of " weakness "
of this kind must not be that of a heart, under ordinary or low
pressures, failing intrinsically. Enlarged such hearts certainly are,
and sooner or later, if an apoplexy be averted, will sutler defeat ;
but we have seen that commonly such overdriven hearts hold
on heroically. With caution, and at certain moments, the
physician must use such cardiac stimulants as digitalis or stro-
phanthus ; yet his main duty is not so much to spur the heart

1 Hecht, Zeitschr. f. klin. Med. Bd. lxxvi. Hte. 1 and 2.

chap, x DIET IN HYPERPIESIA 87

on as to relieve it of its heavy burden. For, even if recovery
of the normal adjustment be past hope, much may be done to
maintain for a while some measure of equilibrium.

In stages of high pressure, early and late, the dietetic cure is
in principle the same. In many instances the rise of arterial
pressure is due to excess of food, positive or relative ; but
whether the harm is done by accumulation of putrefying stuff
in the bowels, or overcharge of the excretory organs by a pro-
fusion of digested but unused food in the circulation, is not
known, and ought not to be taken as known. We do not know
how far luxurious feeding means merely a passage of excess by
the stool, or a taking of food into the blood, only to be excreted ;
or again an incorporation in the tissues with inadequate in-
corporation of oxygen, or of constructive or destructive enzymes.
The subjects of this plethora, large eaters as they may be, may
not be fat, nor ruddy ; often they are so, but not a few are lean
and sallow. In some cases indeed the intake has not been more
than many persons dispose of easily — individuals vary widely in
capacity for disposing of excess of food — but has been more than
the individual capacity. Not a few big feeders, thanks perhaps
to good liver or kidney, manage to attain longevity. Many
of those who suffer, whether stout and ruddy or lean and
sallow, if they do not present a personal history of gout,
yet come of gouty stock, and are wont to regard themselves and
their people as gouty. Moreover, treatment directed against the
supposed gouty habit, especially a spa treatment, often answers
to expectation. If the man be fat, he must gradually reduce his
intake till he brings himself back near to the weight of his
earlier years — say to his weight at the age of 40. In men of
or beyond middle age, to bring the food down gradually, from
the old habit of vigorous youth, even to half the quantity
habitual to the patient, has in many cases the happiest results.
Sir William Osier says that confinement to bed for a couple of
months during severer reduction of the feeding is efficient in
moderating pressure ; a precaution to which I shall return. In
a certain case — one of aneurysm, treated on strict Tufnell diet
and bed — dishing1 noted that the blood pressure fell from a
morbid height to normal, and there remained for two months. If

1 C. Cushing, Boston Med. and Surg. Journ., March 1905.

88 TREATMENT OF ARTERIAL DISEASE parti

alcohol alone does not lead to atheroma (Vol. I. p. 249), yet in
conjunction with other causes — as we may see with lead-
poisoning — it has a strong contributory influence. The same may
be true of tobacco. Alcohol therefore must be cut out, or,
lest we fall into " un certain snobisme d'hygiene," as a French
vintner said of teetotalism, reduced to a nominal amount ; and
tobacco, tea, and coffee must be strictly moderated, especially
if there be any arrhythmia. Some persons find in whey a
pleasant and harmless drink. To " lactate " drinks I will
refer presently.

As regards the chief classes of foods — special dietaries —
temperance rather than exclusiveness should be observed,
especially, it is supposed, in respect of the nitrogenous, and of
those which contain purins ; but really of the effects of purins
we know little, and in most cases the main purpose is the restric-
tion of the whole intake. Erasistratus, who paid much attention
to plethora, preferred strict moderation of diet, and periods of
starvation, to venesection ; but he used some kind of com-
pression of the vessels of which we have no precise information.
A monotonous dietary, which may conveniently lessen for the
gourmand the temptations of the table, may for the temperate
and tractable patient blunt the appetite to some inanition.
Those abstemious persons who are so little able to manage,
normally and completely, even moderate quantities of food that
their habit fails to avert, or to dissipate, pressures morbidly
high, unfortunately for their virtue, have less promise ; the
original bias lies deeper (Vol. I. p. 241). But some of these
patients, such as well-to-do ladies and closet students, are also
of sedentary habits, and their excretory functions are sluggish ;
for them ordinary quantities of food are relatively excessive,
and restriction of food and alteratives may suffice for cure.

As regards particular foods, what are we to say when Brault
and Huchard, both of great authority in this subject, say, the
one (Huchard) that meat is poison to the hyperpietic, the other
that, as atheroma occurs in the herbivora, a vegetarian diet is
fraught with this mischief ! In all these cases the purin-
containing foods should be closely watched, and, so far as the
patient's tastes and appetites permit, reduced, yet again and
again I have placed high-pressure patients on purin-free diets

chap, x DIET IN HYPERPIESIA 89

(Walker Hall, and Haig), or on vegetarian diet with cheese,
milk and eggs, with no appreciable reduction of blood pressure
within such limit of weeks as to satisfy the conditions of an
experiment. Surely, if the purins were the cause of their
increase, the pressures should have fallen notably within a week
or two. Because a food is poor in purin we have assumed in
the past — we may have erred in doing so — that it would not
affect the general purin metabolism ; we have yet to learn
whether this be so or not. However, let us suppose that the
less purin the better, and that all animal soups, gravies, and
other meat extractives should be forbidden. We should forbid
also high meats, such as game and salmon, potted meats,
salt fish, caviare, and all " made dishes." Potain used to assert
that in a case of chronic renal disease a cup of beef-tea
(bouillon de bceuf) would send up the pressure by 40-50 mm. ;
but this might have been due to the salt in it. Dr. Oliver
advises that, in order to reduce extractives, the meat of the
dietary should be boiled. There is no practical difference be-
tween white meats and " butcher's " meat, but as red meat
is more sapid more of it is eaten. The " Salisbury " diet,
of mince-meat and hot water, certainly seems to be remark-
ably efficacious in some of these quasi-gouty cases, purins or
no purins.1 But we are not to overdo even abstinence.

For the following description of a purin-free dietary I am
indebted to an anonymous article in a recent number of the
British Medical Journal ; 2 as it expresses my own experience
I give it in summary :

After a probationary period the "purin-free" diet is thus
prescribed. The term " purin-free " is however a misnomer.
A precisely " purin-free " diet would be composed of milk, eggs,
white bread, cheese, butter, and a few vegetables ; but when
the milk contains many cells, as often it does, and the eggs are
not quite fresh, as often they are not, their purin content
comes within the range of our present chemical methods.
However, to return to a dietary designedly poor in purin.
For this purpose the following foods are at our disposal :
Milk — fresh or soured, buttermilk, or whey ; eggs — boiled,

1 On vegetable diet and viscosity see Vol. I. p. 117.

2 I have mislaid the date, but probably in 1911 or 1912.

90 TREATMENT OF ARTERIAL DISEASE part i

poached, scrambled, or raw ; white (not brown) bread and
butter ; macaroni and cheese ; rice, tapioca, semolina, and
vermicelli. Suet may be used for puddings of all kinds, such
as currant or jam roll, treacle, apple dumpling, etc. Pastries,
pancakes, jellies, and the usual tea cakes are also available.
All vegetables except the pulses (peas, beans, and lentils)
are poor in purin. Practically all fruits may be permitted.
As to drinks, tea, coffee, or cocoa are excluded ; hot water,
claret or burgundy, mineral waters, or hot milk may be
substituted. Beer and porter should be discontinued, and
indeed all alcohol diminished as far as the usual habits make
possible.

After a month or so of this diet some return to customary
food should be attempted. Brown bread, oatmeal, wholemeal,
beans, peas, nuts, asparagus, or mushrooms may be gradually
added ; and if it is desired to employ vegetable protein only,
these should play a large part in the dietary. When animal
protein is permitted, sweetbread should be the first kind of
meat allowed, since the purins contained in sweetbread are
" bound purins," and are hardly absorbed, the greater part
passing out in the fseces. Later, codfish, sole, plaice, mutton,
chicken may be permitted ; salmon, halibut, and beef and pork
being reserved for better days. When meats are taken they
should be stewed, not roasted ; and milk sauce substituted for
the meat gravies.

Even when a return to ordinary diet is made we should still
restrict tea, coffee, cocoa, and soups. With regard to extracts,
there is little to choose between any of the familiar prepara-
tions, all are to be avoided. The purins of yeast extracts
are less well absorbed than those of meat extracts, therefore
presumably less harmful ; but the differences are slight.

But I would not have it forgotten that the prescription of a
diet poor in purin calls for vigilance on the part of the physician.
He will watch for the danger signals of starvation, of glycosuria,
and even of mental bias, while some careful return towards
ordinary diet should be aimed at. We may gain some-
thing by the daily determination of the total purin output or,
when this is impossible, the weight and general condition of
the patient may be a sufficient guide. Under this regime there

chap, x DIET IN HYPERPIESIA 91

will probably be a diminution of the amount of protein con-
sumed, but, as the quantity of food necessary for the maintenance
of life and for the provision of latent resistance to disease varies
with every individual, and with the same individual at different
periods of life, so it is well to realise that prescriptions and
rules as to food can rarely be applied rigidly ; the attain-
ment of good results from the use of a diet poor in purin
depends not a little upon the sagacity of the physician ; even
then I have found it not so successful as enthusiasts suggest.

Milk diet is extolled by some writers as helpful if not curative ;
some say that it substitutes a harmless for a poisonous bowel
content, others that it stimulates the thyroid gland to work
in abatement of blood pressures.1 A milk diet, exclusively
speaking, can be but a temporary resource — say for a few days ;
a drinkable bulk of it contains too little food for a continuous
diet (4 litres = 2*300 cal.), unless the patient be kept in bed. If
we desire to withhold lime, the milk must be decalcified with
sodium citrate. In any case, rice, eggs, and sound cheese, foods
which give nutritive value without bringing in purins (Bradford),
or even a little meat, must soon be added to it.

The Karell cure consists not in the milk only, but also in
Oertel's method of relief of the heart's work (not of the blood
pressures) by reduction of fluid. Many plethorics are copious
bibbers, and bring on " polydipsia " and " polyuria " ; a per-
verse equilibrium. The fluid in the " Karell cure " is cut down
to 1-1| litre, the milk being given in four doses, at 8 a.m., 12
noon, and 4 and 8 p.m. After two or three days some egg,
biscuit, and flour are added. This diet should not be pushed
beyond ten days. Even if the urine be scanty and thick, under the
lesser intake diuresis will set in ; and on the spare nourishment
blood pressures should fall, and probably viscosity also, unless the
patient were hydraemic. Much harm is done at spas by reckless
gulping of waters, under the quackish pretension of " washing
out the uric acid " ; for all the time, especially if the kidneys be
inadequate, the patient may be hydrsemic. This, and such
conditions, must be distinguished from that of essential cardiac

1 Chalmers Watson, Lancet, Oct. 12, 1907, and Brit. Med. Journ., Dec. 21,
1907, who thinks " there is no special therapeutical effect in a purin-free diet,
not equally attained by a carefully planned diet without such special reference."

VOL. II G

92 TREATMENT OF ARTERIAL DISEASE part i

failure, in which the Karell and Oertel plan must be followed
with great caution, if at all. We must not forget that milk is
not by any means a saltless diet ; but of this I shall speak
presently.

A strictly vegetarian diet is bulky, and low in proteid value.
Oliver thinks that under it high pressures are moderated. I have
been disappointed with all these narrow dietaries — the Haig diet,
the vegetarian diet, and so forth ; patients do feel, it is true, mar-
vellously better, even for some months ; they are relieved of the
effects of food too rich or abundant for them ; but in six months
or a year they revolt. Not only is the new diet insipid but they
find it inadequate. Yet as temporary expedients these exclusive
diets, if used with care, are efficacious. It is a common belief,
which I share, that oatmeal is a valuable and wholesome food
deplorably neglected. It is difficult nowadays to get good oat-
meal ; the advertised oatmeals are too often adulterated with
inferior cereals, and the meal of the best oats is spoilt if ground
and bolted on the modern rollers and silks. To be nutritious and
palatable oatmeal should be stone ground from the best oats.
Dr. William Russell says that oatmeal, supplemented by such
booty as they could lay hands upon, was not only the domestic
but also the commissariat staff of fife of the Border raiders.
A vegetarian diet is, of course, rich in lime, a condition of
arteriosclerosis which I have already discussed (Vol. I. p. 504).
An anticalcareous diet, such as Rumpf and others prescribe in
arteriosclerosis, would mean also the exclusion, or great reduction,
of milk. But this mode of degeneration will always find lime
enough ; even if calcification were mischievous, what Ludwig
Braun calls the " naive practice of withdrawal of lime from
the food," is absurd. But calcium salts might perhaps so
increase the viscosity of the blood (Vol. I. p. 110) as to raise blood
pressure, or determine a thrombosis. As to the sum of protein
required per day, or per week, for the permanent support of the
body, the opinions of experts differ so widely that we must
take it as unknown. We are pretty sure however that it is
considerably less than was supposed in the last generation.
Still my experience is that ultimately under an insipid or
monotonous diet the appetite flags, the digestive reactions
grow languid, the spirits sink, and any ill proclivity of the

chap, x DIET IN HYPERPIESIA 93

system is perhaps promoted, or at any rate not withstood.
A good deal of allowance has to be made also for old habits
and individual constitution. A philosopher, whether medically
qualified or no I forget, has said : " Nut cutlets, proteid potatoes,
lentil sausages, mock forcemeat, vegetable sauce, uric-acid-free
marmalade, malted wheat biscuits, sterilised cream cheese, non-
caffeine coffee, apple juice wine : Result, severe domestic dis-
cord ! " It is as a temporary expedient at a time of crisis that
a limited or even an ascetic diet, while working with the
patient's hopes, may be, as often it is, the most effective of all
our therapeutical means.

Fruit, as I have said, is a welcome and usually wholesome
food for subjects of cardio-arterial disease, save those who are
disturbed by dyspepsia, distension of stomach and bowels, gripes,
or lax stools. Dr. Jerome of Oxford found that, so far as
they agreed with the individual digestion, pears, fresh figs, grapes,
dates and oranges might be taken, even by gouty persons, with
impunity, and even with advantage. Apples and pears, apples
especially, agree better when cooked ; mastication is rarely an
efficient pulper of a crisp apple.

Tea and coffee, which contain purins, are less and less well
tolerated as years advance into age ; and thus may carry
some significance as tests of normal circulatory reactions. But
concerning them, and similarly of tobacco, I have written at
length on another page.

Antiseptic measures, addressed directly to the bowel and
given by the mouth, are probably ineffectual. If such an
effect be urgently needed, /3-naphthol is, in my experience,
the best of these drugs ; the sulphocarbolates may have some
value.

Concerning common salt, we have seen in former chapters that
there is much to be said ; and in this respect a distinction between
hyperpietic, renal, decrescent and toxic arterial disease is essential.
Some writers say that salt tends to raise blood pressures, but as
yet on insufficient evidence ; x much must depend on the rate of
its elimination in particular cases. Dr. Leonard Williams says
also — what however is not quite the same proposition — that a re-
duction of salt intake may abate high pressures. The part of the
1 See Boyer, Journ. Exp. Path, el Pharm., July 1907.

94 TREATMENT OF ARTERIAL DISEASE parti

kidney in these ionic balances is still obscure. In hyper-
piesia the kidneys may be intact ; moreover kidneys in
disease may for a short time still let through certain bodies,
caffeine for instance, with no less freedom, even if taken in
excess. In the third stage of hyperpiesia however, when
the heart is getting beaten (" Hochdruckstauung "), the con-
gested kidneys fail duly to discharge the salt, and a fortnight's
salt discipline may be needed. Otherwise a day or two of de-
privation now and then will suffice. During salt abstinence a
little lemon or tarragon will make the food more sapid. A
kidney which is detaining sodium chloride may pass methylene
blue, but it is a long jump from this uncertain ground to Ambard
and Beaujard's conclusion,1 when they assume that plus blood
pressure means plus salt (" chloruration "). They infer that, if
digitalis cause a diuresis of salt, then digitalis is a " hypotensive "
drug, and suggest that theobromine, which has many advocates,
may often compass the same end. Achard, from another point
of view, thinks that salt is retained as a protection against some
toxin ; other writers say that the toxalbumins retain the salt,
whereby pressures are raised. All these conjectures are still in the
clouds ; but we are more and more sure that somehow or other
sodium chloride may be so retained in the body as to cause, or
to be correlated with, oedema manifest or latent (Widal's " pre-
cedema "). Vaquez prescribes complete salt deprivation for two
days the first week, for one day in following weeks ; the whole
salt intake on intermediate days not exceeding 1^ gm. of salt
per diem. If, he says, in a hyperpietic case we notice cough,
distended stomach, mental depression, dyspnea or heart disorder,
withdraw the salt. How, by watching body weight, " pre-
cedema " may be ascertained I have said already. Whatever the
explanation may prove to be, the effect of withdrawal of salt from
the diet in oedema is often amazing ; and if the uncertainty of this
result hitherto shows that we have not yet grasped the full
conditions of the problem, yet the dissipation of serosities often
clears up menacing conditions, even cerebral symptoms, in a
surprising way. Any saline ingredients in the medicines must
of course be taken into the reckoning. Salted meats, often also
indigestible in texture, must be forbidden, and the salt-cellar
1 Ambard et Beaujard, Arch. gen. de mid., mars 1904.

chap, x DIET IN HYPERPIESIA 95

used sparingly if at all. Whether then the salt be held up in
the tissues, or accumulate behind defective kidneys, we do not
yet know, at any rate not in particular cases. We must watch the
bodily weight, and manage the salt accordingly. On the other
hand we shall beware lest we run salt deprivation too hard.
If at a time of urgency all salt must be withheld, even in the
baking of the bread, this rigid exclusion should not last more
than a very few days, if only because of the languor of appetite
and digestion which may ensue.

That there is any harm in other spices and condiments,
which may be grateful to the palate, I cannot say ; but " highly
spiced " food usually means something more, it means rich and
elaborately dressed dishes. In dressings lemon juice must be
preferred to vinegar.

While we were all engaged in lightening the protein cargo,
and filling up with starches, sugars, and fats, we were
pounced upon by Dr. Francis Hare, who urged that the carbo-
hydrate extreme was at least as perilous, if not more so.
We shall go at least this far with Dr. Hare, to admit that in a
being so complex as man, whose body has been developed and
balanced during ages untold by an infinite variety of external
conditions, either, or any, extreme rule of life is to be avoided.
We know by direct experiment, particularly by experiments with
large doses of syrup, that normal men differ widely in their
relative capacities for this function and for that, and particularly
for carbohydrates. It is the delicate office of the physician to
equilibrate, so far as his science can tell him, the natural capaci-
ties of the individual patient and the sum of his conditions.
Senator 1 also, although he dreaded nitrogenous putrefaction in
the bowel, has cautioned us against excess of carbohydrates in
hyperpiesia, especially in fat people ; he preferred to give them
a little meat with fruit and green vegetables. He prescribed
also gymnastics and light purgation. Dr. Graham Steell 2
prescribes a diet much on the same lines as those of Senator's
later papers. I think that, although overfeeding with carbo-
hydrates may be more harmful, and the excess not so readily
burned up as we have supposed, yet the harm of excess of proteid,

1 Senator, Ther. d. Gegenwart, Marz 1907.
2 Steell, G., Med. Chron., Dec. 1902.

96 TREATMENT OF ARTERIAL DISEASE part i

of which we need comparatively little, must be far greater, ex-
cept in persons whose capacity of dealing with carbohydrates
is constitutionally narrow.

Although Chittenden's researches suggest that mental work
makes a remarkably small demand on food, yet unfortunately
sedentary mental work in towns seems to sharpen the appetite.
The standard of the real needs of the body must, more or less,
be regulated by the scales ; but in spare patients who are not
large feeders we must be guided by the progress of the case, and
by clinical observation.

To turn now to the issue of the food ; the abiding high
pressure suggests to us that metabolism is imperfect or perverse,
that waste proteids are re-absorbed, or that certain organs are
in defect. Although it is an error to suppose that an annual
six weeks' " cure " can take the place of a systematic, patient,
and persistent regimen, yet from spa treatment, as for instance
at such resorts as Harrogate, Royat, Evian, Carlsbad, Marien-
bad, Homburg, we shall see (p. 103) that striking results are
to be obtained.

It is in the first, often latent, stages of the malady, in sound
subjects, when the abnormal pressures are not of long standing,
and the consequent ill effects upon the heart and vessels are
incipient, or even yet to come, that cures are to be made. Periods
of five years or more, according to morbid degree and individual
equation, may elapse without permanent strain. In the first and
curable stage, unless the peripheral resistance be unusually high
and obstinate, there are better methods for the restoration of the
circulation than artificial baths and exercises ; namely, natural
exercises. In such cases — and we should now be catching them
earlier and earlier — patients are to be encouraged cautiously to
take more and more exercise. As Thomas Adams said, " Labour
and moderate diet are the poor man's friends, and preserve him
from the acquaintance of Master Doctor, or the surfeited bills
of his apothecary." When the heart has been relieved of stress,
and is pulling itself together, gentle games may be recommended,
especially such as do not require sudden efforts. Gentle cycling
on the level, quiet walking, even on the lower hills, golf, and so
forth, are useful. The efforts of tennis, even of the lawn variety,
are too sudden. It is of enormous advantage if we can throw

chap, x EXERCISE IN HYPERPIESIA 97

open the vast muscular areas to the blood currents, and thus lower
resistance and wash away impurities. Then, if all goes well,
for patients disposed to recurrent hyperpiesis but in whom the
vessels betray as yet no considerable signs of lesion, there is no
medicine like carefully regulated hill-climbing. This " terrain
cure " for rising blood pressure is provided, together with other
appropriate means, in some English health resorts, as at Church
Stretton. The purpose of the method needs little explana-
tion. When a healthy man essays to climb a hill, he will find,
as I have taught for many years, that during the first two or
three minutes the radial artery maintains its calibre ; so
probably do the chief arterial beds in the skin and muscles.
During this period, the exertion raises systolic and diastolic
pressure, embarrasses the breathing, and throws more stress
upon the heart. But on cautiously proceeding, although systolic
pressure may still be high, and even rise, the radial artery
dilates, not gradually but rather suddenly, to perhaps twice its
lumen, and the pulse becomes dicrotic ; this signifies, no doubt,
the opening of other large arterial areas also ; therewith diastolic
pressure falls, and the respiration gains freedom ; we get, as the
phrase goes, our " second wind." During the initial effort no
therapeutical caution can bertoo great ; but after this expansion
the walker will proceed with more and more ease. In an untrained
man this expansion comes later, and in a hyperpietic later still.
Until it occurs, the patient should proceed very cautiously and
slowly in his ascent. Indeed this expansion coefficient should
be our guide in regulating the exertion. The patient may soon
learn to observe it. Arterial (radial) expansion is more important
than pulse rate ; and a few extra systoles during this period need
cause no alarm ; if the exercise can properly be continued these
will disappear. Even in healthy but untrained men some care
in hill-climbing is necessary at first, but it is hill-climbing especi-
ally which is effective in developing the respiration. Potain
made blood-pressure observations on three classes of recruits :
(i.) new recruits, (ii.) recruits after six weeks' training, (iii.) re-
cruits of nine months or more standing. All were between the
ages of 20 and 24. In those of the second class, the blood pres-
sures fell permanently by an average of 10 mm. ; in those of the
third it ranged 20 mm. lower. In their gymnastic teacher it was

98 TREATMENT OF ARTERIAL DISEASE parti

30 mm. less than these, observations which agree with Dr. MichelPs
on undergraduates.1

How far this searching but efficient method may be applicable
to a particular case must depend on the discernment of the
wise and expert physician. Every person from the age, let us
say of 45, would be wise to have the arterial pressure measured
every four or five years ; oftener, if it be found above the mean
for the period of life, or if morning depression of spirits, disturbed
sleep, constipation, biliousness, or other vague discomforts suggest
that the exchanges and discharges of the body are going wrong.
Upon him who comes of a family in which gout or apoplexy has
appeared, such counsels are the more incumbent. The muscular
and fascial stresses forward the blood by pressure, if, indeed,
they do not exert some suction upon it (Braune quoted by Krehl),
and the peripheral vessels dilate. The effect of muscular activity
on the circulation was well illustrated in the days of bleeding,
when, if the stream did not run freely, the operator would request
the patient to clasp and unclasp his hand quickly. The muscular
system is not an organ of locomotion only ; it is also a hearth of
heat generation, and probably an organ of metabolism.

In exercise, natural in early and mild cases, or in severer or
more critical cases artificial, the respiration is of course a large
factor. Although, if exercise be begun gradually, no healthy
temperate man, if 50, 60, or even 70 years of age, should feel
short of breath on climbing hills, at the mountaineer's pace, yet
step by step his breathing becomes deeper.2 Whether chiefly by
washing out carbon dioxide, or by carrying in oxygen, or again by
the " respiratory pump " acting upon the circulation, as exercise
proceeds the mean arterial pressures fall, and the heart, pulling
itself together, diminishes in diameter (de la Camp, and sub-
sequent orthodiagraphists), and viscosity is reduced. The mere
inhalation of oxygen or of carbon dioxide while at rest has
no obvious effect.3 Unless in cyanosis or ansemia, conditions

1 Vide my art. " Heart Stress," Allbutt and Rolleston's System.

2 I need only refer to the well-known observations of Haldane and Smith, of
Pembrey, Oertel, Beddard, Keith, Halls-Dally, Hill and Flack, G. N. Stewart,
and others. Also my "Heart Stress " article (loc. cit.).

3 Stewart, G. N., Journ. Pharm. and Exp. Ther. vol. ii., 1911, and Journ.
Exper. Med. vol. xiv., 1911. But see also Hill and Flack, Journ. of Physiol.,
1910, vol. xl.

chap, x EXERCISE IN HYPERPIESIA 99

in which natural exercise would not be prescribed, or at
any rate not hill-climbing, the bulb has probably less to do
with the benefit than the muscular activities, skeletal and re-
spiratory. The respiratory machine Miura of Tokio calls the
second heart ; it may however be added, as a third, to the
peripheral heart, which also in hyperpiesia is disordered. Miura
says that as in enlarged heart the inspiratory muscles are hyper-
trophied, so in enlarged left heart are the expiratory. In passive
exercise he massages and faradises both sets of muscles.

Familiar as the warning has become, I ought not to omit to
repeat that towards middle life it is foolish, in the midst of
a sedentary life, to try to redress the balance of function by
plunging into unwonted muscular exertion. After long inaction the
peripheral vessels do not respond quickly to sudden demands ;
and after the age of 36 the elastic limits of our tissues are
narrower. If the town worker, even as a comparatively young
man, is to return from his holiday with a purified and invigorated
body, he must train himself gradually to efforts which a few
years before he had found more promptly possible and beneficial.
For a definite task it is calculated that the trained man can get
done by 12 per cent of his possible energy output what in the
untrained takes 30 per cent of it. In middle life such efforts
bring more weariness, and exhaust the animal spirits, at any rate
in the first seven or ten days of the holiday. The recent fashion
of golf, if not a manly game for young men, is [nevertheless an
admirable pursuit for men of or near middle age and after ; for
it can be taken easily or more energetically as the player's state
of training may dictate. It is difficult to speak with patience of
the men who, in the intervals between their feeds, lounge in
motor-cars. Riding on horseback, the best of all exercises for
adults, seems, except in the hunting-field, to be falling more and
more into disuse ; and with this growing indolence and luxury
blood pressures will be augmented. Let us remember then
that with gluttons, as indeed with all well-fed sedentary people,
we must begin exercises very gradually and watchfully, and not
forget that a fall of pressure may be due less to purification than
to fatigue. We shall make ourselves sure also that the heart and
vessels are still sound : no systolic murmur at the base of the
heart ; no bronchitis or emphysema to increase cyanotic viscosity.

100 TREATMENT OF ARTERIAL DISEASE part i

But let us suppose, always in respect of hyperpiesia, for of it,
not of the decrescent disease, we are still speaking, that we cannot
thus develop our exercises from quiet walking to regulated hill-
climbing : how are we to act ? The heart is doing all it can ;
the vessels are not to be trusted, or the patient is elderly. Well,
we must go to the other extreme, and put the patient to bed,
looking forward to advancement by passive exercises, and by
baths. In bed, say for a week or ten days, excessive arterial
pressures usually fall slowly, sometimes near to normal ; prob-
ably because of opening of the periphery by the equable warmth.
In a week or ten days we learn what in the individual can be done
in this way ; the pressures may reach some lower but still per-
sistently high level. Of course other factors, such as pulse rate,
output, cardiac signs, and so forth, must be carefully observed ;
a fall of pressure may be due to declining heart.

This plan of bed for a few days answers very well for the
episodical cases of hyperpiesia in elderly persons (Vol. I. p. 452),
but in no case should it be continued for more than (say) a fort-
night without passive exercises ; and he must be a very sick man
who needs a longer rest in bed, even during artificial exercises.

Of the artificial exercises, for cases in which natural exercises
are inappropriate, massage is perhaps the best. Much depends
upon the skill of the massor, especially in manipulation of the
abdomen, a very important part of the reaction. In massage of
the limbs, Dr. Herbert French lays stress on expert kneading
and stroking of the arteries themselves, whereby a better nutri-
tion of their coats may be obtained (or a morbid constriction
reduced (MacWilliam)). Thus the peripheral or, by abdominal
massage, splanchnic areas may be opened out, the movements
of blood, juices and excretions quickened, and viscosities reduced.
Dr. French speaks of a " stiffening " stage of the muscular
fibres, which later, unless averted by massage of the tunics,
will end in fibrosis. Whether the arterial muscle gets out of
training, and thereupon stiffens, I do not know. Oberndorfer 1
also thinks that by the massage of ordinary exercise the peri-
pheral arteries supplying the joints become less prone to
sclerosis. This direct method seems to be more applicable
in decrescent sclerosis than to arteries under hyperpietic
1 Oberndorfer, Deutsche Arch. f. klin. Med. Bd. cii.

chap, x MASSAGE IN HYPERPIESIA 101

stresses. In this kind, the way to save them is indirectly by
moderating the high blood pressures, to which end also massage is
a valuable aid. The long vessels of the limbs, almost the only
vessels which massage can reach directly, may, as it seems at
present, fall into one or other mode of arteriosclerosis ; the ordi-
nary mode in which the media perishes by the encroachment of the
intimal change upon it, or the mode, or degree, known as Moncke-
berg's (Vol. I. p. 482), a medial necrosis issuing in calcification ;
a dissolution which may or may not be associated with a substi-
tutive fibrosis partly from the intima. In this mode however
fibrosis is not a primary or a prominent feature. Fibrosis, due
to lateral pressures, mechanical stress, is apt rather to arise under
the influence of high blood pressures, primarily in the intima
(Thoma, etc. ; see Vol. I. p. 489); but in the arteriosclerosis of
high pressures (Hyperpiesis) the median muscle can scarcely be
languishing for lack of work. It is in this condition that
large arterial areas may be over active, spasmodically con-
stricted, even in the limbs, as indeed we may often perceive
in the radials. These problems cannot then be discussed fruit-
fully unless the distinction between hyperpietic and decrescent
or senile arteriosclerosis be continually kept in mind ; for in
at least half the cases of sclerosis there can be no fibrosis due
to exorbitant pressures. These reflections are by no means
intended to diminish the value of Dr. French's method, which
will probably prove very useful both in the decrescent and in
the hyperpietic kinds ; if it be not required for the vessels, it is
well adapted to open out peripheral areas such as the musculo-
cutaneous, and to reduce resistance. Massage of the limbs and
back seems normally to cause a rise of arterial pressure, at any
rate at first ; of the abdomen, a general fall ; but if there be a
wide splanchnic constriction, this natural reciprocation may not
follow. Miura's massage and faradism of the muscles of respira-
tion, and the value of " respiratory gymnastics," I have already
mentioned. Respiratory exercises should be practised gently,
the patient being first encouraged to draw deep breaths. It
is said that high arterial pressures may be reduced by breathing
in rarefied air ; of this method I have no experience.

The systematic passive exercises of Lang and August Schott
for cardiac dilatation have no special place in the treatment

102 TREATMENT OF ARTERIAL DISEASE parti

of any kind of high blood pressure or arteriosclerosis, or in
hyperpiesis not until the heart is suffering ; then these methods,
with other means of cardiac therapeutics, may take a secondary
place. Otherwise, both for mind and body, voluntary exercises
are to be preferred. In hyperpiesia the " Nauheim methods "
are not generally required ; the heart, if it can have fair play,
is good enough ; nevertheless, in occasional cases, after reducing
the mean blood pressures, baths, exercises and digitalis may
assist us in helping the heart back to more normal diameters.
Gibson preferred the Swedish to Schott's method.1

Emphysema of the lungs, frequent in the decrescent class,
in hyperpiesis would add to our difficulties. When the patient
has begun to suffer from cardiac dyspnea, and dilatation is
advancing towards mitral incompetency, we must recognise the
unwelcome truth that the heart is undergoing defeat ; a sub-
stantial and permanent restoration of cardio-arterial balance is
not then to be hoped for ; on the contrary, fall of pressure by
heart-failure may be feared. Then the pulse usually rises in
rate. Something may yet be done, but too many leaves have
been torn out of the book.

On climate in hyperpiesis I have little to add to the dictates
of common sense. In high-pressure cases the patient should not
exceed altitudes of 2000-2500 ft., and these heights should be
reached cautiously ; it is better to state 1500 as the limit.
Mountains, and northern and eastern aspects, should be avoided.
Two or three times patients have informed me that it was while
stopping at high altitudes that the symptoms of high pressure
first manifested themselves, especially as dyspnea, chiefly
nocturnal ; and thrice at least under my own observation
subjects of hyperpiesia have been seized at high elevations (4000-
5000 ft.) with apoplexy. Too sudden a change from low to
high altitudes raises arterial pressures (Potain, and others since).2
And as statistics seem to indicate that apoplexy is more fre-
quent in cold weather, we must take precautions accordingly.
Nevertheless, vigorous and undamaged subjects of early hyper-
piesia, who can be gradually inured to moderate heights, and to

1 Gibson, G. A., Section of Pharm. and Ther. Brit. Med. Assoc., 1912 {vide
Brit. Med. Journ., Aug. 17, 1912).

2 See also Oliver, G., Lancet, June 13, 1903. But see Vol. I. pp. 181-2.

chap, x CLIMATE IN HYPERPIESIA 103

hill walking, find in the sweating during exercise in the dry-
evaporating air of the Alps a remarkable effect for good. There
are of course other contingencies to be taken into account, such
as the vasoconstricting effects of cold to the skin.

For decrescent arteriosclerosis a mild and equable cliniate at
moderate elevations is to be preferred from the beginning.

We read of sanatoriums in America where all these methods,
with proper diet and medicines, are co-ordinated and variously
administered according to the needs of particular cases. Dr.
Sprigg has, I believe, opened such an Institute near Banff. In com-
panies people will submit to a drill which singly they would shirk.

Diaphoretic methods, at first sight likely to be useful in high
pressure, are, in my experience, disappointing. I have tried hot-
air baths, such as the " Turkish," hopefully, carefully, and per-
severingly ; but they have not given relief to the patient (often,
indeed, they have caused discomfort), nor established any abiding
reductions of blood pressure. Now I do not advise them.

Of spa baths there is something more to be said, though it
is not easy, in the absence of any discrimination between the
arteriosclerosis of one series and of another, to discern the signifi-
cance of most of the reports of bath treatment. Moreover the
sphere of medical experience at a spa is confined to such cases
as it may be customary to send thither. Notwithstanding,
we may clear the problem to some extent by putting aside, at
any rate for the present, decrescent arteriosclerosis, for which
baths are of no specific service, and keeping our attention upon
excessive blood pressure, a condition over which we might
expect baths to have some influence. In cases of this series
however von Basch, whose experience at Marienbad was very
large, found no advantage from baths ; indeed he thought they
often did harm. Dr. Oliver, on the other hand, from his Harro-
gate experience, has recommended the Aix douche-massage,
followed by a needle bath of alternating temperatures, and warm
pack. Dr. Mantle of Harrogate says that hyperpiesia is quite
curable there if taken in time.1 My observation is that in a bath
of 98-100° F. the radial crimps up for two or three minutes, during

1 Mantle, Lancet, May 6, 1911, p. 1206. A useful article on many points.
See also " Thermal Environment and the Circulation," by Dr. Lyth, 1913 — an
attempt to reduce these problems to scientific method.

104 TREATMENT OF ARTERIAL DISEASE pabt i

which time it is difficult to catch a record ; then the height of the
pulse-wave rises, and the mean pressure falls 15-20 mm. Pawlow,
I see, has demonstrated this fall, and its persistence for some time
after a warm bath. The initial rise of pressure should be avoided.
It was no doubt in the second phase that Schapals, with the ray-
screen, saw the heart diminished in size, and found the arterial
pressures not increased.1 We may anticipate, I think, that
the douche-massage and warm pack, in expert hands, would
coax the peripheral circulation into activity, and with the
alternating needle - bath would re - create a fairly equable
vasomotor system. What is certain is that bath tempera-
tures—whether of hot air or hot water — above or below the
" neutral zone " drive up the arterial pressures, not for the
moment only ; and albumin, as in too cool a bath, may appear
in the urine. It is clear that we must begin at the neutral zone,
and cautiously increase the temperature as the periphery opens
out. Dr. Fortescue Fox,2 for the release of vasoconstriction
and high pressures, advises " subthermal " baths, at a tem-
perature between those of the blood and of the surface, and
with these and even cooler baths he tries to keep these conditions
at bay. He recommends, very reasonably, prolonged baths, as at
Leuk, in natural warm waters below blood heat — say 89-90° F.
Thus any initial rise of pressure sinks to a small proportion of
the whole effect. Ottfried Muller, who has made some careful
observations on this subject,3 says all douches are " cardio-
gymnastics," as they raise the blood pressure, and this the
more if above or below the indifferent point ; it seems desirable
therefore to begin with the warm pack, and follow very
cautiously with " vasomotor gymnastics." A warm bath alone
leaves the skin susceptible to chill ; and Winternitz declares
that friction with water at 40° C. and 8-10° C. alternately, carried
out vigilantly and scientifically by experts, not only prevents the
cutaneous susceptibility, but also lowers the blood pressure on
the whole. This method may be beneficial to persons essentially
sound, such as early non-renal hyperpietics whose heart and

1 Schapals, Zeitschr. f. exp. Path, und Ther. Bd. x., 1912, an interesting
article on baths at various temperatures, etc.

2 Fox, F., Brit. Med. Journ., Feb. 15, 1908.

3 Muller, O., Deutsche Arch. f. klin. Med. vol. lxxiv., 1902, p. 316.

chap, x BATHS IN HYPERPIESIA 105

vessels are still equal to such discipline. Such methods have
another kind of good effect also, a bracing effect upon the
nervous system. Miiller, besides the effect of douches, came
to further conclusions : that water baths a little under the
indifferent zone (say 33-34° C.) raise blood pressure, not
momentarily only but during the whole bath, and retard the
pulse ; that a little warmer, and gradually warmed up to (say)
40° C, they cause a momentary rise of pressure, but then a con-
siderable fall, even near normal ; then comes a renewed rise, which
is persistent : that baths over 40° C. cause a persistent rise,
but with plus pulse-rate ; that " Nauheim baths " raise pressure
more by the temperature than by the carbonic acid gas, but
both affect the pulse (if the Nauheim bath lowers the blood
pressure great vigilance is needed) ; and, finally, that all
sweating baths — hot air or steam — raise both blood pressure
and pulse rate. Groedel says confidently that by careful
precautions rise of blood pressure can be avoided. But nearly
all these baths affect the heart-work, and the greatest care
is needed in cases in which the heart is either overborne or
degenerated, or in which the kidneys are behindhand. Pulsus
alternans would be a bar to bath treatment, and to all " vascular
gymnastics." The function of the kidneys is to be tested by
the diuresis method, as at Roy at, Evian, etc. ; by phthalein,
or, if possible, by Ambard's method (Vol. I. p. 322). Ortner
agrees on the whole with Miiller.1 " Indifference " in a bath —
plain, saline, or effervescent — seems to be an ideal point, or one
would say : Begin at the point of indifference so as not to
start vasoconstriction ; then with care raise the temperature,
opening out the surface vessels gradually. The advantage of
saline, or of a mantle of bubbles upon the skin, is that a cool
bath does not feel chilly, and that changes of temperature are
moderated. In Luftperlbader (bubble-baths) some authors think
it does not much matter, save for suggestive purposes, what air is
used — common air, C02, or 0 ; but it is better to keep to common
air, as the temperature conductivity of gases varies considerably,
and is not parallel with the water temperatures. Moreover air
bubbles are a little less adhesive to the skin than those of C02,

1 See also article by Sadger (of Wien-Grafenberg), " Die Hydrotherapie der
Arteriosklerose," in Ther. d. Gegenwart, Nov. 1908.

106 TREATMENT OF ARTERIAL DISEASE part i

and so in critical cases are less stimulating. H. Senator and
Schiitgen1 find that air and oxygen bubble-baths are less irritant
than those with C02, and that at indifferent temperatures they
lower blood pressures. They relate two cases of air bubble-baths
which lowered pressures more than did warm baths, C02 baths
or 0 baths. Hydropathic systems are not carried out at home
with the same expert supervision and scientific method as in
Germany, too much is left to the attendants ; so, as German
ways of life are unsuited to the habits of most of our country-
men, my experience of hydropathy is not very large. During the
bath or pack, at any rate in new patients, frequent observations of
pressure and of rate should be taken ; there must be no cooling
down ; warm wrappings, and at least an hour's bed, should
follow every bath.

Dr. Groedel,2 who has studied the effects of Nauheim baths
with discernment between hyperpiesia and decrescent arterio-
sclerosis, although he claims so complete a control over their
pressure effects, wisely advises great caution in their use in
cases of high blood pressure or of stenocardial attacks ; though
with care they may be available. Unfortunately after the bath
the blood pressure rises again rapidly, an oscillation which in
stenocardia may be distressing and even injurious. Begin, he
says, as closely as possible to the temperature of the skin, and with
very little gas or saline. It may be judicious at first to give only
partial baths, and of short duration ; though it would seem well,
if some preliminary rise of pressure cannot be avoided, to carry
the bath into the second stage, that of fall of pressures. Peat
baths, with careful grading of temperatures, are said to be
effectual in lowering blood pressure and accelerating the blood
stream through the periphery ; this I am ready to believe, and
their warmth is easily kept constant.

However English physicians have carried out a few careful
observations on both methods ; Drs. Edgecombe and Bain,3
for instance, have published a series upon eleven adults ; and
to Dr. Mantle's observations I have referred. The Harrogate

1 Senator, H., u. Schiitgen, Deutsche med. Wochenschr., 1909, No. 35.

2 In many papers ; one of the latest in New York Med. Journ., March 15,
1913.

3 Journ. of Physiol, vol. xxiv. No. 1, 1899 ; and Lancet, June 10, 1899.

chap, x BATHS IN HYPERPIESIA 107

conclusions did not quite correspond with those of Miiller,
Ortner, and Groedel ; but they indicated likewise that on cool
immersion arterial pressure, both maximum and minimiun, rose
considerably, while venous pressure fell ; though after the re-
action this effect passed off. The effect was still more marked
when the percussion of the needle-bath was added. In these ex-
periments hot immersion and dry heat lowered both arterial
and venous pressures in the second stage, and might double the
output per second. Warm saline baths lowered arterial pressures
more than did plain water at the same temperature. Super-
heated air baths are forbidden by all the experts. Dry massage
of the trunk and limbs lowered the arterial pressure, but ab-
dominal massage, by driving the blood from the splanchnic
area, raised the general arterial pressure. The Aix douche
lowered the general pressure (see p. 103). These various con-
clusions point to great complexity in the problems with which
we have to deal, and to the need of further careful observations ;
the evidence, as Schapals says, is very conflicting. It is said
that in arteriosclerosis the vascular response to baths is
more sluggish. However, unless the transient rises of pressure
be too sharp, or the vessels too frail for any risks, we may be
well rewarded if cardiac balance, output, peripheral activity,
better elimination, and a net fall of pressure be obtained.
The permanent result may be an all-round amendment due
to the cumulative effect of many coefficients ; but it is in
the milder cases, and in persons under middle age and of fair
vascular condition, that such risks may be safely taken. That
we must distinguish the momentary from the permanent effect
of baths on the blood pressure is clear ; but in critical cases a
momentary effect may be all-important.

In England, where the bathing is generally left to attendants,
these scientific niceties are not observed ; it is better therefore in
this country to treat arteriosclerotic patients, whether hyperpietic
or decrescent, by other methods ; for baths are not indispensable.

As regards the drinking of waters, we find no less conflict of
opinions. Ortner says that hot Carlsbad water raises arterial
pressures ; other physicians declare it has a lowering effect.
Bourgouignan,1 a pupil of Huchard, affirms that the Evian

1 Bourgouignan (loc. cit.).
VOL. II H

108 TREATMENT OF ARTERIAL DISEASE part i

cure (and Vittel and other springs are probably as efficacious)
doubles the output of urea, triples the output of uric acid, and
increases the chlorides (on which he lays much stress) by one
half. Dr. Leonard Williams gives a like report of it, and adds
that it does not lose its virtues by export, so that it may be used
at home. If the water is not so quickly absorbed as to produce
prompt urination, the difficulty usually lies in the stomach or
bowel ; therefore during the digestion of the water abdominal
massage is ordered, and hot applications are placed upon the
belly ; or the kidneys may be at fault, if so, warm baths and
tepid drinks are employed ; or, thirdly, the delay may be due to
some obscurer conditions of the system, to be met by cutting
down the quantities of all other liquids, and administering the
Evian water in small doses to the patient on bed or couch.
Bourbon-Lancy is strongly recommended by French physicians ;
but the choice of the spa and the course of the cure must be
adapted to the individual case. Of the use of the Marienbad
waters, especially for persons of gross habit, we have abundant
testimony in von Basch's writings ; his results do not differ much
from those now generally accepted. Yet, to tell the truth,
I am reluctant to pour large volumes of fluid, fluid which may
contain common salt, into the bowels of persons with high pres-
sures. Their ingestion must add to the work the heart has to do,
and dispose to that latent oedema which, as we have seen, is so apt
to impair the elasticity of the peripheral circulation (Vol. I. p. 38).
Vaquez,1 1 see, has taken up this problem. In the normal state,
he says, the kidney responds by adequate functional activity to
the ingestion of 600 cc. of water taken in a morning before food ;
but more readily if the patient lies down. In renal inadequacy
the discharge is much slower and may only be fulfilled, if it be
fulfilled, during the night ; and this only if no further dose be
taken : then, if day by day some undischarged remnant is not
got rid of, an accumulation gathers for mischief. Thus when,
in arteriosclerosis of any form, the renal values are in doubt,
exact observations must be made for a few days before spa
waters are used freely.

Waters containing radium emanations, as at Bath, Kreuznach
and elsewhere, are now in much request, and are credited with
1 See, e.g., Vaquez, Arch, des mal. du cceur, avril 1913.

chap, x ELECTRICITY IN HYPERPIESIA 109

virtues which, as yet reported, rest on very unsubstantial
evidence. Plesch, no mean authority, says that under careful
use of radium waters both maximum and minimum pres-
sures fall, and metabolism is rectified. The supposition is
that they greatly increase diuresis, excretion of uric acid,
and exhalation of carbonic acid ; that they lower blood
pressure, and diminish blood viscosity. They are not to
be used in " Granular kidney." It is claimed of course
that the natural radium waters are far more efficacious than
the artificial. The natural bath should be given about the
indifferent temperature, and should never last longer than
twenty minutes. Radium emanation has been used by many
physicians in the treatment of high blood pressure, and while
some of them urge caution, and note some unpleasant effects, all
seem disposed to admit that it has some influence in reducing
pressures, and perhaps in diminishing the viscosity of the blood.
Dr. Lowe * of Bath has discussed the arguments on both sides
of the question.

Light baths, a system of incandescent electric lamps giving
off indeed both heat and light, were recommended by Huchard
and others, and have made some way since. If the lamps be
turned on suddenly, the blood pressure of the patient rises ;
the rule therefore is to bring the lamps gradually forward from
60° to 80° F., and then, if no ill effect, to increase the heat from
85° to 100° F. ; at this point both maximum and minimum
pressures are said to fall, and the heart to empty itself more
rapidly and completely. This amelioration is said to last for
some hours. But baths again can be thus used only for persons
whose cardio-arterial system is not undermined. That they
act by way of reducing adrenal activity is one of those many
guesses which obscure the discussion of these subjects.

Electric Treatment. — Faradic baths, cutaneous stimulants,
such as saline or gaseous baths, or fresh air, are of no service
in hyperpiesia. Reports of the therapeutic value of high-
frequency currents in cases of high blood pressure are not very
consistent, and some are contradictory. My own impression of
the method, and I have used it in many cases, is decidedly favour-
able. In three cases, which I was able to watch for three or four
1 Lowe, T. P., Brit. Med. Journ., April 20, 1912.

110 TREATMENT OF ARTERIAL DISEASE parti

years, one of them under Dr. Roberts of Harrogate, the not incon-
siderable reduction of pressure at each sitting persisted for two or
three days or more, and proved to be the forerunner of an abiding
amendment ; although in each patient the malady, being only too
well established, ultimately returned. In another case, a lady
under the care of Dr. Philpot of Chester Square, Dr. Philpot told
me that at the first sitting the pressure (over 160) fell a little, but
fell still further afterwards. After the second sitting it fell to 133.
This fall after the sitting I have observed in other instances. It
is very important therefore that after the sitting the patient
should remain at rest. Dr. Sloan of Glasgow,1 who has used the
method for more than two years, finds it effective in high-
pressure cases ; it lowers peripheral resistance, and must not
be used in low-pressure cases, as the reduction might be harmful.
He advises a rest before as well as after the sitting. Dr. Sloan
considers it proved that the current influences the alimentary
canal ; and he adds a conjecture that it modifies metabolism
and dissipates toxic substances. Dr. Somerville 2 agrees with
this suggestion, and emphasises also the influence of the current
in relieving insomnia, and promoting renal excretion. One
may hazard guesses of this kind but, although Dr. Somerville
alludes to some stricter researches of his own, so far as I know,
no systematic experimental proofs are produced as yet. It
seems at least as likely that a diathermic effect upon the vaso-
motor nervous system relaxes arteriolar spasm (Lewis Jones).3
Dr. Somerville, whose conclusion was based upon 266 clinical
cases, says indeed that among the after-effects is a rise of the
surface temperature of the body.

Some authors suspect — Kraus, for instance, who seems rather
sceptical of this method 4 — that the fall is due to suggestion.
One can scarcely suppose suggestion to act without a concept in
the patient's mind ; and a concept of falling blood pressure can
scarcely be formed ; all we know of expectant attention in this
matter is in the direction of a rise of pressure. Kraus admits
however that by the current the pressure is lowered, even

1 Sloan, Brit. Med. Journ., 1907 and 1910 ; see also Sayer Ettie, Brit. Med.
Journ., 1910.

2 Somerville, W. F., Lancet, Aug. 6, 1910.

3 Jones, L., Lancet, Feb. 7, 1914.

4 Kraus, Berl. med. Gesellsch., Feb. 24, 1909.

chap, x ELECTRICITY IN HYPERPIESIA 111

in chronic nephritis ; also that the effect is more or less abid-
ing, and no harm comes of it. Dr. Oliver who, when in Harro-
gate, had found no help in hyperpiesis from other modes of
electrical treatment, contrasted them with the high-frequency
current, which on the contrary he had often found effectual. A
Zurich physician, Buhler,1 observed the good effect of the high-
frequency current, even in severe cases ; the falls were decisive,
and after six or seven sittings persistent. He attributed the
effect, at any rate in part, to considerable (deutlich) fall in viscosity,
which he says he has verified. All his patients have assured him
that they have suffered no disadvantage from it. His best
results were in early cases of high pressure. From the Zurich
school also I have obtained a Dissertation (of 1911) by
A. Anton jewitsch on " Arteriosclerosis and High-Frequency
Current." The author works in the usual confusion between
high blood pressures and any arteriosclerosis, but testifies to the
potency of high-frequency current in moderating high pressures ;
he regards it as the most efficient of our means. He found that
the nervous symptoms and insomnia also were often relieved.
Normal and subnormal arterial pressures were left unaltered by it.
That the current is usually harmless is true, perhaps true of all
cases in which it has been used carefully ; in skilled hands it is
without danger ; but Dr. Sloan's warning is echoed by other
physicians. In a discussion at the French Medical Association of
1906, Doumer and Chanoz stated that by " Arsonvalisation " they
found abnormally high pressures to be reduced ; and with their
experience other speakers were in agreement, and I have heard at
second-hand that Vaquez and other French physicians are using
the remedy with success. Schurig 2 says of it that " above all
things it has a favourable influence upon arteriosclerosis (sic)."
The method is probably quite impotent to dissipate any kind of
arteriosclerosis ; but the author evidently means high pressures,
for he proceeds inconsistently to say that it is especially useful
in " presclerosis," gradually reducing the arterial pressures, and
therewith the associated symptoms, such as headache, vertigo and
insomnia ; that it quickly restores energy and good spirits, and
lifts up the general well-being. His report is perhaps a little too

1 Buhler, A., Schiveiz. Korresp.-Bl. No. 13, 1911.
2 Schurig, Deutsche med. Wochenschr., Feb. 6, 1913.

112 TEEATMENT OF ARTERIAL DISEASE parti

sanguine ; yet many clinical observers speak in like manner.
After these words were written, Dr. F. H. Humphris read an
important paper to the same effect before the British Medical
Association in 1913. x The author, who evidently writes with
considerable experience and technical skill, protested against the
objection that the treatment of hyperpiesia by high-frequency
currents was disappointing ; that if so, either the choice of the
case or the technique was at fault. Too often, he said, the current
used (d'Arsonval) was limited to 250-300 ma., whereas it should
run at 1000 ma. The sitting should last for 15 minutes. A
pleasant feeling of warmth and comfort then pervades the body,
with somnolence. The blood pressure should fall 20-40 ; say
from 200 to 180 or 160. Towards the following day it will
gradually rise, but not always to its original point, when another
sitting should be given ; after a time it will be observed that the
pressure no longer rises between the sittings ; but to keep the
pressures about this range will require further sittings, from time
to time as the course of the case may indicate. Dr. Humphris
wisely did not pretend to explain the good effect, but guessed
at vasomotor relaxation, and " improved metabolism." He
stated indeed that the solids of the urine and perspiration were
increased, but gave no detail of analyses, nor references. If
the effect be directly and only vasomotor, presumably some
further treatment would be required, but the author thinks
that, by setting the peripheral circulation free, metabolism
is thereby freed also, and a vicious circle cut. He spoke
also in favourable terms of the influence of the electric light
cabinet.

On the other hand, Carriere 2 warns us that in one case,
in which the pressure stood at 260, it was reduced by the current
to 160 (!) ; but the urine fell too, asystole set in, and in four
hours alarming symptoms of dyspnea, convulsive spasms, and
acute pulmonary oedema. Happily the crisis was surmounted.
Probably this was a renal case, and we have seen that in
chronic renal cases this method is to be used cautiously, if at
all. Martinet gives us the same caution ; indeed he says plainly
that in albuminuria with imperfect renal excretion it is contra-

1 Humphris, F. H., Brit. Med. J own., Oct. 11, 1913, p. 935.
* Carriere, Paris mid., 1912, 191-194.

chap, x ELECTRICITY IN HYPERPIESIA 113

indicated. It seems then that in this agent, if carefully used,
we have a potent means for good, if ill-managed, for harm.
The doses should be exactly measured, and the sittings timed ;
the first few sittings should be tentative. As with the bath a
brusque start would jerk up the pressures. To persons whose
pressures are disposed to fall, it is said to be unpleasant. The
patient should feel warmer and better after it, the peripheral
circulation being so expanded as sometimes to cause a limb to
swell, as in hot weather. In elderly persons with fagged heart
it should be applied meticulously, and for decrescent arterio-
sclerosis, even if the pressures should range 150-160, the method
is neither indicated nor effectual ; in no case can I think it desir-
able to reduce the pressures by 100 mm., or even by 50 mm.,
as is not infrequently recorded or advised.

I have said more than once that to mistake early stages of
hyperpiesia for neurasthenia is no infrequent error in diagnosis,
and it is chiefly in these early cases, or in some of them, that the
high-frequency current may prove to be permanently effectual.1
The reports are still rather inconsistent ; in some cases, cases
probably of advanced stages, the reduction of pressure may
fail to do any good. However, if in particular instances 2
it has had its failures and disappointments, especially in the
earlier attempts, yet there is a strong current of opinion in favour
of high-frequency treatment of non- renal hyperpiesia, especially
in earlier stages. Fortunately* it is a remedy whose doses can
be measured, and the effects appreciated, with some accuracy.

It is not unlikely that the effects of the current are due,
not to electric, but to diathermic action ; this question the
therapeutist may leave to the experts.

No other form of electricity is of any service in hyperpiesia.
The effects of the sinusoidal current have been carefully in-
vestigated by Albert Weil and Mongeot.3 It raises pressure, not
by stimulating the heart, but by constricting the periphery, an
effect which could play only a subordinate part, as a " vasomotor
gymnastic," for which purpose graduated baths or gaseous
douches are more convenient and manageable.

1 See, e.g., Macnamara, Lancet, July 18, 1908.

2 See Guilleminot, Arch, a" elect, nied., Aug. 25, 1911. I have seen only the
column of abstract in Epit. Brit. Med. Joum., Jan. 20, 1912.

3 Weil and Mongeot, Bull. Therap., 1906,

114 TREATMENT OP ARTERIAL DISEASE part i

At the Peebles Hydropathic Institute Dr. Luke tells me
that he is getting good results in hyperpiesia by " rhachidian
vibrotherapy."

For the mental depression, insomnia, and other nervous
symptoms of hyperpiesia, I have in several patients tried, and by
certain experts well tried, "suggestion" (p. 110), but so far in vain.

Venesection we may consider from two points of view —
from that of prompt relief at a crisis, and, again, from that of a
gradual remedial means, repeatedly and systematically used over
long periods of time. A crude measure no doubt it is, but it may
be serviceable until more scientific methods are available. By
a single large bleeding a threatening condition of high arterial,
or high venous, pressures may be averted for the time being ;
or a pulmonary oedema dissipated, or an eclampsia cut short ;
but can we by bleedings repeated at intervals mitigate or cure an
obstinate hyperpiesia ? On critical bleedings, as in pneumonia
or mitral disease, I have not in this place to dwell ; our concern
now is with Hyperpiesia. If we have reason to believe that a
persistently high blood pressure is associated with chronic renal
disease, a disease apt to impoverish the blood, at least in respect
of its red corpuscles, we may hesitate to bleed so freely or so
frequently as to be of much use in reducing high pressures ; but
if the state be one of hyperpiesia, a disease in which usually the
blood is not thus reduced in value, and may indeed be hyper-
globulous, is venesection here likely to be at least harmless, or
has it indeed proved to have a curative or moderative effect ?
At first sight, it is true, the promise would not seem great. If we
reduce the content of the peripheral vessels, and they contract
down upon the smaller content, unless the supply of blood is to
fall, the velocity must be increased ; that is, the heart must work
so much the harder, and for the time we are back where we were.
Furthermore, in a few hours, or in a day or two, as resorption
proceeds, the vascular system will refill. For this however the
vessels may dilate — it appears that they do — and thus pressures
may not rise, though, as there may be a reduction in blood value,
a larger quantity of blood may have to be delivered in unit of
time. Cook and Briggs x say that experimental venesection
on the one hand, or transfusion on the other, cause on the
1 Cook and Briggs, Johns Hopkins Reports, 1904.

chap, x VENESECTION 115

pressure curve but transient drops and rises respectively — acute
angular excursions. Of these phases all old pupils of Ludwig
and Roy were well aware ; but such experiments do not tell us
of the subsequent effect on plethoric men. Saline, it is true, is
readily absorbed, and transfusion of blood is efficient in raising
and sustaining arterial pressure, yet the effect is transient.
If we turn to experiments on the normal animal, we observe
that a rise of venous pressure does not, within limits, raise
arterial pressure, either generally or locally ; but in mitral
regurgitation, where venous pressures had gradually risen,
Dr. Mann x observed that bleedings of 10-23 oz. (in adults),
by abating irregular maximum readings, and enabling the
diastolic to pull up, steadied the heart. At first there was
no gain in mean systolic pressure, but in about four hours it
would rise, and in all his cases did so. Again we are told that
on venesection there is an increase of agglutinins, and probably
of other " antibodies." Evidently, here again we have very
complex conditions to deal with, and clinical experience must not
yet be disarmed by experimental bleedings on normal animals ;
nor indeed by the fluctuations of single symptoms of the series.
Besides, as we have seen (Vol. 1. p. 86), we are ill-informed
on diastolic pressures, with which nevertheless in this problem
of venesection we are very closely concerned. My impression
is that venesection has some abiding effect of moderation of
diastolic pressures.

Let us turn then to the evidence of empirical treatment. Of
the vast abuses of bleeding I will say nothing ; I remember the
last of them too well, in Bouillaud's wards. As in Sangrado's
day in Western Europe, so of this fashion in ancient Rome Celsus
sagely writes : " Venesection is no new thing ; what is new is
that there is scarcely any malady in which it is not practised."
But amid the crowd of Sangrados there were, as amid all contro-
versies, wise and thoughtful men who used their remedies
with sagacity and economy ; such men, for example, as Wepfer,
of whose sensible practice we may read in his book on Apoplexy.
They bled " not pale and delicate persons, but those who loved
meat, generous wines and choice dishes . . . such have much
blood, their urine is thick, and some ebullition of humours is

1 Mann, Guy's Hospital Gazette, Jan. 25, 1908, and Guy's Reports, vol. lxii.

116 TREATMENT OF ARTERIAL DISEASE pakt i

to be feared in them." Now such urine indicates not chronic
renal disease but hyperpiesia. Lancisi, after pointing out the
benefit of blood-letting in plethora, proceeds to warn the reader
against bleeding too heavily, " which may lead to cachexia and
dropsy." He reflects " adeo verum est prudentiam in medico
potiorem esse virtutum partem."

When we leave the ancients for our own day, we may ask
ourselves if now we have not gone, in this respect, to the opposite
extreme of inaction. We are indisposed to listen to the testi-
mony of our fathers on behalf of bleeding ; partly for the good
reason that they had not modern methods, nor modern thoughts
moulded on modern methods, wherewith to criticise their own
results. Yet it is not improbable that, in their confused experi-
ence of bleeding, our fathers were encouraged in their practice
of it by a substantial, if indiscriminate, admixture of good results
with bad. However, more absolute, and perhaps no less indis-
criminating, has been the revolt from venesection, so that it is
not easy now to obtain evidence concerning this practice, for
good or harm. In my own practice I have found experience
very hard to attain. Only in a small minority of cases other-
wise appropriate for this means are the patients, or their friends,
or their family physician, ready to agree to periodical bleedings ;
and of those in whom it may have been advised and practised,
too many pass unrecorded out of sight and memory.

Yet of venesection for Hyperpiesia I have some increasing
knowledge. I began some years ago to use it where I dare, and
I had experience enough to recommend it, for Hyperpiesia, in
1907.1 Recently I have had under observation for some time
three patients who have been bled at least twice a year. They
look forward hopefully to the operation, declaring that the
symptoms of excessive blood pressures are marvellously relieved
by it. And a permanent improvement seems to be thus
maintained ; but these three cases are beyond the stage of
cure, though not of substantial amelioration. It was in such
cases, which they recognised by the tight pulse, that our fore-
fathers were wont to take blood freely ; and, I believe, with
great benefit. One lady, who has now been bled for some years,
after the first bleeding wrote to me a letter of the warmest grati-
1 C. A., in The Hospital, Nov. 17, 1907.

chap, x VENESECTION 117

tude, saying she had found astonishing relief from it, and that
many obscure and troublesome symptoms had been dissipated.
Her own medical man — Mr. Day, of Baldock — added his testi-
mony to the same effect, and told me that he and his patient
together had learned with some precision when venesection
should be repeated. Swollen veins on the arms and hands are
among the indications of the need. Usually the interval is about
six months ; but if the operation seems to be required sooner,
there need be no hesitation in shortening this interval. This
lady, in later middle life, had been subject for ten years or more
to very high and sustained pressures, with a tightly contracted
radial artery, and an enlarged left ventricle. There have been
no renal symptoms or signs. I cannot doubt that venesection
has not only ameliorated her discomforts, but has greatly pro-
longed her life ; for the range of her blood pressures has been
very materially moderated from about 200 to about 160.

As regards the testimony of others, I may refer to Felix Mendel
of Essen,1 who, while disclaiming " Vampyrismus," illustrated
some judicious remarks on venesection by cases of which I will
quote one example, that of a male, set. 50.

There was a very high range of sustained arterial pressures.
Family and previous personal history good. No infection. Com-
plained of vertigo and distressing fulness of head and headaches.
Pulse very tense. Second aortic sound very loud, and left ventricle
hypertrophied. No albumin in urine, or other renal sign. No
sugar. Was bled (200 cm.) with great relief, especially to the head ;
and under vegetarian diet with milk and massage, and iodide of
potassium for three months, was better every way for eighteen
months. Then returning symptoms indicated a second bleeding,
which was likewise efficacious. After a while the symptoms increased
again, but for some reason reliance was placed on diet, he was
not bled ; he grew worse and fell in an apoplectic attack with
hemiplegia.

Mendel thinks that for a long time after venesection the
viscosity of the blood is less, the stream rate accelerated, and the
heart's work reduced. Although Mendel is the more inclined to
bleed if the carotids are full and throbbing, and the face ruddy,
yet he recognises also the many high-pressure cases in which, in

1 Mendel, F., Ther. d. Gegenwart, July 1907.

118 TREATMENT OF ARTERIAL DISEASE parti

spite of a spare frame and sallow countenance, it is none the less
needed. A more rapidly oblique descent on the sphygmographic
curve on compression of the brachial suggests a gain in velocity.1
The apparent gain in velocity persists for a few days, though
the systolic pressure may increase, but not to its former
degree. Some years ago Dr. Oliver Withers, of Sidmouth,
published in the Practitioner two cases of excessively high blood
pressure with oppression of the head and vertigo, in which
bleeding gave remarkable and persistent relief. Purgatives had
availed little. Dr. Fortescue Fox 2 has had many opportunities
of bleeding in these cases ; a lady, suffering from high blood
pressure, he bled regularly from the age of 55 to 60 ; the heart
was large and labouring, and the peripheral vessels thickened ;
he attended this patient for twenty years for rising pressures
which first showed themselves at the age of 48, but after
the menopause became aggravated. Among other symptoms
were fulness of the head, dyspnea, vertigo, and a slight apoplectic
attack. As all ordinary means had failed to give relief, she
was bled. The relief was striking and immediate, and for some
time persistent. It was found necessary however to bleed her
every six months for six years, taking usually from 10 to 20 oz.
(on one occasion 24 oz.). At length something like recovery was
attained, for at the age of 68 she was reported to be in good
health. He describes other like cases : in one of them, with
threatenings of apoplexy, an immediate bleeding, and two in the
year following, gave permanent relief. As I write these words
he is using this method successfully in the case of a gentleman
of middle age whom I had seen with Mr. Wingate. Eulen-
meyer 3 narrates many instances of repeated bleedings in these
hyperpietic cases. By it, he says, viscosity is reduced (p. 147),
and velocity promoted. He prefers to make small and frequent
venesections. Broadbent practised venesection not infrequently,4
and urged its use in high-pressure cases, especially in patients
menaced by apoplexy. If the immediate fall of pressure after
venesection be not considerable, 30-40 hours later it becomes

1 See also Lewis, T., Practitioner, Feb. 1907.

2 Fox, F., Lancet, April 23, 1910, and Nov. 4, 1911.

3 Eulenmeyer, Deutsche med. Wochenschr., 1906.

4 See Broadbent, Sir W., Treatise on the Pulse, 1887 ; vide, e.g., p. 287.

chap, x BY MEANS OF DRUGS 119

more definite, and the pulsations more ample ; as if the bleeding
had relaxed arterial spasm. Ortner testifies to the same effect.

In hyperpiesia venesection is not only well tolerated — even
40-45 oz. may be taken before the radial pulse softens — but its
effects seem far-reaching. It compasses some profounder altera-
tion lying beyond our direct appreciation, emancipates the
system from some burdens unknown ; cuts vicious circles perhaps,
or alters the solids of the body. Under no head of treatment is
the discrimination between hyperpiesia and decrescent arterio-
sclerosis more imperative. This remedy, so efficacious in
hyperpiesia, in the decrescent form of sclerosis would rarely,
if ever, be called for, and might be disastrous. And yet
influential physicians are now talking of " bleeding in arterio-
sclerosis " !

Dr. Herbert French1 has proposed, as a less formidable opera-
tion, " venepuncture " instead of venesection, the blood being
drawn off through a hollow needle. He thinks this method might
facilitate small and frequent bleedings, if these be preferred.

When headache is severe, the brain oppressed, and the blood
pressures very high, lumbar puncture may be thought of. I
have never used it deliberately for a hyperpietic case, but I
have used it for like conditions in chronic renal disease with
advantage. I think I got the suggestion from Vaquez ; the
operation is one which might come more into use in phases of
these maladies.

For those physicians who seem to know that high pressures
are " compensatory," and therefore to be maintained, most of
our therapeutical means will seem worse than idle. I cannot
pretend to be more than an empiric in this matter. Yet it is
with some disinclination that now I pass from the physical
methods 2 to the use of drugs. It would be ungrateful to forget
that in hyperpiesis we owe much to certain drugs, but it is reason-
able to remember that in adding drugs to toxins we may be piling
poison upon poison without full recompense.

1 French, H., Guy's Hospital Gazette, Feb. 15, 1913.

2 The Greek physicians of the Empire (Celsus, Galen, Antyllus) called
bleeding, cupping, purging, emetics, massage, gymnastics, fasts, sweats, their
"common aids" (kolvcl ^orjOrifxara, or Troocrcpepo/xeva).

120 TREATMENT OP ARTERIAL DISEASE parti

In entering upon the discussion of direct vasodilators, as con-
trasted with agents which bring about this change indirectly by
modifying the causes of morbid constriction, we have to con-
sider how far mere dilatation — brought about, that is to say,
immediately and singly — serves any good purpose. We are told
that to act thus directly upon the vessels is but to " treat a
symptom," and is therefore absurd. But whatsoever be our
judgment on this or any such particular effect, the common
denunciation of " treating symptoms," which sounds very philo-
sophical, is surely but a parrot phrase. Why should we not
treat a symptom ? If in Granular kidney by mere pressure
reduction the grievous headache be abated, or if in angina pectoris
the pain be thus charmed away, we have so far at any rate a
substantial gain. In renal disease it is generally agreed that on
the whole, with due caution, to lower pressures is helpful.
Moreover, if by mitigation of his suffering the patient gets a
chance of picking up in many other ways, are we not more than
justified in our interference, narrow as it may seem ? We never
know what interference may cut a link in a " vicious circle." x
To deprecate a therapeutical means as mere treatment of a
symptom is idle, unless by this step we are doing some incidental
mischief. If we cannot stop the crack in the water-pipe we need
not throw away the mop. The warning should run not against
the treatment of a "mere symptom," but lest while giving our
attention to the symptom, and snatching at an immediate advan-
tage, we lose our grip of the case as a whole. If it be argued that,
in chronic nephritis for instance, the high pressure is a cardinal
condition of an artificial but critical balance, and that to reduce
it without counteraction of its causes is to upset the unstable
machine, we shall reply that the appeal must be to clinical ex-
perience, to empirical results. We have gone back to learn of
nature, though not obsequiously. That ultimately we shall have
to be guided by the intimate physiology of these processes is no
doubt true, but true of a more or less remote future ; at present
we are working in the dark, and must grope by touch. It is too
readily assumed, without any definite data, that every natural
coefficient is for the advantage of the system. How do we know

1 See Dr. Hurry's book on Vicious Circles in Disease. " One could win the
fight with the other fellow if his terrier were not biting one's leg."

chap, x VASODILATORS 121

that, in current jargon, these high pressures are "compensatory" ?
How do we know that they are not the result of some poison
acting upon the bulb or other vasomotor centres, driving up the
pressures in sheer mischief, and straining the mechanism to no
purpose ? We do not know even the outlines of an answer, and
seem not to be near such knowledge. We are agreed that when
called to a patient whose machinery has thus for some time been
carried on upon a compromise, if we cut in upon an abnormal
but provisional balance, if we depress one pan of it too
sharply, we may endanger the temporary adaptations, and even
add to, rather than alleviate, the patient's discomfort ; but if
brusque practice of this kind may be unwise, a more circumspect
intervention in the same direction may be as wise. Indeed
under urgent circumstances, such as stenocardia, or menace of
apoplexy, a brusque interference, with vasodilators or otherwise,
even at the cost of some other obliquity, may be imperative ; and,
with time before us, we may continue such remedies with caution
and discernment, in combination with other measures which we
flatter ourselves are more rational and comprehensive.

Whether then as swords for a knot, or as more continuous
aids in perplexity, whether quickly to lull the agony of an angina
or slowly to moderate the stresses of an arterial plethora, the
nitrites are often valuable, and sometimes invaluable means ; but
we must use them with this discernment. Their effect in lower-
ing arterial pressure, it may be by 25-30 mm.,1 is prompt and
remarkable ; and in hyperpiesis lasts longer than in health.
When pressures are acute and menacing, we shall betake
ourselves to the Liquor trinitrini ; for more continuous use
sodium nitrite (usually prescribed in solution with 5 or 10 grains
of potassium nitrate) is more suitable, and usually answers well.
Unfortunately however the drug is unstable, and apothecaries'
samples are variable. It varies least in tablets, yet of one
sample an ordinary dose may be almost too prompt in its
effects, whilst of another a dose three times as large may
appear inert. Not only so, but the margin between therapeutic
and toxic doses is somewhat uncertain, and vertigo and nausea
may ensue on a dose too large for the individual (Vaquez).

1 See Matthew, E., Quart. Journ. Med., April 1909. Dr. Matthew reports
comparative tests of several of these agents.

122 TREATMENT OF ARTERIAL DISEASE part i

The degree of tolerance of nitrites varies considerably in various
patients ; the first doses should be prescribed with caution.
This is especially true of sodium nitrite. Some persons bear all
nitrites badly, when not doses but frequency of doses may be
increased. This salt must not be combined with potassium
iodide, nor with any oxydising agent. Erythrol tetranitrate
may be better suited for prolonged depressor influence ;
being less soluble its effect comes on more gradually, and is
more persistent than that of sodium nitrite, as this in its turn
is more gradual and persistent than nitroglycerine. One of
our medical graduates — Dr. Newmarch — in a private letter told
me he had found long courses of erythrol efficacious in some
melancholic patients with high blood pressures. This drug
is said, by a gradual moderating influence, to restore sleep
to those sufferers from high pressures in whom insomnia is a
distressing symptom.1 As a chronic remedy then erythrol is
convenient, but it is explosive and, like sodium nitrite, unstable ;
still if kept in a cool dark place it should last well enough
for a season. It is best given in tablets of a half to one grain,
or more. But I shall be pressed to say plainly if I advise the
use of vasodilators systematically and continuously in all high-
pressure cases. To this question I am almost ashamed to con-
fess that I cannot give a definite answer. I think not. When
the heart is beginning to yield nitrites must be avoided, or, if
urgently needed, guarded with digitalis. Rest in bed would
be essential, and the doses anxiously watched. If there be
reason to infer loss of conductivity, even this combination may
be unsuitable. But we cannot enter here upon the field of
cardiac therapeutics. My own practice is to try first what diet,
frequent calomel (in non-renal cases), and saline laxatives will
do ; then, if more interference be needed, I try courses of physical
methods, of baths, of the high-frequency current if available,
and so forth, and sometimes venesection ; if, after a fair trial
of these measures, some relaxant seems called for, I then betake
myself to a systematic if not prolonged course of vasodilators,
watching their effect on all sides ; yet always under the pre-
judice that there is something too artificial, too rule-of-thumby,
about the method.

1 Bruce, M., Sc. Med. and Surg. Journ., 1900.

chap, x THE NITRITES 123

How is the depressor effect obtained ? It is agreed that
diastolic pressures are lowered. Is it by peripheral dilatation, or
wholly or in part by splanchnic dilatation ? If by splanchnic
dilatation only, what do we gain ? Apparently nothing more
than a transference of part of the bulk of the blood from one
area to another. And may not the heart then endeavour to
counteract this kind of fall by a quicker rate, more energy, and
more output per minute, so as to restore the systemic arterial
pressures to their former levels ? x Again, one cannot feel sure
that the depressor effects of the nitrites are merely by vasodilata-
tion ; I ponder uneasily whether some part of the relaxation be
due to a lowering of the cardiac energy, with a consequent fall
of stream velocity. It is stated indeed by Russell- Opitz 2 that
nitrites accelerate the stream in the femoral artery, and by others
that they tone up the heart ; but we cannot argue from the
normal animal to the abnormal man — or even to the normal
man, whose splanchnic mechanism is correlative with the up-
right attitude. Certainly during their use the heart sometimes
dilates, and there are phases in which hypotensive medication
seems mischievous. Unfortunately, the consultant can watch
few of his cases so continuously as to enable him to form any
steadfast opinion about long courses of treatment. In angina
pectoris, it is true, one sees nitrites used in large doses
continuously for many months, and from these perseverances
I have seen no harm ; but here the arterial pressures may not
be deranged. For hyperpiesia, then, I cannot at present advise
the use of nitrites as more than adjuvant, when some rapid
relief is called for, as in stenocardia or paroxysmal dyspnea.
The doses ordinarily prescribed are but initial ; to produce a well-
marked effect, sodium nitrite may be pushed carefully up to a
rate of eight to ten grains, or more, in twenty-four hours — with
twice as much saltpetre — but in frequent and limited, not in
larger and rarer, doses. Some physicians indeed, relying upon an

1 Since these words were written I have come across a paper by Laidlaw
(Journ. of Physiol, vol. xl., 1910), who, experimenting with a depressor drug
(tetrahydropaperveroline, not as yet suitable for medical use), recorded just this
effect : the dilatation was chiefly abdominal (splanchnic, etc.), and the cardiac
rate, and output, and energy of beat, were so much increased that (under normal
cardiac conditions) the arterial pressure did not fall much, or for long. The
circulation time must have been shortened.

2 Russell-Opitz, Journ. Exp. Med., 1910.

VOL. II I

124 TREATMENT OF ARTERIAL DISEASE part i

acquired tolerance of nitrites (Osier, Passler, Vaquez), run them
up to very large doses, to m. 30-40 of the liquor trinitrini, for
example, without apparent harm. In all these therapeutical
tests we should try to watch not systolic pressures only but also
the minimum, and therewith the amplitude. A run down of
diastolic pressures, like a rise of rate, is ominous. I have never
seen a " nitrite habit " established in hyperpiesia, but I have
seen it in angina ; a malady in which the patient's sufferings
may justify his addiction to the remedy.

Dr. Hobhouse kindly reported to me the following observations
made by a medical man upon himself while at rest. He was the
subject of aortic aneurysm, and I had seen him in consultation.
He used tetranitrin in slightly increasing doses His pressure
on the first day, at 11.30, was 136 ; at 2 o'clock it was 128 ;
at 5 it was 137 ; i.e. it returned to the former and usual
level. But at 8.30 (without another dose) it fell to 120.
Another dose was then taken, and the pressure fell to 112. This
experiment was repeated day by day, falls of 136-120 or there-
abouts being noted. The fall usually became apparent in five to
thirty minutes, and occupied about five hours, when it would
rise again to its previous level. But the observer found that
without the drug the fluctuations were nearly as large. In spite
of cutting down food, alcohol, or tobacco, rises would occur ;
and the tetranitrin did not always cause a fall. After lunch,
whether it were with or without a little alcohol, there was always
a rise. On one day a pressure of 140 at 8 a.m. fell, under the
drug, by 10.30 a.m. to 123, but in seven hours more it had risen
to 134. (See daily phases, Vol. I. p. 21.)

Vasodilator drugs then, when the pressures are acute or
urgent, have a certain but not a predominant part to play. Of
stovaine, alleged to be a vasodilator, I have no experience, nor
have I any important information concerning it in this respect
from others ; nor again of sparteine, proposed as a vasodilator
remedy by Professor Dixon. Acetylcholine is said by Reid-Hunt 1
to have an amazing depressor activity, " a hundred times more
activity " in this sense than has adrenalin in pressor activity, and
a hundred times more activity in the depressor sense than nitro-
glycerine ; but its mode of action and its possibilities in thera-
1 Reid-Hunt, Sect. Physiol., Brit. Med. Assoc, Toronto, 1906.

chap, x MERCURY 125

peutics are unknown. Choline we know, by Dr. Mott's experi-
ments, to be a depressor by way of the heart, not a promising
function for therapeutical values. Both choline and acetyl-
choline are opposed by atropine, which suggests that those sub-
stances act through the vagus ; but it is not easy to see how by
this route acetylcholine can exert effects so enormous. By
thyroid extract, given in ordinary doses in high-pressure cases,
I have gained no advantage ; but the doses of 30 to 40 grains
of which we read assuredly ought to set up some disturbance,
good or bad. Dr. Oliphant Nicholson,1 speaking of high pressures
in pregnancy, says that in this condition thyroid extract is very
efficacious ; headache and other untoward symptoms are abated,
and the transition to well-being is remarkable.

Of the more specific drugs in hyperpiesia, none is equal
to mercury, especially — for the many who tolerate it well —
as calomel ; for others, blue pill. The calomel is to be given in
fractional doses, say \ grain once, twice, or thrice daily for four
or five days ; or \ grain every night : the course to be repeated
from time to time. A saline laxative is required by many
persons ; in others the calomel may have to be guarded by a
grain or two of Dover's powder. The patient soon learns when
to repeat his course, and to expect the benefit to be had from
it. In the intervals, small frequent doses of podophyllin — y^
to \ grain thrice daily — or of euonymin or iridin, may be
prescribed. From day to day some notion of the effects may
be guessed at by the finger, but the blood pressure should be
measured at least once a week. It is desirable, as I have said,
to keep the patient in ignorance of the figures, lest he worry
about them, or disturb the record by expectant attention.
In the cases of intercurrent high pressures in elderly persons,
with or without decrescent arteriosclerosis, mercury is marvel-
lously efficacious ; by its means insomnia and other discomforts
are often dispelled at once. Of other laxatives some are useful,
not so much for expulsion of water, as to provide for excretion,
and for the activity of the lymphatic system. Thus the morning
saline draught, though by itself it is not efficacious, is a valuable
aid to other measures. In several instances of hyperpiesia I
have been surprised to find how little amendment long courses
1 Nicholson, O., Brit. Med. Journ., Oct. 3, 1903.

126 TREATMENT OP ARTERIAL DISEASE part i

of laxative saline achieved alone ; and this in cases which after-
wards responded to calomel. They may increase viscosity. A
good habitual laxative is the old-fashioned electuary of sulphur,
senna, pepper, tamarind, etc.

The general faith in the iodides as moderators of high arterial
pressures is curiously robust and perennial, notwithstanding the
default of any definite evidence of this virtue in them. Their
reputation was first gained in the field of aneurysm, a some-
what dubious test ; for, as about 90 per cent of aneurysms are
syphilitic, the virtues of the iodides in syphilis may bring about
some amelioration by way of their specific influence. It was by
See and Lapique 1 that they were carried forward into the general
field of arteriosclerosis. Pal seems to me to speak in exaggerated
terms of their value in reducing high pressures. Syphilis apart,
I have never been able to satisfy myself that the iodides, either
as vasodilators, by reduction of viscosity, or otherwise, have any
effect, direct or indirect, in abating arterial pressures (see Viscosity,
Vol. I. p. 145). Still, we have to meet a heavy phalanx of empirical
observers on the other side. Dr. Edwin Matthew (loc. cit.) classes
the iodides with the nitrites as pure vasodilators, especially in
hyperpiesia before vascular strain has appeared ; a remarkable
definition, for Huchard, as definitely, deprecated their use in the
" presclerotic " period, the only period in which Matthew, and
Graham Steell with him, thinks they are of service. Matthew
begins with 10 grains thrice daily, increases the doses rapidly
for some days, and then decreases them. Ludwig Braun of
Vienna follows the same method.2 In my own practice I have
not followed this method precisely. Ortner's method 3 is different
from that of Dr. Matthew. He orders 3 to 5 grains of potassium
iodide, with a little sodium of carbonate, copiously diluted,
thrice daily after meals ; omitting each week a day or two, but
not more. Acids in the meal should be avoided shortly before
the dose. He advises against its use in renal disease or in
anaemic conditions ; and it should not be given while the patient
is under calomel. Von Romberg, Klemperer, and Ewald
still prescribe the salt in moderate doses. Sir L. Brunton says

1 See and Lapique, Rev. de la science med., 1876.

2 Braun, L., Med. Klinik, No. 26, 1911.

3 Ortner, Jahreskr., Feb. 1911.

chap, x THE IODIDES 127

many patients can tolerate a dose of 25-30 grains at bedtime,
well diluted, when 5 grains thrice daily cannot be borne. He
also believes that the drug is effectual in abating pressure.1

Various explanations are given of the virtue of the iodides
in alleviating excess of arterial pressure but, as in the old
story of Charles II. and the bowl of fish, without first ascertain-
ing whether the alleged effect follows, or not. In so far as
therapeutics are to be rational, before we discuss the mode of
action of a remedy, we must clearly understand the problem
before us. Some authors assert that these salts act thus by
releasing arterial spasm (Ortner, Matthew) ; some that they act
by reducing viscosity (Erlenmeyer, Komberg, Ludwig Braun of
Vienna, Martinet and others) ; others, by the oracular assump-
tion of "some kind of metabolic resolution or elimination."
Miiller and Inada's paper,2 in which these investigators alleged
that potassium iodide reduces arterial pressure, not directly but by
reducing viscosity, is discussed in the section on Viscosity (Vol. I.
p. 145). Their statements found much acceptance in Germany ;
but we have seen that, although viscosity must be a considerable
factor in the labour of the circulation, upon arterial pressures
it has less effect than was anticipated ; though notwithstanding
the cardio-arterial work may be much affected. However, it
was upon this paper that Romberg's and other opinions 3 on the
influence of the iodides were based. Dr. H. D. Rolleston suggests
that the abating effect may be compassed by a mediate excite-
ment of the thyroid (p. 134). Erlenmeyer, on his hypothesis,
orders the iodides to be administered in long courses after the
manner of Ortner, and combines this treatment with small and
frequently repeated venesections.4 Erlenmeyer's article was
written to dispute Krehl's objection to their use, which was
not that they lack the effect attributed to them, but that they
were too effectual in reducing the high pressures, which in
"arteriosclerosis " Krehl believes to be essential to the defence.
Krehl is beset by the notion that any reaction in a perverted
body is compensatory, and so to be respected. Hochhaus of

1 Brunton, Sir L., Clin. Journ., August 28, 1912, sect. vii.

2 Miiller and Inada, Deutsche med. Wochenschr., 1904, No. 48.

3 Romberg, Deutsche med. Wochenschr., Aug. 31, 1905, and in his book
{Herzkrankheiten, 1906).

4 Erlenmeyer, Deutsche med. Wochenschr., 1906, No. 7.

128 TREATMENT OF ARTERIAL DISEASE parti

Cologne,1 a very able physician, urges long courses of iodides,
but prescribes also diuretin, the milder baths, and exercises.
But he does not make his argument clear, he regards arterio-
sclerosis throughout as one disease, not distinguishing between
its several modes and issues. In this confusion treatment goes
utterly astray — perhaps with all of us.

However, in the present debate the argument may be about
moonshine. We have had it on the high authority of Stockman
and Charteris 2 that in man the iodides, pressed even up to iodism,
fail to bring about any fall of blood pressure, whether by dilating
the arterioles, by reducing the heart, or otherwise. In animals
they injected sodium iodide intravenously (the sodium salt to
avoid any effect of potassium on the heart) without any
pressure reduction, though as regards the heart Professor Stock-
man says that the amount of potassium in its iodide is so
insignificant that it is scarcely worth while to substitute the
sodium for the potassium salt. Dr. James Burnet,3 by the test
of subcutaneous injections of iodipin, came to the same negative
result in man. It is sometimes forgotten however, especially in
experiments on animals, that in certain morbid states reagents
may prove efficacious without manifesting the like phenomena
under the conditions of health. My attitude for the present is to
remember that many experienced observers are convinced that
in high arterial pressures the iodides are potent for relief, and
that accordingly, unless we ourselves have some strong reason
to the contrary, we are in a measure bound to give our patients
the benefit of the chance. Josue likewise seems to continue to
prescribe them, although he frankly says that, however ad-
ministered, he has never seen any benefit from them. The
difficulty is that to many persons iodine is always a nasty and
often a depressing drug, and yet one which, if it is to be of any
use, must be given in full doses and over a long period. My
custom therefore is to explain the position to the patient, and
to invite him to try the drug at will ; some persons have less
distaste for it than others. I have tried many of the prepara-
tions alleged to be less disagreeable than the ordinary salts of

1 Hochhaus, Deutsche med. Wochenschr. vol. xxxviii., 1912.

2 Stockman and Charteris, Brit. Med. Journ., Nov. 23, 1901.

3 Burnet, J., Lancet, Sept. 6, 1906.

chap, x THE IODIDES 129

iodine, but without any notable advantage. Some physicians
of repute recommend, especially for cerebral symptoms — head-
ache, vertigo, loss of memory, or speech arrests, and paresthesias —
" tiodina " (whatever this may be) in subcutaneous injections of 3
grains, for 16 doses. They are said to be painless. For " arterio-
sclerotic " (high pressure ?) headache Neusser prescribes a com-
bination of bromide and iodide. It will be seen that from any
point of view these clinical records, as described, are too often
a muddle of high pressure and decrescent disease.

If a case be altogether or in part syphilitic the iodides are of
course indispensable ; but in the arteriosclerosis of syphilis, as
such, local or general, the blood pressures are not raised. In
this infection the relief given by these salts is often marvellous,
especially to the cerebral symptoms ; but no such case should
escape a full course of mercurial treatment. In arterial disease
of syphilitic origin, unless the heart be much degenerated, or
the lungs emphysematous,1 salvarsan also should be used
carefully but promptly by an expert.

It is impossible here to enter fully upon the treatment of
syphilis. How successful specific treatment may be, and
permanently successful, in curing cerebral and other arterial
disease of this kind is happily well known to us all. As a mere
illustration I insert the following case :

At the Leeds Med.-Chir. Soc., March 20, 1903, Dr. Churton showed
a woman, aged 39, who had been under antisyphilitic treatment
since December 1901. At first the subclavian arteries, especially
the left, were thickened and greatly dilated, the pulsation being
visible above the inner and below the outer part of the clavicle
(see Vol. I. p. 395). The carotids were similarly, but less, affected,
and pulsation was felt behind the manubrium. All these arteries
now appeared perfectly normal, and the other symptoms were
relieved. Of course the speaker did not assume that the case could
be dismissed as cured. We know but too well how relapses will
occur. It is to be hoped that salvarsan may control them.

To judge by the mode of action attributed to the iodides,
these salts would probably not be recommended for decrescent
arteriosclerosis, in which state arterial pressures are not char-

1 See Grassmann, Milnch. med. Wochenschr. No. 42, 1910 ; a helpful
article.

130 TREATMENT OF ARTERIAL DISEASE parti

acteristically augmented ; if perchance they rise episodically
(Vol. I. p. 452), mercurial and other remedies for this transitory
condition are more efficacious. However, I am driven to repeat
that in the published papers the confusion between the terms
arteriosclerosis and high arterial pressures, or the acceptance of
arteriosclerosis as " a disease," is so incessant as to make their
message too often unintelligible. Erlenmeyer (loc. cit.) indeed
looks upon arteriosclerosis without high pressures as so eccentric
and improper that he advises a cautious raising of the level by
gaseous baths at temperatures about 30° C.

For raising pressures, in case of a lurch to the falling side
(usually a heart failure), Dr. H. C. Mann (loc. cit.) found no drug
equal to strychnine. He says that morphia also often acts well
in raising diastolic pressure and steadying the systolic. He
finds also that in " second wind " the diastolic pressures rise
and the systolic abate in the same way.

Of other salts in the category of remedies there is not much
to say : nitrate of potassium is an old diuretic, and in hyperpiesia
is conveniently prescribed with other and more specific agents ;
it often contains some nitrite. Salts containing much potassium
may reduce pressures, but at the expense of cardiac energy,
the very opposite is what is needed. Dr. Gee used to say
that whey — a breakfast-cupful two or three times a day — has
an excellent effect in dissipating uratic deposits. Ammonium
chloride is said to have a relaxing effect on the vessels, while
leaving the heart intact ; I have no experience of its value —
it may merit more attention than it has received. The part of
sodium chloride, the alleged retention in high pressure of sodium
chloride in the tissues, and its comparative scantiness in the
blood, the urine, and certain viscera I have discussed already
(p. 93). Certain authors recommend tablets of sodium chloride,
sodium sulphate and phosphate, magnesium phosphate, and
calcium glycerophosphate in due proportions, for "arterio-
sclerosis " ; it is not easy to say why. Of the calcium salts we
shall hear more presently. Dr. George Oliver at one time recom-
mended the hippurates as moderators of high pressures — he
knew better than to speak vaguely of remedies for " arterio-
sclerosis " ; but subsequently I think he preferred to them the
benzoates of potassium. A diuretic influence should be the sign

chap, x CALCIUM AND OTHER SALTS 131

of their benefit. Gouget recommends sodium silicate ; * he gives
1-3 grams of a 35 per cent syrup much diluted, and reports
fall of pressure in " arteriosclerosis " (presumably he means
hyperpiesis ?), and therewith relief of vertigo, headache, etc.
He states that by a previous administration of sodium silicate
the damage to the rabbit's aorta by adrenalin may be prevented.
In respect to the salts of calcium there is not much to be
said of therapeutical value. In passing from practice under the
conditions of the extremely soft waters of the West Riding to
the chalk and gypsum waters of Cambridge, I have not observed
any difference in the incidence or mode of arteriosclerosis or
blood pressure. That without excessive pressures lime salts
are conspicuous in arterial decay we know well enough, but we
know also that this deposition of the lime is but a secondary
event. If an excess of lime in the blood augments the viscidity
of this fluid we shall be careful to avoid it ; but we are far from
assurance that such is the case. Opinions differ widely on this
matter ; our own investigators, such as Professor Dixon and
Sir James Barr, and many foreign observers likewise, hold
sundry opinions.2 Certainly in the malady before us we
are no gainers by administration of lime salts, and in this
obscurity we may as well forbear from any use of them in medicine
or diet ; but let us be clear at any rate about the maladies with
which we are dealing ; let us not continue the habitual confusion
of distinct affections under the name of " arteriosclerosis " ; let
us recognise that if lime salts be early and conspicuously de-
posited in decrescent arteriosclerosis, in which blood pressures are
not much affected, in hyperpiesia, in which augmented pressures
are the first obvious deviation from the normal, lime deposits
are tardy and, at any rate till protracted stages, inconspicuous.
Thus the effects of lime ingestion, if any, on the regulation
of function, and on the coats of the vessels, respectively must be
considered apart ; the processes are independent. The heart
cannot be short of its own calcium requirement.

1 Gouget, Presse mid., Dec. 6, 1911, quoted Arch, des mal. du cceur, avril
1912.

2 See Report, Brit. Med. Assoc. Mtg., 1912. Rumpf was the author of the
lirneless cure. Voorhoeve, who has made a recent study of the subject, says
(Berl. klin. Wochenschr. Nr. 36, 1912) (see vol. i. p. 499) it is possible to
increase the lime content of the blood by administering it in large doses, but
that there is no evidence that it has then any important effect.

132 TREATMENT OF ARTERIAL DISEASE parti

The antisclerotie serums, or tablets, invented by Truneczek,
Natterer, and others for the treatment of " arteriosclerosis,"
without regard to its kind or to the initiatory processes of its
manifestation, are pedantic ; and to the best of my belief
useless. On empirical grounds, they are falling into discredit.
Some of them are proposed on the shallow hypothesis that
arteriosclerosis is due to an abnormal saline constitution of the
blood. After the manner of other proprietary remedies, they
have been advertised without criticism.

If diuretin (5-7| grains ter die) be of service in arteriosclerosis,
it must be in the secondary form of it, secondary, that is, to
abnormally high blood pressures ; it does not counteract
mechanical strain, but it may counteract, or eliminate, the
causes of vascular strain. The assertion that it relaxes vascular
spasm rests, so far as I am aware, on no verified data. Dr.
Haynes, in our laboratories, showed that diuretin increases the
flow from the coronary arteries ; but we also know that such
outflow depends less on pressure than on activity of cardiac
metabolism (Barcroft and others). That it has some virtue in
high pressures I believe, on empirical grounds, for in angina
pectoris it seems to moderate relatively high arterial pressures.
On its effect in hyperpiesia we need some careful continuous
observations ; somehow or other it seems to do good in this
disease. It should be prescribed in as little water as possible.
Aspirin and sodium salicylate are prescribed also in excessive
blood pressure. In one case, which came under my notice, we
quickly relieved a grievous cough and bronchitis, which had
tormented the patient for five winters, by reducing the diet by
one-half and administering aspirin ; it was not easy to discern
which of the two was the crucial step, but the amendment certainly
was accompanied by a reduction of the arterial pressures which
before had ruled too high. Twelve years later this patient died of
angina pectoris ; five years before this event the arterial pressures
had again gone up, and sclerosis of the mitral valve had given rise
to an audible murmur. Dr. Core (loc. cit.) thinks (without ex-
periment?) that sodium salicylate "neutralises some pressor
toxins." Guaiacum, for its supposed virtue as a hepatic stimulant,
is credited with a " katabolic neutralisation of pressor excretory
toxins " ; it may be worth a trial, and a better explanation.

chap, x SUNDRY DRUGS 133

Adonis vernalis has been recommended — two grammes of the
extract (better than the infusion) per diem * — in more than one
quarter, for rising blood pressures, and even for " abdominal
angina."

Viscum album, at one time classed with the digitalis group,
more recently has been credited by certain French physicians
with a depressor influence upon the vasomotor centres and
arterial muscle ; and also with a diuretic property. Ortner,2
on the contrary, found the fluid extract quite useless. Yohimbin,
which for a time had a run as a pressure reducer, seems also to
be useless,3 though Frankel has some faith in it ; Ortner also
still recommends vasotonin (Lippmann), which is a combination
of yohimbin and methane. This remedy is supplied in sterile
bulbs for subcutaneous injection, once a day for 20-30 doses ;
the pressure is said to fall with relief to the symptoms ; but in
Ortner's opinion the reduction, if harmless, is transient. He
thinks diuretin and agurin more efficacious, but that even these
are wanting in abiding effect. I suppose little more, if so much,
is to be expected from Senecio jacobaia, which is described
in small doses as an augmentor of arterial pressure, in large
doses (08-10 gm.) as a depressor ; fluctuations attributed to
constriction or dilatation of the intestinal vessels. Aconitine,
veratrine, and antimony prove at best to be useless (Cash and
Dunstan). There is a little evidence however in favour of arsenic,
which may have some adjuvant metabolic effect ; it is said by
Coley 4 to be not a direct reducer of pressures, but by more
intimate alterations to bring about an improved condition in
these cases. Ortner also has a good word for it in certain cases
where, in alternation with more direct treatment, a general
" tonic " may seem indicated. The use of fibrolysins seems a blind
suggestion ; if they have any influence on the vessels it might
well be an injurious one. When the heart is suffering under
excess of pressures the inhalation of oxygen has been advised, in
order to counteract any increases of viscosity by cyanosis.5

Professor Osborne of Yale and others have recommended

1 E.g. by two Russian physicians quoted Sem. med., No. 25, June 18, 1913.

2 Ortner, Jahreskr., Feb. 1911. See also Selig, A., Med. Klinik, 1912.

3 Pongs, Zeitschr. f. exp. Path. u. Ther., April 12, 1912.

4 Coley of Philadelphia, Brit. Med. Journ., 1906, No. 24.
6 See Bence, Julius, Deutsche med. Wochenschr., 1905.

134 TREATMENT OF ARTERIAL DISEASE pakt i

thyroid extract in hyperpiesia ; I had already tried it without
success, but perhaps my doses were not sufficiently liberal.
Strychnine, in hyperpiesia, would be suggested only at a time
of crisis, as of failing heart ; but, as on occasion such aid
may be desired, I may call attention to certain observations of
Cabot,1 which suggest that this drug does not of itself drive
pressure upwards. He says, " The average pressure in the 50
cases that received a daily dose of strychnine was no greater than
in 18 cases without any drug." The records varied of course, but
" the total result was negative."

For the cardiac or respiratory distress hypodermic morphia,
as first advised by me in 1869, has found acceptance. If on
repetition its influence wanes, Frankel 2 advises injection of
heroin hydrochloride (O'OOOS-OOl) ; there is no call for increas-
ing doses, though, like morphia, it does induce a craving.

The reference to remedies for yielding heart opens out the
way to discuss that sovran drug, without which no discussion
on cardio-arterial disease is complete, digitalis. There is an
opinion abroad, and not without good reason, that in cases of
high arterial pressure digitalis is contra-indicated. If we are
still to suppose that digitalis promptly constricts the arterioles
in most areas of the system,3 and if we suppose also that
hyperpiesia consists in such a general constriction, to propose
to use digitalis in such cases would seem to magnify the evil.
But now we hear that this constrictive quality of the drug
rests on opinions which may need some considerable modifica-
tion ; 4 be this as it may, no physician would propose to administer
digitalis whilst against an abnormal peripheral resistance a big
heart was working not unsuccessfully. But when at length the
brave heart is worn down by the intolerable strain under which
for many years it has been too often permitted to strive ; when,
in spite of alleviated peripheral resistance, it is yielding in its
walls, and perhaps leaking at its valves, when in an unequal strife
it is giving way, our treatment will fall into line with the general

1 Cabot, Bost. Med. and Surg. Journ., Oct. 1, 1904.

2 Frankel, Berl. klin. Wochenschr., 1913, No. 17.

3 See Bradford, J. R., Clin. Journ., July 27, 1904.

4 Among other papers see Price, F. W., Section of Pharm. and Ther. Brit. Med.
Assoc, 1912 {Journal of Assoc, Aug. 17 and Sept. 21, 1912). Probably a good
deal depends on the relation of the dose to the individual, and to his state.

chap, x DIGITALIS 135

treatment of heart failure. At such a time, if cautiously used
and with full knowledge of the conditions of the particular case,
digitalis is for mitigation invaluable, although the time for cure,
or even for any abiding amendment, be now past. It is absurd
to say that digitalis is inadmissible — this would be to treat a name,
not a patient ; but, on the other hand, when to exhibit it is one
of the most critical dilemmas in medical practice. The strife
is killing the heart ; the state is an unnatural one, and only by
some compromise is any rally possible. Traube saw clearly,
then against adverse opinion, that at such critical stages of
the malady digitalis must be admitted, and in his own practice
he proved its efficacy. Dr. Graham Steell, while warning us
against the use of digitalis in the earlier stages of hyperpiesia,
recognises its value in the later, when the heart may yield. Sahli
says, paradox as it may be, that when the heart is overdone by
prolonged excessive pressures, and is dilating, digitalis must be
used. Dr. Mackenzie however wrote that " digitalis is rarely
of much service in dilated heart secondary to arteriosclerosis."
May I, with the greatest respect, demur that there is not such a
heart ; or, if there be, that it is in decrescent arteriosclerosis
with coronary obsolescence, a condition which neither he nor we
had in view. The heart and the sclerosis of which we are now
speaking are, on the contrary, consequent upon high pressure ;
the heart by hard work is forced and dilated, it is succumbing
in the main not to diseased vessels, nor to intrinsic default, but
to peripheral resistance by unknown causes ; probably by
extensive vasoconstriction. In all stages of such a strife it
is clear that our first duty is continually to lighten the burden
by whatsoever means may still be practicable ; but, while not
forgetting this, the heart must occasionally be lifted over a
crisis. When the cart sticks in the mire we first lighten
the load, yet, notwithstanding, a touch of the whip may
also be needed to bring out for the crisis what reserve may
be latent in the weary horse. But this metaphor, like many
another, is not quite parallel, for the use of digitalis in this
emergency is not the dilemma it appears to be ; the case is not
one simply of pull devil pull baker ; there is, as I have argued
elsewhere,1 something more than a mere reinforcement of intra-

1 Musser and Kelly's Practical Treatment.

136 TREATMENT OF ARTERIAL DISEASE part i

aortic pressure ; by the action of digitalis we gain some re-
distribution of pressures, whereby particular stresses may be
resolved or alleviated. The rise of intraventricular pressure, if
any, may be but momentary and tidal.1 We shall not how-
ever betake ourselves to the drug until the heart is yielding ;
until then we shall pursue the more rational method of trying
to reduce the resistance. If I were to make a clinical maxim I
should say — turn to digitalis when diastolic pressure is rising
and amplitude therefore narrowing. If signs of "steno-
cardia " appear we should perhaps avoid even a relief thus
purchased at the cost of aortic tension, and still endeavour to
soothe the strife by less direct methods — by rest, venesection,
mercurials, and so forth. But this is not the place to enter
at length upon the treatment of heart failure. If there be any
indications of pulmonary oedema, venesection may be specially
indicated. If digitalis is to be used I suppose that we must
hearken to Dr. Mackenzie and Professor Dixon,2 who assure us
that the galenical preparations of the plant are as efficient as
the active principles, or the much advertised novel preparations.
But for this opinion of my colleagues I should have allowed
myself too much reliance upon certain striking results with
Nativelle's granules, which I have used since their first intro-
duction ; results due, it may be, to the more careful manage-
ment and attention which a less familiar remedy requires.

We must not be led by the sallowness of some hyperpietics
to give them the feeding tonics required by white flabby people.

How near after all modern medicine lies to the principles of
our fathers, witness this extract from the Tractatus de infirmorum
sanitate tuenda, Londini, 1726, by George Cheyne, M.D.,3 an
Edinburgh student, who practised in London and Bath :

Quae autem his neglectis Corporis Plenitudo succrescit, Lentoris
Humorum et Infarctionis Canaliculorum parens ; hanc diuturnorum
omnium Morborumpraeproperae etinfirmae senectae, Vitaeque medio
in Decursu recisae Causam facile agnoscas, si attendas Evacuationum
maxime Usu illos sanari, haec praecaveri. Venae etiam Sectione,
Cucurbitulis, Vesicatoriis, Fonticulis, Catharticis, Geneticis, Sudori-

1 Josue has some useful reflections on this subject, Soc. mid. de Paris
Nov. 8, 1912.

2 Dixon, Quart. Journ. of Med., Jan. 1912.

3 Cheyne was a pupil of Pitcairn.

chap, x THE DECRESCENT DISEASE 137

ficis annon rnanifesta sit Evacuatio et supra Modum ingestorum
Absumptio. Sed et ipsius Abstinentiae Exercitationis, Medica-
mentorurn item alterantium ; etc., etc. . . . Quod enirn, Venae
Sectio, quod Cathartica, quod Hidrotica praestant, idem in
diuturnis Morbis (celeres enim lenta Medicamina antevertunt)
praestat per Quatriduum aut quinque Dies Caena abstinuisse,
Carnes non attigisse, Vino caruisse.

Decrescent Arteriosclerosis. — For arteriosclerosis secondary
to hyperpiesis we have seen that much can be done ; not, it is true,
for the sclerosis itself, but for that exorbitance of arterial pressures
to which it owes its origin. Indeed, but for the high pressures
the sclerosis is, comparatively speaking, of little importance.
In this case our argument must be not of the " arteriosclerosis,"
which is so incessantly put forth as " a disease," but of the hyper-
piesia, or the chronic renal disease, one of which is the main morbid
process. This, or these, we treat, not the sclerosis. So also with
the decrescent mode ; here again we treat, or should treat, not
the sclerosis but the morbid changes, toxic or other, to which
it owes its origin. In this mode of arterial injury the
degeneration often depends more directly upon the condition of
the vessels themselves ; essentially it is, or often is, their own
default ; in hyperpiesis this is not the case. The contrast is there-
fore not directly between two primary diseases of arteries, but
between a mode which is not primarily a disease of arteries at all
but some one or more morbid processes setting up internal stresses
under which the vessels suffer, and a degenerative process seated
primarily or chiefly in the walls themselves. Now if this change
be, as it is commonly called, " senile," we are as little able to
" treat " it as we are to treat grey hair, or arcus senilis. Although
the results of decrescent sclerosis may be far worse than of these,
yet in principle our medical disability remains much the same.
If there be any mitigation of local anaemias, of waning energy and
heat, due to silting up of arterial twigs, it is these which we must
deal with ; how to arrest the vascular depravation which lies at
the bottom of these failures we cannot tell ; at any rate I know
nothing of such means. Sometimes, it is true, decrescent arterio-
sclerosis comes on precociously ; in these cases the lesions of the
vessels, as revealed without to the touch and inferred within from
the waning of function, are so malign as to suggest virulence, and

138 TREATMENT OF ARTERIAL DISEASE paet i

we find ourselves suspecting some instant toxic cause. Arterial
disease of such kinds may be transitory (Vol. I. p. 288). But
a precocious atheroma is usually accompanied by other and
less equivocal signs of early senility, local and general ; and
is progressive. In more • benignant cases however, although
the vessels within reach may be greatly deformed, often
indeed much more tortuous, lax, and calcareous than in the
hyperpietic form, the general health is so little affected and
life, speaking within limits, so little shortened or dimmed, that
we may suppose the changes to be mainly of the long vessels of
the limbs only, and, if so, relatively unimportant (Vol. I. p. 482).
Too often however the memory trips, the flow of ideas is
tardy, the feet begin to slur, the facial expression to fade ; and
we can do nothing but watch and lend a hand here and there as
it may be wanted. Decrescent arteriosclerosis is immedicable.
We " cannot hold time by the wings," and with some men it
flies faster than with others.

In decrescent arteriosclerosis it is evident that we must not
interfere with the moderate rise of pressure which belongs to all
elder life ; with increase of friction, and loss of the energy which
the less resilient arteries now fail to restore, the stream velocity
slackens ; and if to meet this there may be some increase of
cardiac energy — in some cases obviously there is, in others
apparently not — we shall not try to counteract it. But we may
try to improve the quality of the circulating blood, so that what
reaches the periphery may be the better worth having. By airs
fresh but mild and equable, we shall try to lessen the viscosity
due to degrees of cyanosis, and to promote respiration in lung
and tissue ; by iron we may redden the corpuscles, and by gentle
alteratives, gentle baths, and exercise carefully moderated
within the nearer approaches of fatigue, we may try to keep the
excretory organs at work. Concerning the conditions of the
kidneys in this mode of arteriosclerosis, I have said enough in
the proper section on this subject. On the other hand we have
seen that in the decrescent disease an access of hyperpiesia may
be attended with great peril to vessels already fragile. For these
episodes the treatment recommended for hyperpiesia must be
employed, and attacks of hyperpiesis, from which these patients
are no more immune than other people, must be warded off ;

chap, x THE TOXIC SERIES 139

happily in decrescent cases intercurrent plethora is even more
readily dissipated than it is in early hyperpiesis.

Iodide of potassium, useful or not in hyperpietic cases, can
be of little service in the senile. And the consequences are not
those of the hyperpietic form. We have not to guard against
apoplexy in its sanguineous form.

The heart, being more disposed to deteriorative than to
hypertrophic change, is less apt to burst the vessels ; so that
the bodies of decrescent arteriosclerotics often survive to great
and even to extreme old age. In these cases treatment has to
concern itself with nutrition and economy rather than with
depletion. By adapting the diet to a diminishing output of
work, by providing for the best assimilation of the simpler
foods, by the addition from time to time of ferruginous
and other tonics, by gentle exercises in fresh air, by mild
winter climate, and by some relaxation of work and care, but
by encouragement of a fair activity of both mind and body
and dissuasion from elderly indolence, the tendency to cardiac
degeneration or strain is to be counteracted ; on the whole by
a restorative strategy as patient as the morbid proclivities
themselves. Fibrolysins have been suggested, but, in so far as
they act as such, they might act injuriously in dissolving the
remnant of the framework of the vessels.

Of toxic arteriosclerosis the treatment is that of the particular
infection or poison concerned, be it in some one or other of the
specific fevers, as in syphilis or typhoid ; or again in diabetes or
plumbism. In the large majority of these cases the blood
pressure is not raised, depressor remedies are not required.
The most general rule is to make for elimination by rest, with
massage baths and diuretics. In early stages vaccines may be
required. Free urinary and hepatic action must be encouraged.
Every organ must be vigilantly examined, especially the states
of the heart and its valves. Except in syphilis, mercury, so
valuable in hyperpiesia, is to be eschewed. Even in lead poison-
ing, often accompanied as it is by high arterial pressures, this
drug, save in occasional doses for contingencies, is inappropriate.
In cases where a specified vaccine or serum or other antidote is
obtainable, as in diphtheria or syphilis, this means will enter
into the therapeutical method. But the myocardium is often

VOL. II k

140 DISEASES OF THE ARTERIES paet i

affected as much as or more than the arteries. The long survival
of microbes, such as the S. pallida, in many of these distempers,
even after the carrier is wholly or partially immunised, is only
too well known. The urine should always be examined bacterio-
logically. We have, as yet, little knowledge of the ultimate
effects of a toxic arteriosclerosis ; life may not be so much
abbreviated by it as impaired in its energies. We have seen
that these influences may tend rather to connective fibrosis than
to atherosclerosis. Above all things we shall be warned that in
such maladies lie dangers to the heart and great vessels, and thus,
foreseeing and vigilant, we shall try, during the acuter stages, to
prevent the fixation of these poisons on the tissues. " These foxes
must be taken while they are little."

To sum up : involutionary arteriosclerosis is intractable. The
toxic forms of arteriosclerosis seem to undergo some mitigation in
time ; but, syphilis apart, we have few specific means of cure.
The use of vaccines may come hereafter ; meanwhile we must
prevent the engendering of toxins, and promote their excretion.
As life goes on, these cases may merge into the involutionary
mode. It is in the hyperpietic mode that treatment is most
efficacious. If this malady be discovered before it has impressed
itself indelibly on the vessels, we may wholly drive it away, or
by no very irksome watchfulness dispel it again and again : even
if we do not detect it till a later stage, we may still control it,
and postpone, if we cannot avert, its extremer perils.

PAKT II

AORTITIS
ANGINA PECTORIS

SECTION I

AORTITIS

The preceding pages are occupied chiefly by a considera-
tion of arteriosclerosis as a whole, and in respect of the body
as a whole. But disease, when seated in the vital thoracic
aorta, and especially in the ascending arch, produces some
peculiar effects ; and if inflammatory, or acutely disintegrating,
the issues may be correspondingly grave. Disease thus seated
requires therefore some more intimate and special considera-
tion. It was with this object in view that I chose this section
of arterial disease for the Cavendish Lecture to the West London
Medical Society in 1903.1 This address, with some additions
derived from later experience, and without some parts already
included in previous or subsequent pages of this work, I
venture to reproduce, as it bears closely upon the succeeding
subject of Angina Pectoris (p. 211).

In a little tract of the brain, one so small that an infant
might grasp it, lie the ministers of all that makes life worth living ;
and but a few inches below it, where brain and spine unite, is
a still smaller tract, where lies the knot of life itself. The upper
tract has its times of energy and of repose, by sleep its ravelled
sleave is knitted up ; but the knot of life itself knows no pause,
no quiescence ; let its vigilance be at fault for a few seconds,
and the busy frame it governs will drop into silence. Save as
a lesson in physiology, these parts are strange to us : yet with
it is united another unsleeping minister of life, our familiar, of

1 The Cavendish Lecture, delivered June 26, 1903. Reported West London
Medical Journal, July 1903.

143

144 AOETITIS part n

whose pulses Harvey was rapt into saying, after Aristotle, that
they "are of the spirit of the blood acting superiorly to the powers
of the elements . . . and that the soul in this spirit and blood is
identical with the essence of the stars." When the pulses of this
instrument beat in harmony we feel within us that all is well ;
when they are jangled and out of tune we are dismayed. Often
when in the still night I hear, as I he, the calm and continual
rhythm of my familiar spirit, ever winnowing boon from bane,
I am lost in wonder at the long procession of these notes of human
time, at this perpetual beat of the manifold tides of life. As I
listen to its notes they seem to fall into the burden :

So schaff' ich am sausenden Webstuhl der Zeit,
Und wirke der Gottheit lebendiges Kleid.

Sixty times a minute, at least ; 3600 times an hour, 86,400
times per day, for us heedful and heedless, does this shuttle of
life flit to and fro ; for us in tireless periods this pendulum of
man's gravitation tells the seconds which will never return.

Tireless as it seems, tireless as sin, yet it will cease ;
nay, when youth is gone, in every beat there may be an
irreparable wound. Hour after hour the blood leaping against
the vault of its conduit strains the bonds of it, searching its
strength, testing its elasticity. Although, from Professor Mac-
William's researches, it would seem that Roy's estimation of fail-
ing aortic elasticity in elderly persons was defective by some
ignorance of post-mortem and other variables in arterial tissues, yet
it is clear enough that some such loss of elasticity is inherent in
all men ; and in the large majority of aged bodies is in its effects
visible to the naked eye. Nevertheless, the endurance of the arch
of the aorta under the incessant lashing of the blood for three-
quarters of a century is marvellous ; in some old persons in whom a
constant immunity from toxic influences has coincided with an in-
herited tenacity of structure, astonishing. I have spoken already
of the necropsy of a patient who had died of a gall-stone at the
age of eighty-three, how we admired the soundness of the heart,
the translucency of its valves, and the uniformity and smoothness
of the aorta and its lining. But for the most part it is otherwise,
often far otherwise ; we expect to find, and usually we do find,
in the aorta of persons after the age of fifty no inconspicuous

sec. i AOETIC STKESSES AND TOXINS 145

signs of these years of stress. And, again as we should expect,
it is in the arch of the aorta more than in any other arterial
tract that these signs of injury prevail, and prevail densely
and widely in persons whose lives had been spent in strenuous
muscular labour. All this we have considered in the chapters
on Atherosclerosis. But, as regards aortitis, with none of its
kinds have abnormally high blood pressures any essential concern ;
if now and then in aortitis they be present it is by accident.

Such being the conditions under which the work of heart
and aorta is performed, the stress upon the first or curved portion
of the great vessel being thus heavy and perpetual, while we
admire its tenacity we shall assume that, to whatever other
injurious influences it may be obnoxious, stress must enter
for more or for less into the sum of the lesions, and into the
election of their seat or seats of greatest severity. Let me
suggest a common case ; the aorta of a man of some fifty-five
years of age, who has taken freely of drink and suffered from
syphilis, lies before us. The vessel is heavy, baggy, and hard ;
its walls are beset with knotty masses. On laying it open we
find the stretching had told chiefly upon the ascending arch
and vault, and that, besides the old syphilitic pouches and
scars, and engrafted upon them, atheromatous bosses and plates
also, some calcareous, some " ulcerated," now occupy its inner
face. The aortic cusps are thickened and deformed ; the
sinuses of Valsalva are contracted, and the orifice of the heart
is altered. The orifices of the coronary arteries also are
invaded by atheroma ; the orifice of the right coronary occluded
perhaps, that of the left barely admitting a bristle. The cusps,
altered as they are, may be competent against regurgitation ;
the heart in substance looks healthy, and to the naked eye
and the microscope, in spite of the interference with the
mouths of the coronary arteries, presents in its muscular tissue
no worse sign of degradation than a moderate fibrosis. The
disease was not cardiac, it was arterial. Here then we find
the combined effects of mechanical stress telling upon a
vessel formerly attacked by syphilis and further reduced
by age and alcohol ; to this infection and stress we shall
attribute the pouchings of the arch, specific and atheromatous,
and so much of the consequences of the mechanical and toxic

146 AOETITIS part n

lesions as may be due to the incessant agitation of an afflicted
organ which, to heal its wounds, needed rest, but to which rest
was denied. For this reason disease of the thoracic aorta
has always an additional and very grave element of peril.
Under the beating of the pulses no lesion, however slight, can
be wholly repaired. In favourable cases, by fibroid growth
and condensation, a patch of disease may become a patch of
repair ; for an indefinite time the damaged wall may resist
destruction : but restitutio ad integrum, or, if the lesion be
extensive, even practical efficiency on the computation of an
uninjured life, is contrary to experience.

In this case I have spoken of the luetic poison, already
fully considered : this however is but one poison out of many
by which the integrity of the arch of the aorta may be
imperilled. We have seen that the aorta enjoys no immunity
from the attacks of the ubiquitous bacterium : although of the
kinds and degrees of its liability we are still in some ignorance,
yet such lesions may end in atheroma, or directly produce
it ; but in their acuter stages, the syphilitic, and many other
infectious lesions of the aorta, are not arteriosclerosis but
inflammatory — are, strictly speaking, aortitis. In syphilis at
any rate it ends in scar. Systematic examination of the aorta in
respect of infectious lesions, save in syphilis, is much neglected ;
in infectious diseases, or indeed under any circumstances, careful
sections of the ascending arch, not to mention the abdominal
limb of the vessel,1 are very rarely made, or even thought of.
Not infrequently I propose the subject to candidates for our
higher degrees, but little work of the kind is sent in.

We may anticipate that the self-purifying virtues of the blood
and the scour of the aortic stream may give the aorta some
advantages against microbic invasion from within ; and that, when
infection of it occurs, it occurs under conditions of high blood
impurity and high microbic or toxic virulence. The microbe
may be chased along swifter currents to settle in regions of more
sluggish irrigation. We are familiar with it in many cases of
malignant endocarditis. Nevertheless, microbic attacks upon
the aorta are much more frequent than is generally suspected,

1 Morgagni always opened the aorta in its full length, and advised that this
precaution should not be omitted.

sec. I ACUTE AOETITIS 147

and we have surmised already that passing poisons or toxins,
apt to enter into chemical relations with the wall of the vessel,
may be the causes of some of that atheromatous decay which
we call senile. But, speaking generally, as we have seen, infec-
tions attack the vessel by way of its vasa vasorum.

Disease of the aorta has not only a certain independence
of disease of the heart, but also of the aortic valve itself. When
we speak of diseases of the " aortic area," we mean, no doubt,
something more than the arch of the aorta ; we include the
mouths of the coronary arteries, the valve, the base of the heart ;
even the large anterior limb of the mitral valve, the smaller
being related rather to the auricular side of the heart. We
observe accordingly that the larger mitral limb is often associ-
ated in disease with the aortic valve, whereby, independently of
dilatations, it comes about that a systolic mitral murmur may
follow aortic disease ; in atheroma it commonly does. Not-
withstanding, when we consider the part of the aorta itself,
we shall see that disease of the base of the vessel may not invade
even its valve ; or may involve it gradually, secondarily, and
from above. Clinically also, as I shall presently set forth more
at length, disease of the arch of the aorta forms a chapter apart
from that of the heart.

Aortitis may broadly be divided into Acute and Chronic,
a division corresponding with some difference of symptoms, at
any rate in respect of intensity, from a course wholly latent,
to a more or less transitory stenocardia, to a fuller angina, or to
the racking agony of the status anginosus.

More than once I have recalled a case of acute aortitis
in which I was concerned when clerk to Dr. Bence Jones at
St. George's Hospital, about the year 1860. The symptoms and
their origin made an ineffaceable impression on my memory,
and from that time forward aortic disease engaged my interest.
And as, a few years later, in the diagnosis of disease of this great
vessel I became much indebted to the teaching of Professor
Potain, I have made from all available sources of observation
and reading no inconsiderable a collection of facts. Acute
aortitis is not always the perilous disease I once supposed it to
be, and it is part of my present purposes to insist upon careful
heed to the state of the vessel in diseases wherein aortitis may

148 AOETITIS part ii

enter and depart, often unawares. That acute aortitis is apt to
arise in the course of infectious diseases, even in the course of the
milder exanthems, rests upon a collection of facts now large
enough to carry conviction ; though perhaps in the majority of
cases it is betrayed by no telling symptom. Incidents of this
kind are now no curiosities, but integral, if not common, terms of
various series ; terms which range in significance from transitory
and superficial affections to terrible and even mortal calamities.
Acute aortitis, as well as atheroma, was not unknown to the
immortal Morgagni ; and near our own time, Hodgson, in
his notable Jacksonian Essay of 1814 to which I have often
referred, carefully distinguished the signs of inflammation from
those of imbibition ; and, besides his leading description of the
aortitis we now know to be syphilitic, described a remarkable
case in which a fibrinous deposit lay upon the inner face of
the great vessel, and was continued as a thrombus into one of
the carotid arteries : a case presumably of bacterial infection.

Causes. — In the infections due to acute aortitis the occur-
rence of microbes, known or assumed, is beyond cavil. It is
far more frequent in the exanthems than we have been wont
to suppose. Often mild in degree, transient in time, secret in
its approaches, the affection may be revealed, if at all, only to
him who is on the watch for it (p. 260). Physicians in charge of
smallpox, if they will use the means of diagnosis to be discussed
hereafter, may detect the lesion not infrequently, or so it would
appear from the reports of Therese, who records six cases, and of
other physicians. Brouardel 1 also gives the sanction of his
authority to variolous aortitis, and tells us that it arises during
the suppurative period, and disappears during convalescence.
In some cases it seems to have determined a fatal issue, but
often, as it usually appears in cases of gravity, the mortal
effects of the aortitis itself cannot be precisely decided.
Portal 2 recorded a case of a young man, who died of small-
pox " with violent suffocations and palpitations," the wall of
whose thoracic aorta was swollen and soft, especially the

1 Brouardel, Arch. gen. de mid., 1874.

2 Portal, Anat. Med. vol. iii. p. 127 ; quoted Corrigan, Dub. Med. Journ.
No. 35.

sec. i DUE TO INFECTIONS 149

internal membrane. Happily our experience of smallpox is
now very small. In ordinary cases of variolous aortitis the
lesion seems to disappear in a few weeks.

It is remarkable that in an infection so trivial as measles,
if we may judge by the testimony of physicians so well known
and careful as Sansom and Dr. Samuel West, the intercurrence
of acute aortitis of a mild and transitory kind is not very rare.
Of scarlatinal aortitis I know nothing, of scarlatinal myo-
carditis only too much ; but we have the authority of Landouzy
and Siredey, and of other authors, to testify to its occurrence ;
and this the more commonly perhaps for the well-known co-
operation with scarlet fever of a process very like rheumatic
fever, like it not only in its arthritic but also in its endocardial
manifestations. Simnitzky of Prague,1 who worked with Chiari,
reckons that aortitis occurs in half the mortal cases of scarlet
fever ! Both intima and media are attacked. Wiesel 2 includes
scarlet fever, with diphtheria, measles, pneumonia, and influenza,
among the infections causing aortitis. He warns the pathologist
that in these diseases microscopic evidence of aortitis is often
found in cases where to the naked eye the vessel seems normal. A
remarkable case has been published by Minet 3 : — soon after
defervescence a fresh rise of temperature occurred with pain in
the epigastric portion of the aorta, which dilated and throbbed.
There was no other affection of heart or aorta. I shall discuss
these cases again later (p. 304). One or two other instances of
abdominal aortitis after this infection are on record. The follow-
ing deserves notice :

Mr. Z., set. 26, sent to me, April 30, 1908, by Dr. Glasier of
Mildenhall. Scarlet fever three years ago ; remembers that he had
some rheumatism with it, especially in the legs. On rising from
bed was seized with severe pain, at first in the subepigastric region,
but far more intensely, and afterwards wholly, in the chest. This
pain was paroxysmal and intolerable, and for some weeks never
went entirely away. It " screwed him through from the breast

1 Simnitzky, Zeitschr. f. Heilkunde, April 1903, and Bull, de la Soc. de
Pediatric de Paris, Nov. 1902.

2 Wiesel, " Erkrank. art. Gefasse in akut. Infect.," Zeitschr. f. Heilkunde,
1906.

3 Minet, J., " Aortite abdominale, angine post-scarlatineuse. Guerison,"
Soc. mid. des hop., juillet 12, 1912.

150 AOKTITIS part ii

bone (midsternum) to the back, and went across the left upper chest
and down one or both arms (not quite sure about the right)."
Does not smoke ; syphilis absolutely denied. The paroxysms were
only to be calmed by subcutaneous morphia. To his doctor's
surprise after some weeks' illness, and a month's vacation, he
recovered completely. Last summer the pains returned, but only
for a few days. Last Christmas they again appeared, and he is
still subject to them. He is obviously no complainer and presents
no sign of " neurosis " ; although no leading questions were asked,
he did not readily speak of these facts. His description now is
that of classical angina. He grips his waistcoat at midsternum.
The only point of peculiarity is that below the elbow the track is
that of the musculospiral rather than of the ulnar nerve. Heart
enlarged considerably to left, and heaving, but the radial artery,
although little thickened, was either so constricted or of such low
pressure that in determining the systolic pressure (which was about
110 mm.) only with the greatest pains could I keep in touch with
it. (Atheroma of subclavian orifice ?) The aorta was not palp-
able in the notch, but there was a very strong basal thrill and
murmur, rasping and in systolic time. No first sound audible.
At the apex a brief and distant first sound was heard with a
systolic murmur. No murmur of regurgitation. No Flint sound.
No dyspnea, but in attacks sits up with a sense of oppression. As
he did not volunteer an apprehension of death I forbore to ask
the question.

The poison of rheumatic fever prevails of course rather in
the mitral area ; but of its power to attack the aortic area, and
the aorta itself, we are becoming better aware. In its position
in the ascending limb, and in its tendency to aneurysm, it comes
nearest to the syphilitic kind. The syphilitic kind grows con-
tinually worse, but happily the rheumatic tends to recovery.
If in rheumatic fever aortitis may be an extension from the
heart, it is not always so. Klotz * gives a plate showing a
strip of healthy aorta lying, as in syphilis, between a rheum-
atic valvulitis and an aortitis. Renon, Klotz, Barie and
others testify to the independent position. In 1901 2 Barie
described such a case of aortitis in a child. I have seen not a
few cases in which during life it seemed to have an independent
seat in the aorta ; and others in which it seemed to be an exten-
sion of pericarditis to periaortitis (p. 454). In such extensions

1 Klotz, 0., Journ. of Path, and BacL, Nov. 1913.
2 Barie, Soc. med. des hop., 1901.

sec. i IN RHEUMATIC FEVER 151

of rheumatic inflammation to the aorta, and in rheumatic
pericarditis about the base of the heart involving the aorta, as
Pawinski x and many others have demonstrated, new and strange
symptoms may awake in fierce activity.

In my clinical lectures I have been used to make the con-
trast, to which I have alluded, of rheumatic valvulitis with
atheroma in respect of the directions of progress : usually in
rheumatism the mitral valve is attacked first, and the disease
advances to the aortic valve from the anterior mitral cusp to
that aortic cusp with which it is practically continuous ; thence
it creeps upon the other cusps of that valve, and often extends
a little upon the aorta : in atheroma the disease usually extends
in the contrary wise, creeping from the aortic valve to the
anterior mitral cusp. In the few cases of death during the
acute stage of double rheumatic valvulitis, I have seen at the
necropsy not only the path of this upward propagation of the
inflammation from valve to valve, but also an extension upon
the suprasigmoid portion of the aorta ; now when this happens
we have, in my opinion, the pathological substrate of angina
pectoris. Of two cases to be mentioned presently, in that
of Dr. Simpson the angina was only too convincing ; in the
Royston case the process was more stealthily at work ; the pain
did not transcend the degree of angina minor. After a while
these attacks also died out, and this patient likewise, so far as
the primary illness was concerned, recovered.

That in rheumatic fever aortitis is no very rare event yet
nevertheless often an event of no little gravity, is a conclusion
which I found, on the delivery of my Cavendish Lecture, was
scarcely realised by English physicians. For this reason I re-
newed the subject before the Association of Physicians, at the
London Meeting in 1907. Concerning the rheumatic we have been
even more in the dark than we have been in respect of syphilitic
aortitis. It occurs not very rarely, but it is mirecognised.
Desportes (loc. cit.), so far as my reading goes, was the first to
describe a case of rheumatic aortitis, in a man, aet. 25, with
anginous symptoms ; and it is to French physicians that we are
indebted for the best of our recent knowledge of it ; but Welch
also had clearly pointed it out, on pp. 70-74 of his admirable essay.

1 Pawinski, Deutsche Arch. f. klin. Med. Bd. Ixiii., 1897.

152 AOETITIS part n

In most instances it arouses no subjective symptoms ; if signs
there be they are unsought : in a few cases subjective symp-
toms are present (symptomes attenues) but ignored ; as Barie
says, " elle pousse souvent inapercue . . . eHe demande a etre
cherchee."

Among the first recent cases, fully recognised as aortitis, to
receive careful clinical study were two published by Marfan
(p. 157),1 in boys aged respectively 12 and 13 ; and a third, in a
girl aet. 13, was published by Mery and Guillemot ; 2 but in 1863
H. Roger had published a case of aortitis followed by aneurysm
of the ascending aorta in a child aged 10 ; and in 1881 Hippolite
Martin 3 published cases of aortitis in acute rheumatism (as
also in smallpox, diphtheria, and typhoid fever). Sanne,4 in 1887,
made such a collection of cases of aortic dilatation and aneurysm
as was then possible. I have in my possession an M.D. thesis,
of Kiel (in 1891), by Dr. Walther Richter, a pupil of Heller, on
the implication of the aorta in endocarditis (■" Die Beteiligung der
Aorta an endocarditischen Prozessen "). Richter had before him
four specimens, and concluded that endocarditis, of whatsoever
kind, might invade the aorta in two ways, usually together,
sometimes severally ; namely, by contiguity or by continuity.
Thus an aortic cusp, or a polypoid appendage of it, may, as
it flaps, carry infection to a contiguous area of the aorta, where
an ulceration may be established from which an aneurysm
may arise.5 Marfan, in a criticism of the relevant physical
and clinical signs, brought out certain diagnostic criterions ;
some of his cases being " trouvailles d'auscultation." He was
then of opinion that angina pectoris (by which he meant a
full attack with radiating pain and dread) does not occur in
children ; yet in both his cases there were peculiar recurrent
suffocative oppressions and distresses with " douleurs sternales."
He also discussed cases drawn from previous authors in which he
believed himself justified in diagnosing, or at least suspecting,

1 Marfan, Semaine mid., mars 27, 1901.

2 Mery et Guillemot, "Aortite rhumatismale avec dilatation," Bull, de
la Soc. de Pediatrie de Paris, Nov. 1902.

3 Martin, H., Rev. de med., 1881, vol. i. p. 369.

* Sanne, Rev. mens, des maladies de Venfance, fev. 1887.
6 Professor Teacher showed four or five striking specimens of this kind at
the Brit. Med. Assoc. Meeting, Aberdeen, 1914 (see p. 161).

sec. i IN EHEUMATIC FEVEE 153

unrecognised aortitis of rheumatic or other infective origin. The
alternative was a precocious atheroma, of which a very small
number of examples have been recorded from the time of Andral,1
who noted calcareous atheroma of the aorta in a girl set. 8, and
of Peter, who described a like condition in a child set. 2.2 This
subject has been well considered by Simnitzky (loc. cit.). (See
Vol. I. p. 175.)

In the case of aortitis reported by Mery and Guillemot in
a child aet. 12, the dilatation of the aorta was considerable and
easily defined. It occurred during an attack of acute rheum-
atism. The "cimier de casque" extended 3 cm. beyond the right
border of the manubrium. In 1901 Barie 3 published his similar
case with the same diagnosis, and Queille 4 likewise ; but they
verified rather than increased our knowledge of the subject. In
1903 Zuber 5 reported that he had re-examined one of Marfan's
patients at the age of 16. In the previous year signs of general
heart failure had set in, with nocturnal attacks of cardiac dyspnea,
" and, moreover, during the last year a new trouble, resembling
angina pectoris ; namely, violent pain in the chest about the
sternum and radiating into the shoulder and arms. The aortic
dulness extended 4 cm. to the right."

In the same year de la Riie6 published a book on the subject.
His first two chapters are given to aortic valvular disease ; the
third to aortitis, which in children he regards as most frequently
rheumatic. Now de la Riie was, I think, the first to point
out the febrile phases which may accompany aortitis, as in
my Royston case ; in illustration of this process he published
extracts from temperature charts. The aortitis itself, he says,
is apt to bring on pain, radiating to the left shoulder and arm ;
or passes more covertly as a retrosternal oppression, weight, or
constriction. He says also that in rare cases the aortitis may
lead to aneurysm. He had seen two instances, of which however

1 Andral, Clin, mid., 1834. 2 Peter, Union mid., Paris, 1890.

3 Barie, Presse midicale, 1905, No. 24.

4 Queille, These de Paris, avril 1906.

6 Zuber, Rev. mens, des mal. de Venfance, Turin. 1903.

6 De la Riie, Affections acquises de Vaorte (orifice et crosse) chez V enfant,
These de Paris, 1903, an able tract of 160 pp. De la Riie says that the first
case of aortitis in a child was published by Moutard-Martin in 1875. But this
may have been a case of congenital syphilis ; and see pp. 151-2.

154 AOETITIS partii

I gather that Mery's case (reported above) was one. This case
de la Rue verified by radiography. He adds that these aortitic
cases may end in sudden death by angina pectoris, or by laryngeal
spasm. The author industriously collected, from English and
French sources, a very important series of cases of aneurysmal
dilatation and of saccular aneurysm of the aorta in children ;
a substantial proportion of which seem to have taken their rise
in rheumatic aortitis : in some of them angina pectoris is
definitely described. In these descriptions the author pays
the conventional compliments to the coronary arteries.
Gibson 1 exhibited a child with double aortic and pulmonary
disease — the result of acute rheumatism ; she suffered during
the attack with pain " which resembled that of angina pec-
toris." Again, Josue and Solomon 2 in an autopsy on a case
of very extensive and acute rheumatic disease, found " on the
aorta at the origin of the coronary arteries some gelatinous
'patches"

In 1905 M. Triboulet,3 the cordial friend and host of English
physicians, published an article on rheumatic aortitis producing
cylindroid dilatation of the ascending arch, or of the whole arch ;
but he had not seen a case of consequent aneurysm. In respect
of this consequence however it is interesting to find that Triboulet
also detected changes especially in the media ; and he reminds us
that in Boinet's 4 well-known statistics of aneurysm 7 cases in 240
were attributed to acute rheumatism.

In 1906 (Edin. Med. Journ., June 1906) Dr. Hugh Stewart,
then house physician to Dr. Gibson, published a case of severe
rheumatic fever in a boy aged 7. The case presented some
curious valvular lesions, mitral and double aortic, but incident-
ally it is reported that two months after the onset, when hardly
convalescent, he was seized repeatedly by angina pectoris of the
typical characters, radiating into the left arm. " He was fixed
in position not daring to move : pale, anxious and fearful."
The attacks would last ten to fifteen minutes, and on some days

1 Gibson, Med. Chir. Soc, March 1903. Also Dis. of Heart and Aorta, 1898.

2 Josue and Solomon, Lancet, Nov. 21, 1903.

3 Triboulet, Soc. med. des hop., mars 10, 1905,

4 Boinet, E., " Aortites," etc., Tr. de med., Ed. Brouardel, 1907. Idem,
Arch, de med. exper., Sept. 1897 ; and " Atherome aortique exper.," Soc. de
Biol, juin 1906.

sec. i IN EHEUMATIC FEVER 155

were as many as six. The pains did not wholly subside for
some two months.

In a volume of Conferences pratiques sur les maladies du
cceur, etc., published in 1906, M. Renon x has a chapter on Rheu-
matic aortitis and aneurysm, in which he reports a case of his
own in a boy, set. 16, in the Pitie. The patient was then suffering
from acute rheumatism with aortitis. He was seized at the level
of the fourth right rib by a sudden violent pain in the breast
with " etouffement syyicopale" but without change of cardiac
signs. These attacks were repeated, and radiated to the
right arm and shoulder, then subsided with the develop-
ment of aneurysm. Briefly, the author had the remarkable
experience of seeing an aneurysm form under his own eye. It
was revealed by radiography. Professor Vaquez saw the case,
and agreed in the diagnosis of rheumatic aortitis with formation
of aneurysm. The boy had suffered from previous attacks of
rheumatism, and rheumatic aortitis had occurred in him before
that attack which culminated in the aneurysm. In the next
year the following case was recorded in the Miinchener med.
Wochenschrift (1907), p. 2330 :

Male set. 46 ; good health till the attack of acute rheumatism, on
the eighth day of which he had sudden occlusion of the left brachial
artery. " Recovery nevertheless complete." But six months later
an aneurysm became manifest, with palsy of the left recurrent
nerve. It was seen by radioscopy, and proved mortal by rupture.
The diagnosis made was Aortitis rheumatica, with embolism of
" brachial " artery from the primary patch, and development of
aneurysm later.

Bennert 2 has described two cases of aortic aneurysm following
rheumatic fever. Both patients were under 20 years of age.
Syphilis was definitely excluded. This author had collected twenty
cases, and laid down the rule that aneurysm in children and
youths is a result of acute rheumatism. Ruppet 3 again reported,
in a patient set. 10, aortic regurgitation and aneurysm of the
ascending aorta, due to an attack of rheumatic fever five years

1 Renon, Mai. du cceur, etc., Paris, 1906 ; an interesting book in many
ways ; also Presse med. vol. xxxviii., 1912.

2 Bennert, Zeitschr. f. klin. Med. Bd; lxix. Nos. 1 and 2.

3 Ruppet, Med. Klinik, 1910.

VOL. II L

156 AOETITIS paktii

before. Feytaux 1 reported 5 cases of rheumatic aneurysm in
patients set. 12-16.

Eare then as it may be, aneurysm of rheumatismal origin is
definitely to be accepted. As to physical diagnosis little has been
added since Potain's well-known lecture in the Clinique de la
Charite, 1894.

Some authors think that the aortitis is due to inoculation by
an affected semilunar cusp, as in malignant endocarditis ; in a few
cases it may be so (p. 160), but in a fair number of these cases
no valvular disorder was audible. In aortic valvular disease
I have observed small patches of inflammation extending from
the cusps to the sinuses, and it may travel farther up the arch.
But this rheumatic aortitis is but one of many specific kinds, and
in syphilis we know the rule to be suprasigmoid aorta first,
valvular involvement in the second place. Rheumatic in-
flammation reaching the aorta from an endocarditis falls into
a secondary category.

How, if unsought, this lesion escapes notice I may illustrate
by two instances which I discovered accidentally in patients
with cardiac disease, due to recent attacks of rheumatic
fever, who came in a batch of cases called into Adden-
broake's Hospital for one of our final M.B. examinations.
In both besides the heart disease, to one who looked for it,
were definite signs of dilated aorta. I brought them under
the notice of my colleague Dr. Rolleston, the only examiner
who happened then to be disengaged. In neither case had
a note been made of this complication ; it was, as usual,
lost in the cardiac malady. On the independent notes of one
of these, a girl named Jeeves, set. 15, passed over as aortic
regurgitation (and query mitral stenosis ?), I found she had had
three attacks of rheumatic fever ; the second " was far the
worst." She was then in bed twenty - three weeks, and
" suffered severely from attacks of pain at the breast-bone and
down her left arm." 2 The other patient, a man set. 30,
also had had three severe attacks, and spent months in bed.
In one of the attacks he suffered from severe mid-sternal pain.
In both these cases the aorta was much dilated submanubrially,
and to right, and up in the neck : throbbing and thrilling.

1 Feytaux, These de Paris, 1906, » See Appendix ix., I. p. 210.

sec. I IN EHEUMATIC FEVER 157

Marfan,1 out of twenty-four cases of aortic disease in children,
found three cases of aortitis (set. 9, 12, 13) attributable to
rheumatic fever. Many of the others were hereditary syphilis. A
very curious case is reported by Hennig,2 in which aortitis was
found in the body of a child born of a mother who during that
pregnancy suffered from severe rheumatic fever. Valvulitis
may spread by the anterior mitral curtain to the aortic valve,
or perhaps the aortic valve may be attacked independently,
but I feel sure that in some instances aortic regurgitation,
consequent upon rheumatic fever, is due to the extension of an
aortitis.

So much for latent cases : the following typical instance
will illustrate how slight symptoms of the kind might be
neglected by physicians not awake to the process. Master B.,
set. 16, a patient of Dr. Windsor of Royston ; seen also by Sir
Bertrand Dawson and myself. Dr. Windsor, who watched the
boy anxiously, wrote, " he should be through a severe attack of
rheumatic fever, with a damaged heart, but does not come quite
through." He had had several returns of fever, not high but
recrudescent ; periods which recurred after as before our meeting.
In these recrudescences the temperature rose in a flat curve to
about 100*5 or 101, or occasionally near 102 ; and in a few days
slowly fell again. Now during these relapses the boy made an
anxious if indefinite complaint. He dreaded them ; he felt very ill
in them, ill beyond discoverable reason ; moreover he complained
definitely of an oppression about the sternum, so that he
would sit up in bed, looking anxious and disturbed. Signs of
dilated aorta, dulness and jugular pulsation, were clear and
unmistakable. This case was a good example of Leger's rheu-
matic aortitis " par poussees." 3 I have chosen a fairly obvious
instance, but there are plenty of such aortic intercurrencies
in rheumatic fever, if less well marked than this one. In a few
cases the symptoms, anginous in kind and degree, are actively,
even furiously, present, but too often are attributed to the
heart, or to transitory spasms of the nerves. In such cases

1 Marfan, "Lesions acq. de 1'orifice aortique et de l'aorte dans l'enfance,"
Sem. med., 1901.

3 Hennig, " Angebor. Aortitis," Jahrb. f. Kinderlieilk. Bd. xxx.
3 Leger, UAortite aigue, These de Paris, 1877.

158 AOETITIS paktii

the rheumatic aortitis is violent and agonising ; angina pectoris
appears in full dress, as in the case under Dr. Christian Simpson
to which I shall refer again (p. 274). A like case, with necropsy,
Dr. Poynton also described in the Lancet of May 20, 1899 : a
woman, aged 38, attacked by rheumatic fever with not only
mitral endocarditis but also aortitis (fuller report, p. 275). After
death numerous fresh patches were found upon the aorta.

Now although necropsies in cases of rheumatic aortitis are
infrequent, as in its acuter stages rheumatic fever is rarely mortal,
yet they are less infrequent and more decisive than we suppose.
Dr. Andre wes l writes : " Professor Klotz informs me that he
commonly finds similar changes in acute rheumatism " — similar,
that is, to acute aortitis in typhoid fever, scarlet fever,
diphtheria, influenza, etc. To Klotz's paper on rheumatic
aortitis 2 I have referred already ; he likewise describes in the
ascending aorta, more rarely in the descending thoracic and
abdominal portions, a " fairly typical lesion, after the manner
of syphilitic aortitis " (but not syphilitic). The coronary trunks
may or may not be affected in this way, though their finer
twigs are " invariably " involved in the myocarditis. Klotz
gives three necropsies of consecutive cases of rheumatic fever
in patients whose ages were 9, 16, and 19. The aorta on closer
scrutiny presented in each " a striking picture " : the intima
was not altered, but the media was thickened by vascular
increase, oedema, and perivascular infiltration, with abundance
of leucocytes and plasma cells. Many elastic fibres were
" split and feathered," and much muscle had perished. The
adventitia was infiltrated by inflammatory non-suppurative
lymphoid cells. There were signs of fibrous repair. These
histological features were different from the gummy and
granulomatous process of lues,3 though the seat and mode
of access were similar. In the older cases patches of sclerosis
are formed, chiefly fibrous, but extending to the deeper layers,
and with evidence of fatty and even calcareous decay. In one
mortal case of rheumatic aortitis and aneurysm, in a child set. 6,

1 Andrewes, Sept. Med. Off. L.G.B., 1913, App. B. No. 1, p. 254.

2 Klotz, Trans. Ass. Amer. Phys. vol. xxvii., 1912. But see also the later
essay in Journ. Path, and Bad., loc. cit.

3 The words are those of Klotz; but, as the description is a little abbreviated,
I cannot put these sentences as a quotation.

sec. i IN EHEUMATIC FEVER 159

the author found a pure growth of a streptoccocus in short chains.
In his later paper (1913) however, he separates two forms :

(1) inflammatory hyperplasia in the media and adventitia (as if
it approached after the manner and by the ways of syphilis) ;

(2) an endarteritis after the obliterans mode. To the first
form he attributes the ectasies and aneurysms. Sir William
Osier,1 who was, I think, somewhat sceptical concerning
rheumatic aortitis, now agrees that " in rheumatic fever the
resulting endaortitis may be serious." Syphilis then is not the
only grave toxic invasion of this vessel, nor the only cause of
aneurysm, in which, unless the process or its reactions reach
the extremer degrees, the intima is primarily unaffected.

Barie,2 returning to this subject in a recent paper, discusses
it as a whole, including peripheral arteritis. This he says
occurs more frequently in the arms ; in typhoid in the legs.
It may occur in the carotid ; with fever, pain on palpation,
throbbing, and perhaps thrill, with some dilatation. In smaller
vessels it may take the obliterative course. In cases of death
after bygone rheumatic fever Klotz has shown old thickening
of the adventitia and media. He also has demonstrated rheu-
matic arteritis occasionally in peripheral vessels, as in the
posterior tibial.

After my London paper was read, Dr. Cowan of Glasgow
sent me a reprint of one of his own,3 wherein he stated that in
acute rheumatism he had found aortitis, and arteritis of its vasa
vasorum. In a covering letter he says " the subject (and in other
acute infections also) is of far more importance than has hitherto
been supposed. In nearly all cases however post-mortem evidence,
if obtained at all, is not obtainable till later life, when the incidence
of other diseases has vitiated it." Dr. Carey Coombs 4 of Bristol,
to certain autopsies of acute rheumatic cardiac disease, adds the
following sentence : " At the root of the aorta, about the coronary
openings, little white patches are generally visible ; these prove
on section to be areas of subendothelial inflammation with small-
celled infiltrations, proliferative, and fatty change."

1 Osier, W., Brit. Med. Journ. and Lancet, Aug. 1908.

2 Barie, Paris med. tome xxi., 1913.

3 From The Practitioner, March 1906.

4 Coombs, C, Brit. Med. Journ., Nov. 23, 1907 ; and Q. J. Med., Oct. 1908.

160 AOETITIS part ii

Pericarditis as a cause of aortitis, acute or chronic, I
shall discuss in the essay on Angina Pectoris (p. 454). It is
generally a periaortitis due to extension into, or arising in,
the cul de sac of the basal pericardium, contiguous to the
aorta. It is said that in rheumatic fever this periaortitis may
occur as a local and independent effect (see p. 457).

In my essay on Angina Pectoris I shall explain that the
presence or absence of sternal oppressions and of radiating pains
probably depends — as it does in atheroma — upon the precise seat
of the process ; whether or no it engages, or at any rate by
swelling distends, the investing coat. Now the demonstrations
of Carey Coombs, Poynton and Payne, and others, prove
that rheumatic carditis is perhaps never confined to a valve,
but enters more or less deeply into surrounding tissues ;
or "it begins in the deeper parts and spreads towards the
surface."

From rheumatic fever we pass easily to the " malignant "
forms of cardiac inflammation, where again we find the aorta
by no means outside the sphere of several kinds of virus. In
an aortitis which formed part of such a case Dr. Maguire found
streptococci. A remarkable case, published by Pagliano,1 pre-
sented the features of malignant endocarditis, but at the necropsy
this kind of mischief was found confined wholly to the aorta.
Sir Dyce Duckworth has published a case of acute verrucose
aortitis ; and Boulay 2 also has described a case, in a man aged
36, in whom from a verrucose aortitis, also confined to the
thoracic aorta, embolisms in the mesenteric area proved mortal.
In three necropsies — two of malignant endocarditis and one of
erysipelas — Boinet and Bomary 3 found bacteria in patches of
" endo-aortitis." (See Morison, Petit, etc., p. 276.)

Pechter of Kiel, a pupil of Heller, was early in emphasising
the extension of malignant endocarditis to surrounding parts, and
to independent foci in the aorta.4 In one case the posterior
aorta was much inflamed, and its sinus full of vegetations ;

1 Pagliano, " Aortite chronique terminee par etat infectieux sans lesion
d'endocarde," Marseilles med., 1886 ; quoted in other journals.

2 Boulay, Bull. Soc. Anat., 1890.

3 Boinet et Bomary, " Recherches exp. sur les aortites," Arch, de med.
exper., Sept. 1897.

4 Pechter, Beteilungen d. Aorta an endocarditischen Prozessen, Kiel, 1891.

sec. i SEPTIC FOKMS AND PEEFOEATION 161

above it were several foci up to the size of a linseed. In a second
case the same disease extended to the aortic wall, and had set
up ulceration of it. In a third a coagulated deposit, 1 cm. long,
was attached to the wall (see Hodgson's Case, p. 148). In a
fourth the aortic intima was thickened by proliferation, and in
one place about the size of a linseed a superficial ulcer, with
ragged edges, and a loss of substance. In a fifth this process
was deeper in the wall of the vessel, both media and intima being
attacked, with extrusion of the adventitia (clinical notes of
this case would have been of much interest, but the author writes
only as a morbid anatomist). In a sixth was a small ulcer upon
the wall (with aortic valvulitis). In a seventh an endarteritic
process had extended to the aorta. Heller himself published
a similar case with extension to the aorta, and to the pulmonary
artery also.

The verrucose or ulcerative aortitis of malignant endo-
carditis does not usually tend to perforation ; in some cases
perforation occurs (see Teacher's specimens, p. 152 n.), but the
evidence seems to indicate that perforating aortitis is usually
a result of other kinds of microbe. In the well-known case of
perforative aortitis of Oliver and Woodhead {Lancet, 1891) it
was the B. anthracis which was detected in the parts attacked.
These perforating cases, in which the disease penetrates rather
than diffuses itself, are not very rare ; though too often the
bacteriological evidence is wanting. I shall refer presently (p.
273) to a case of perforation attributed to influenza. So luetic
disease sometimes by concentration sets up saccular aneurysm,
sometimes is more diffuse. Perforation may make its way
into pericardium, pulmonary artery, or auricle ; Dr. Lumsden's
case of perforative disease of the aorta just above the valve in
a young woman of 23, was fatal by penetration and haemor-
rhage into the pericardium ; the aorta presented only some
spots of disease on its inner face. There was no bacteriological
record. Thoracic aneurysm of course may take rise in such a
process. One of our graduates — Dr. Jordan — has recorded x
a fatal aneurysm of the ascending aorta in a boy of 6 ; the
aorta and heart seemed otherwise healthy, but a septic focus was

1 Jordan, A. C, Lancet, Feb. 21, 1903. The specimen is in St. Bart.'s
Museum with a somewhat similar specimen from a boy of eleven.

162 AOKTITIS paetii

discovered in one ear. He had suffered from an arthritis and,
presumably, from a septic ulcer of the aorta, due perhaps to
septic embolism of vasa vasorum. Nordmann and Maurin 1
publish two cases (set. 15-17) of pyaemia upon tuberculosis, in
which patches of aortitis were formed in the descending aorta.
There was no syphilitic infection.

Suppurative aortitis seems to be rare, or, as it does not
break into the channel of the vessel, is apt to be overlooked after
death. The pus lies in foci in the adventitia and in the sub-
stance of the middle coat ; it is a periarterial affair, and usually
but a small and secondary item in some much more extensive
pycemia ; as for example in some recorded cases of puerperal
infection. Indeed in pyaemia, as in other septic maladies,
such an aortitis is not uncommon, and may be due to
septic thrombosis or small emboli. Dr. Charlewood Turner 2
has collected cases of this kind ; Brouardel and Bureau have
recorded others ; and at a still earlier date Rokitanski and
Lebert had observed both the event and its associations.

Boinet has recorded an instance of aortitis in erysipelas,
the nature of which he verified by bacteriological tests.
Klotz and Sumikawa report that, in some contrast with
other infections, the streptococcal set up proliferation of the
intima. Staphylococci attack both coats (Saltikow). Klotz
says that this infection also enters by the vasa vasorum and,
before the intima, attacks the media where, and in the adventitia,
small cell infiltration is to be seen. Koritschoner 3 publishes
a remarkable case in a man, set. 30, who died of haemorrhage
by rupture of the aorta into the pleura just posterior to the
left subclavian. The cause of the rupture was a perforating
phlegmonous inflammation of the media and adventitia, which
had arisen " metastatically " from a phlegmon of the hand.

The occurrence of aortitis in typhoid fever, as Louis first
pointed out, might be recorded more frequently were it more
diligently sought for ; but in this malady aortitis presents itself
in a superficial and transitory form. In typhoid we look for
the specific changes rather in the peripheral arteries (see

1 Quoted in Zentralbl. f. Herz- u. Gef.-kranlchtn., March 1912.

2 Turner, C, Trans. Path. Soc, Lond., 1886.

3 Koritschoner (Wien), Zentralbl. f. pathol. Anat. Bd. xxiii. No. 3, 1912.

sec. i IN TYPHOID AND INFLUENZA 163

Vol. I. p. 283) ; still Potain has published two cases of
definite typhoid aortitis,1 and a few more are on record.
Gilbert and Lion produced typhoid aortitis experimentally,2 as
after them did Chantemesse likewise. The episode, for it is
rarely much more, occurs during the later weeks of the fever,
or even during early convalescence, when it is very apt to
escape observation. [Scarlet Fever, see p. 309.]

The occurrence of j aortitis in the course of influenza, or
during the convalescence, has been observed by Lancereaux,3
by Hanot,4 by Pawinski,5 by von Leyden and others ; and
in England has been so well described by Sansom 6 that I
must not linger on this section. (See also Vol. I. p. 291,
and Angina Pectoris, p. 268). Some of Sansom's cases came
to autopsy, when grey translucent raised patches of aortitis
were found. In some necropsies the aortitis had become ulcera-
tive, and in some a mixed infection was verified. Sir Richard
Douglas Powell has fully recognised post-influenzal aortitis,
often with symptoms of angina pectoris (p. 272). Three or four
definite cases, and others of less certainty, have fallen under my
own observation ; one patient, whom I visited with Dr. Humphry
of Cambridge, being an eminent instance. A man, then about
60 years of age and, before his influenza, of excellent health,
while apparently convalescent was walking in the fields near his
college, when, as I shall narrate in the essay on Angina Pectoris,
he was seized in an instant with a severe attack of this malady.
He crawled home with great difficulty, and, so intense were the
attacks, that he seemed for some weeks to be in hourly jeopardy
of life ; but ultimately he made a complete recovery, and to this
day — many years later — remains well. Kraus7 says that " grippal
aortitis " is not so well known in Germany as it ought to be.
He supports also the important rule of prognosis that in this

1 Quoted in Bureau's Etudes sur les aortites, 1893.

2 Gilbert et Lion, " Arterites infect, exper.," Comptes rendus de la Soc. de
Biol, oct. 12, 1899.

3 Lancereaux, Soc. Anat. de Paris, 1886. See also Traite d'anat. path.
tome ii. and atlas, 1871 ; and Gaz. des hop., juli 6, 1899.

4 Hanot, Arch, de med., 1886.

6 Pawinski, Berl. klin. Wochenschr., 1891.

6 Sansom, Roy. Med. Chir. Soc, 1894 ; and Lancet, Oct. 21, 1899. See
also Fiessinger, Gaz. med. de Paris, Nov. 1892.

7 Kraus, Deutsche med. Wochenschr., 19. Marz 1914, p. 578.

164 AOETITIS paet n

kind of aortitis the symptoms and the dilatation usually recede.
Sansom records recovery likewise in most of his cases ; though
others, in which the pathological changes were verified, were
mortal. For the records of von Leyden and other observers of
this sequel of influenza I must refer to Sansom's paper.
Dr. Mitchell Bruce 1 records a case in a man, set. 54, in whom
after influenza angina pectoris appeared. The aorta was dilated.
The disease progressed to a mortal issue, when the aortitis was
verified by necropsy. In 1908 Marmorstein 2 recorded two
notable cases, both in women, aet. 20 and 24 respectively,
in whom syphilis could be certainly excluded. In the second
patient the aortitis was betrayed by a disagreeable sensation
referred to the upper sternum ; it was observed to extend to the
aortic valve, first with a systolic, then with a diastolic murmur,
which were permanent. The former patient died of basilar
thrombosis : within the arch of the aorta were patches of acute
inflammation, showing abundant cell proliferation, here chiefly in
the intima, but penetrating to the middle and outer coats. The
vasa vasis were injected and infiltrated around with small cells.
Influenza bacilli were found definitely here, but more abundantly
in the cerebral tissues. (See also Cooper, p. 273.)

Of aortitis following diphtheria many instances are on
record.3 This infection attacks the media distinctively (Klotz),
a simple medial necrosis ; not with a proliferation of the intima,
as in typhoid, streptococcal, etc., aortitis. But we may agree
with Marchand that it is not infrequently impossible to dis-
criminate between an acute aortitic atherosclerosis and mixed
conditions. Curschmann4 describes such a case in a boy, set. 16,
who died after severe diphtheria of five weeks' duration. The
front wall of the aorta was thin and pouched, and its inner face
was beset with a network of whitish streaks of disease. The
heart and other vessels were examined, by the naked eye and
by the microscope, but no changes were found in them. I will
stay to cite only one more case of diphtheritic aortitis, in a
horse, examined by Boinet, which had been poisoned by a pro-

1 Bruce, M., Lumleian Lect., Lect. III.

2 Marmorstein, Rev. d. med., 10 mars 1908.

3 E.g. Mollard et Regaud, " Ath. de l'aorte avec diphtherie," Soc. de Biol.,
juillet 17, 1897 ; and Klotz later.

4 Curschmann, Pathol, d. Kreislaufs. Art. med. klin. zu Leipzig, 1893.

sec. i IN DIPHTHEPJA, PNEUMONIA, MALARIA 165

longed and severe course of injections of diphtheria toxin ; acute
aortitis, of which illustrative microscopic sections were published
by the author, was found at the necropsy.

That aortitis may arise in pneumonia, not as a direct exten-
sion of this disease, but as a several function of the pneumo-
coccus, from certain observed cases seems probable. Dr. Poynton a
narrates a well-marked case, in the main a severe pneumonia ; but
after death marks of a separate point of attack were found in
the first portion of the aorta. The endothelium was destroyed,
and the subintima infiltrated with leucocytes. Luzzatto 2 also
narrates a case in a man, set. 45, ill with tedious chronic pneumonia
for twelve months, when suddenly an ulcer of the ascending
aorta, 1 cm. wide, perforated. The intima was thickened and
split, and the media " sclerosed," besides hyaline foci of softening
in the muscularis, and abscesses. The elastic fibres had perished.
Pneumococci were abundant in the affected parts. The mischief
seemed chronic and of some duration, and as if due to direct
attack of the diplococci from the blood stream. Barie (loc. cit.)
has found the pneumococcus in the wall of the aorta.

Malarious aortitis, which attacks the arch especially, does
not rest upon the well-known testimony of Lancereaux alone ;
Herve 3 published three cases, and Sansom, adding the weight
of his authority to theirs, recorded another in a lady in whom
gout, rheumatism, syphilis, and other known causes could be
excluded. Nevertheless, as this form of aortitis is not always
benignant or transitory but, as Sansom points out, is apt to
linger for years and to leave permanent lesion of vessel or valve
behind it, we may be thankful for its apparent infrequency. Dr.
Theodore Fisher,4 late of Bristol, notes however that among
men who have frequented tropical lands disease of the
aorta is prevalent. He thinks syphilis insufficient to account
altogether for this prevalence, and suggests that it may be
due in part " to some infection of the blood which is more
common in warmer climates than with us." Eight of thirty-seven
collected cases were attended with the formation of aneurysm.

1 Poynton, Heart Dis., p. 273.

2 Luzzatto, A. R., Biv. d. sci. med. vol. lii., 1912.

3 Herve, " Symptomes de l'aortite chron.," These de Montpellier, 1885.

4 Fisher, Theo., Brit. Med. Journ., Feb. 21, 1903.

166 AOETITIS part n

Lancereaux, as we shall see (p. 403), spoke of angina pectoris
as an eminent feature of the disease ; x and Dumolard 2 and
fellow-workers have brought testimony from recent experience
in support of his opinion. In malarious districts, in syphilis-
free individuals, in both sexes, and often before the age of 30,
they found dilated aorta, and even aneurysm. They cited only
cases in which the Wa.R. was negative. In diagnosis they relied
upon the X-rays ; but they had one autopsy, in an Arab, set 20,
who died of malaria. The internal tunic was affected, not the
adventitia nor media. But the description of the intimal disease,
so far as quoted, was not convincing ; it seems no more than
Hollis, and many others, have described in young subjects.

Tuberculosis of the aorta has been studied by Flexner,3
Hanot, Blumer,4 Boulay {loc. cit.), Faber (loc. cit.), and others.
Tubercle, only too common in small arteries, especially in miliary
form, as in those of the brain, lung, or kidney, is rarer in the large ;
and in the aorta its presence is rather curious than important.
Its patches are distinguished from syphilitic patches partly by
their greater propensity to caseation ; the discrete nodules are
most frequent in acute miliary tuberculosis. The epithelium
and adventitia long remain intact, the media undergoes necrosis.
Woolley 5 collected fourteen cases. Little nodules may be found
on the inner surface of the vessel not continuous with tuber-
culous foci elsewhere ; or the aortic disease may form part of
a chronic tuberculous mediastinitis. In the discrete foci
tubercle bacilli are to be found. Blumer readily demonstrated
the specific bacillus in both his cases.

Brodier and Laroche 6 have published two cases in which
gonorrheal aortitis was almost surely diagnosed. In both
a dilatation of the vessel receded with the subsidence of the
acute attack. Probably in many of these infections aortitis
(as arteritis elsewhere and phlebitis, with thrombosis) is no

1 I am indebted to Dr. Francis Hare for the following references on this
subject : Broadbent, Lumleian Led., 1891, rep. Brit. Med. Journ., p. 748 (see
also Heart Dis., 1807); and Anstie, Neuralgia and its Counterfeits, 1871, p. 74.

2 Dumolard and others, Revue med. d'Algerie, dec. 2, 1913 ; quoted in
other journals.

3 Flexner, "Tuberculosis of the Aorta," Bull. Johns Hopkins Hosp., 1891.

4 Blumer, Amer. Journ. Med. Sci., 1900.

5 Woolley, Johns Hopkins Hosp. Bull., March 1911.

6 Brodier et Laroche, Gaz. des hop., mai 22, 1900.

sec. i IN TUBERCULOSIS SYPHILIS 167

uncommon occurrence, but is latent, or masked by the general
symptoms. On this subject Wiesel (loc. cit.) has made some
interesting observations.

Syphilitic aortitis I have considered in the essay on
Arteriosclerosis, and shall have to deal with it again in the essay
on Angina Pectoris ; but here it must take that chief place which
the gravity of the disease imposes upon us. Syphilitic disease
of the aorta is far more common than of the heart. Deneke x
reckons that in adults syphilis doubles the mortality of diseases
of the circulatory system ; that the aorta is the most frequent
seat of the infection, and that in its tale of deaths it is exceeded
only by General Paralysis. The inflammation in syphilis is usually
chronic ; though some cases of syphilitic aortitis are of rapid course,
and may do more grievous, or swifter, injury than the more gradual
phases of extensive chronic disease and dilatation. Many years
ago Dr. Pye-Smith put such a case on record, in a syphilitic
subject, set. 32, in whom was no history of rheumatism or chorea.
At the necropsy a patch of recent aortitis was found ; soft,
injected, and crescentic at the edges like a cutaneous syphilide ;
it had advanced rapidly, invading and destroying the valve.
Brault, quoted by Letulle,2 examined a fresh and acute syphilitic
patch which will be referred to presently in the pathological
paragraphs of this chapter. In the essay on Arteriosclerosis I
have described how syphilitic aortitis passes into or blends with
atheroma, or may even be concealed by it ; in persons of and after
middle life, as Welch pointed out, we have no clear local demarca-
tion— in many cases at any rate — between the syphilitic and
the atheromatous processes. Hodgson, Wilks, Moxon, Davidson,
Jaccoud,3 Potain,4 and many others taught us much about
syphilitic aortitis ; but it is to Francis H. Welch, sometime Pro-
fessor of Pathology at Netley, that we owe our full knowledge of
this subject. It cannot be too plainly declared, in these days of
" Doehle-Hellersche Aortitis," that Welch, in his comprehensive

1 Deneke, Th., of Hamburg, " Die syphil. Aortenerkrankung," Deutsche
med. Wochenschr., 1913, p. 441. Seaport statistics are over the average.

2 Letulle, Anal, path., 1897.

3 Jaccoud, " Aortite et aneurysme de l'aorte d'origine syphilitique," Sem.
med., 1887.

4 Potain, " De l'aortite," Union med., Paris, 1889 ; also Charcot, (Euvres
completes, tome x.

168 AORTITIS part 11

and judicious essay, if in places a little old-fashioned in expres-
sion, described nevertheless all the essential features of the
process, macroscopic and microscopic. In November 1875 * he
read his paper upon 117 cases of " fibroid aortitis " ; in 46 per
cent of which was a clear record of syphilis. Again, of a series
of 56 cases of fatal syphilis, 34 presented aortic lesions, mostly
severe. If extensive, it may produce Hodgson's dilatation ; if
circumscribed and penetrative, aneurysm. Welch's opinions
were strongly contested at the time in the Royal Medical and
Chirurgical Society, and later, through his pupil Orth, by von
Leyden, and even by Virchow himself. Herein Orth's pupil
Bruhns must have differed from his master, for Deneke says
Bruhns was the first to describe a congenital case.

In discussing the syphilitic aorta I shall pass by, for the most
part, the large subject of aneurysm ; my concern is rather with
those parietal changes of which aneurysm, if a very obtrusive,
is an incidental offspring. Hodgson, in the admirable description,
in his Jacksonian Essay of 1814, of this preternatural dilatation
of the ascending aorta, beginning just above the semilunar valve,
seems to me to have suspected syphilis as the cause of it (see
pp. 9-10) ; and he quotes, of those before him, Morgagni, Senac,
Lieutaud, Haller, and Scarpa ; now Scarpa clearly apprehended
the specific cause as Lancisi had done. Scarpa says, " Syphilitic
patients are very liable to steatomatous [an unlucky adjective] and
ulcerative disease of the coats of the aorta" He gives a case, with
aneurysm, in a corporal, set. 22, who had been treated with
mercury ; though he was disposed to ascribe this effect rather to
the mercury than to the syphilis itself. But, as Hodgson says,
these authors confused this chronic aortitis with aneurysm. In
the original and still unforgotten sense of the word aneurysm
they had their excuse ; Welch in his classical paper compares
fusiform and saccular aneurysm. Hodgson did good service
moreover in emphasising clearly that post-mortem imbibition
was not disease. Other authors contended, not that syphilis
set up its own specific process, but that it gave a bent to ordinary
atheroma. Now we know that of mere atheroma aneurysm is a
very rare consequence ; indeed the great Neapolitan surgeon as-
sociated what he definitely named as the " Aneurysma Gallicum "
1 Welch, F. H., Med.-Chir. Trans. 2nd ser. vol. xli., 1876.

sec. I IN SYPHILIS 169

with " impure coitus " and signs of syphilis elsewhere in the
body ; a and attributed the aortic lesion to the " principia
ichorosa " and " humores erodientes " of it in the blood ;
though he is puzzled to know how, while in the current, they
can fasten upon the wall. Kayer 2 likewise was convinced that
syphilis played a part in this aortic lesion ; and later Gueneau
de Mussy, whom I often find reason to quote, published, in the
first volume of his Clinical Medicine, an admirable study of the
subject, with its pathology well up to that date. Edgren3
was clear about the lues, but was not clear about the peculiar
histology ; even my friend von Schrotter never quite saw his
way to accept this distinction. Sir William Osier 4 says that
Helmstadler 5 drew attention to the rupture and necrosis of the
elastic fibres, causing grooves, which he pictured ; but this author
again did not realise the specific nature of the lesion he had under
his eye. For I may note that, thus far of course, this process
is not necessarily specific. Osier adds that Koster, in 1875, stated
that " mesarteritis " is a mark of syphilis — which is true, if not
critical, for the same is true of rheumatic and other kinds of
infectious aortitis originating by way of the vasa vasorum — and
that in 1877 " gummous " deposits were recognised in the media.
We have seen that it is difficult, save in a few cases, to assure
oneself by the eye of the " gummous " nature of these foci (Vol. I.
p. 300 and II. 181). Eppinger's work on aneurysm (in 1887) Osier
esteems as " one of the most exhaustive ever written." In the
same year Jaccoud 6 described a case of syphilitic aortitis ; and I
well remember that about these years, or sooner, my old comrade
Dr. W. H. Dickinson was demonstrating to us " syphilitic
atheroma." Great progress then was made ; albeit the syphilitic
was not yet clearly distinguished from the atheromatous process,
which, as I have said, practically never leads to aneurysm.

We shall not forget what is due to Heller (1885), to Dohle
(Inaug. Diss., Kiel, 1885), or to Saathofi ; nor our earlier debt to

1 Lancisi, De novissime observatis abscessibus, c. xviii., ed. 1724.

2 Rayer, Arch. gen. de med., 1823.

3 Edgren, Arteriosklerose, Leipzig, 1898.

4 Osier, Sir W., Schorstein Lecture, Brit. Med. Journ., No. 27, 1909.

5 Helmstadler, Formation des anevrysmes spontanees, Strasburg, 1873.

6 Jaccoud, " Aortite et aneurysme syph.," Sem. med., Penis, 1887. See also
Faure, Arch. gen. de med., 1874 ; Kundrat, " Aortitis acuta," Allg. Wien. med.
Zeitung, 1885 ; and Broadbent, Heart Diseases, 1897.

170 AOETITIS part ii

the Scandinavian physicians — to Heiberg (1876) and to Malm-
sten ; to Benda again about 1888, and later to Chiari.1 It is
not surprising that our more intimate knowledge of syphilitic
aortitis has come from great seaports, such as Kiel, Hamburg,
and Christiania. Reuter of Hamburg (in 1906) was perhaps the
first to find the spirochseta in these cases. It is however to
English medicine, to Hodgson and especially to Welch, that
we owe our knowledge of this disease, debts too much ignored
by German writers who, too exclusively, claim the honour of
its description for the Kiel School ; and our debt herein is not
much less on the whole to Wilks, and his pupil Moxon.

Professor O'Sullivan 2 has graphically described, in two cases,
the features of this characteristic form of aortitis. Some years
ago he had received the heart of a young soldier who had dropped
dead on the march. He was apparently perfectly healthy.
The appearance of the aorta struck him as abnormal, for he
observed that a little above the origin of the aorta, parallel
with the valves, there was an abrupt rise in the surface level
which continued in breadth for about an inch upwards into the
vessel and then as abruptly descended again, forming an elevated
partial ring, a quarter of an inch or more higher than the rest of
the surface. The left coronary artery was obstructed by the
excrescence of the surface, which obstruction he took to be the
cause of death. That specimen had gone astray, but he ex-
hibited a similar specimen from a young man who a few days
before had been found dead in a lavatory. The condition of
the part in the two cases was almost identical. There was very
little degeneration, as compared with an ordinary case of
atheroma ; and the amount of overgrowth of the inner coat of
the vessel, as compared with the amount of degeneration, was
enormous. The orifice of the right coronary artery was practi-
cally closed ; the opening of the left was likewise reduced to
small dimensions. A small depressed area, about an inch from
the sinuses, was stained red and exhibited a lesion different from
atheroma. The tumidity of the inner coat, as seen under the
microscope, was composed of a reduplication of the inner

1 Chiari, many papers : the earlier in discussions of Deutsche path. Ges. in
1899 and 1903-4.

2 O'Sullivan, Session Roy. Acad. Med. Ireland. Rep. Lancet, April 11, 1908.

sec. I IN SYPHILIS 171

tissue ; in the middle coat the elastic tissue was cut, torn, and
split by masses of cell infiltration which ran along the course
of the vasa vasorum. The natural conclusion was that,
although there was no direct evidence of it, both cases were
syphilitic.

But the weight of the incidence of syphilis upon the aorta and
its valve is even yet not fully recognised. Oberndorfer,1 in a
recent discussion, reported that of 1436 autopsies on adult bodies
during the previous two and a half years, " Aortenlues " was
found in 99 — nearly 7 per cent — and that it stood next in fre-
quency to diseases of the heart. In 40 of these cases the aortic
disease was discovered at the necropsy. He urged the importance
of suspecting syphilis in all slow and obscure cases of disease of
the heart or aorta. He emphasised the larger pulse amplitude
(dilated aorta), the (occasional) angina, and the usually normal
systolic pressure, unless of course the valve be injured and the
left ventricle hypertrophied. Gruber of Strassburg,2 who followed
this speaker, stated that he had searched the records of 6000 cases,
and found luetic aortitis in 4 per cent ; or, taking cases since the
vogue of the Wa.R., 4-5 per cent. I may say here that with
expertness in the Wa.R. method, the proportion of positive results
is increasing. Of 256 autopsies on bodies with acquired syphilis
in Leipzig, between 1906 and 1911, Marchand reported aortic
syphilis in 211 (about 82 per cent) ; and in 67-4 per cent of
autopsies on the congenital disease ; in but few of these was
the pulmonary artery the vessel attacked. So large is the post-
mortem incidence that Marchand suspects that in the slighter
invasions the local disease peters out more or less harm-
lessly. Citron 3 used the Wa. test in all chronic cases of aortic
regurgitation, and found it positive in over 60 per cent, a much
larger percentage than that of a history of infection ; and recently
even this estimate has been exceeded. Deneke, in cases

1 Oberndorfer, E., Milnchener drzt. Verein, Nov. 20, 1912, reported in
Munch, med. Wochenschr. Bd. x. S. 506, 1913 ; report contains precise records
of morbid histology. See also idem, Berl. klin. Wochenschr. Bd. xlix., 1912.

2 Gruber has since published a monograph on " Dohle-Hellersche " Aortitis
(1914), too late for this book. It is rich in pathological material, and contains
some important statistics. It is well illustrated. But in the results there is
nothing new.

3 Citron, Berl. klin. Wochenschr., 1908.

VOL. II M

172 AOETITIS part II

apparently specific, is still improving upon his positive percentage
of 88-6. Out of 71 pronounced (ausgesprochenen) cases of
aortic syphilis Oberndorfer (loc. cit.) reported a positive
Wa.K. in 67. Collins and Sachs x tested 13 cases of aortic
valvular disease sole : in 10 the reaction was pronounced,
and in one more it was apparently positive ; these cases they
contrasted with an equal number of mitral disease only, in
which the reaction was positive but twice. Allen2 however
obtained a positive Wa.R. in some cases of mitral stenosis,
in which the fibrous circumference of the orifice proved to be
thickened by syphilis, so that we cannot confine our suspicions
to aortic disease ; in a few cases of mitral stenosis of obscure
origin the same infection may be at work. Indeed we should
bear in mind the possibility of an element of syphilis in cases
of heart disease apparently of other causation, for by a positive
Wa.R. we may be directed occasionally to find no little aid from
the addition of specific to other remedies.

Oberndorfer {loc. cit.) has suggested that a syphilitic spot
might give a starting-point to a verrucose or other septic
cardio-aortitis.

As regards sex, aortic syphilis occurs, according to the
records, more frequently in men than in women ; but this pro-
portion, being about three to one, probably depends on more
than one factor other than the intrinsically sexual. Allen
{loc. cit.), while reporting the heavy prevalence of syphilis
in Victoria, found there the proportion of this aortic lesion
in women relatively large. In 1906 he had 31 deaths from
aneurysm in women, as against 57 in men ; and he found
a similar unusual relation of aortic insufficiency in the two
sexes. Of 173 cases in Deneke's report {loc. cit.) of his pre-
vious four years, 148 were men, and only 24 women (the remain-
ing one was a congenital case). In one-half of Benary's 3 cases
the aortic disease was the only manifestation of syphilis ;
concomitant symptoms were most frequently the " para-
syphilitic.'' In one-third of them some tabi-paralytic symptom
was detected. There was valvular (aortic ?) lesion in one-half

1 Collins and Sachs, Amer. Journ. Med. Sci., Sept. 1909.

2 Allen, Intercol. Med. Journ. of Australia, March 1909.

3 Benary, a Kiel student, Diss. Kiel, 1912.

sec. i IN SYPHILIS 173

of them. A frequent symptom was angina pectoris. Stadler
reports a case of aortic syphilis in a widow whose husband was
syphilitic, and likewise had this aortic disease. When I read
this story it flashed upon my mind that I had seen the same
consequence. The husband was syphilitic, and both he and I
feared his wife had become infected ; she underwent a course of
specific treatment, and we hoped the matter, equivocal at worst,
was at an end. After her husband's death, when she was under
60, she came to me for angina minor with aortic dilatation ;
the angina slowly increased, and caused her death.

In respect of age the average falls between 35 and 50 ; much
earlier than atheroma. Like tuberculosis, the disease mars and
kills its victims in the prime of life. Benary, of 54 cases of
syphilitic aortitis, found the mean age to be 48*6 ; the mean
period after infection 22-9 years. The majority of these patients
die between the ages of 40 and 50 (Lippmann, Deneke, Stadler,
etc.) ; and no small number present symptoms between the
years of 30 and 40. Sir W. Osier, in his Schorstein Lecture,
reports two cases of patients aged about 21 ; and Lippmann (p.
181, note 5) a case of a young man, set. 20, who had been infected
very soon after (possibly before) birth. His father was syphilitic.
Benda 1 has described a case in a woman, set. 22, who died on
the third day of acute anginous symptoms : P.M. moderate
aortic insufficiency, and starting from the first portion of the aorta
a severe scarring (schwielenbildend) inflammatory process, with
dense thickening about the root of the aorta, suggestive of gumma ;
and of this nature under the microscope it proved to be. Benda
showed the sections with the lantern. (See also Case II. p. 375.)

Congenital cases of this disease, noted at such ages as 15
or 20, are not infrequent. Rebaud 2 reported an examination of
the aorta in 17 syphilitic foetuses and infants. In 13 he found
specific aortic disease, and in 5 of them the spirochseta. He
found most in one case, a severe one, in which the mischief had
extended to the intima. Marchand has reported a case in a
virgin, a subject of inherited syphilis, in whom aortic lues did

1 Benda, at a meeting of the Berlin Medical Society on Jan. 19, 1910 :
protocol in German journals about date ; also in AschofFs Lehrbuch, Bd. ii.

2 Rebaud, Munch. Monatsschr. f. Geburtsh. u. Gyn., July 1912 ; and Berl.
klin. Wochenschr., Aug. 5, 1912.

174 AOETITIS part n

not reveal itself until the age of 27 ; and Ziegler in another
case recorded a like protraction. In many cases of young
children dying of congenital syphilis some measure of this
peculiar affection may be found on scrutiny of the aorta
(Heller, Chiari). Klotz (loc. cit.) and others have dwelt fully on
this part of the subject (see also Vol. I. pp. 174 and 293).

As this aortic disease, before it descends upon the valve,
is often latent, we are deprived of many data and of many oppor-
tunities : for example, we cannot say how long an interval elapses,
or may elapse, between the primary infection and the aortic
lesion. Probably the interval is very variable, and the extremes
wide apart. Aortic disease has been recorded so early as eighteen
months after the primary infection, and so late as forty years
after it ; though in these belated examples the aortic mischief
had probably lain latent for years. A. Frankel x quotes a case
of " cardiovascular syphilis " two years after infection. To
illustrate this latency I might refer to many a necropsy on cases
of tabes and of general paralysis of the insane ; for in such cases
Hodgson's aorta, in its various degrees, is no uncommon trouvaille
d'autopsie.2 It is, as I have said, because of this latency of the
early stages that the period between primary infection and aortic
lesion is so difficult to calculate. Estimates vary widely because
the intervals vary widely. In two cases of Stadler's,3 only five
years elapsed between infection and the first symptoms of
aortitis. Brooks 4 relates two cases in which aortitis appeared
with early secondary symptoms (roseola, etc.). The speakers at
the Inner Medicine Congress at Berlin in 1914 agreed that the
intervals might vary from 2 to 5, 13, and 39 years. Frankel said
the aortitis might appear " very early," or be deferred 20-30
years. In a coloured picture of a section in Letulle's Path. Anat.
(1897), which shows subintimal as well as medial and adventitial
lesions, the age of the patient is not given, but the whole process
seems contemporaneous. In one of my cases the infection was

1 Frankel, A., Berl. Bin. Wochenschr., 1913, No. 17. See also Deutsche med.
Wochenschr., 1908, No. 12, and Munch, med. Wochenschr., 1908 and 1912.

2 So far as my notes go, the first pathologist to observe, but not at that
date to explain, the concurrence of aortitis with general paralysis was Bordes-
Pages, in a These de Paris of 1885, in my collection.

3 Stadler, Die Klin. d. syph. Aortenerk., Jena, 1912.

4 Brooks, Amer. Journ. Med. Sci., Oct. 1913.

sec. I IN SYPHILIS 175

at the age of 18 ; the aortic symptoms appeared about the age
of 41 or 42 ("set. 43 to 45," Deneke) ; death occurred at 51.
(See also case, p. 516.) At Milbank, of 44 cases in soldiers
15 were under 30 ; 36 under 40 (quoted by Osier). It
seems that intervals between twenty and thirty years are
not infrequent. Lippmann notes intervals of fifteen to twenty
years after infection ; Deneke a mean interval of twenty
years, with extremes of five and forty-four years. Osier quotes
a case in a man, set. 36, in which aneurysm of one coronary
artery appeared only eighteen months after the primary infec-
tion. Lubarsch, in 1911, reported two cases of specific cerebral
symptoms in which this arteritis occurred in seven and fifteen
months after infection respectively. Data of this order are
sought from the point of view of " tertiary " versus " para-
syphilitic " phases ; and to ascertain whether, if " parasyphilitis"
specific treatment be effectual. The frequent association of
aortitis with tabes and general paralysis does not by any
means necessarily pass on the lesion to a " parasyphilitic "
category, if such there be.

Occupation and other circumstantial determinants, if any.
are not known. By my own experience I should be led to say
with some decision that laborious or athletic pursuits are import-
ant determinants. Deneke and others do not regard alcohol
as an important determinant, and I agree with them. It so
happened that few, or none, of my many cases in private practice
were in sots ; two or three were in abstainers.

Two cardinal methods of diagnosis have opened out to ua
almost a new field of diagnosis in aortic disease, the X-rays
and the serum test ; devices by means of which we are extending
and confirming our data very largely indeed. As concerns the
lesion under discussion, they aid us to determine its seat, its
nature, and its extent ; great gains, if not all we could desire.

The seat of the mischief in the suprasigmoid area, in its first
stage a single cushion less than a sixpence, is a matter of the
gravest import, because it threatens precious limbs of the arterial
system — the aortic valve, and, at their orifices, the coronary arteries.
It is therefore of the utmost urgency to discover, or even to
surmise, the initiation of such an evil, which, " working on
in its still design," will wreck the frame on which it has made

176 AORTITIS part ii

its settlement. Of late years I have had the satisfaction of
believing that by prompt diagnosis, and prompt treatment,
I have been able to save from invasion the valve — which how-
ever may be distorted by a peri-cicatricial process, the cusps
being still of fairly normal quality — and probably, as results
have suggested, the coronary orifices also. For we shall see that
cases of syphilitic aortic regurgitation, perhaps crippled because of
this common association of closed coronary orifices and aorta,
do on the whole badly, very badly — far worse than rheumatic
cases of equal reflux ; although, as Grau points out, in rheumatism
the vascular signs are usually far more salient.1 In syphilis the
left ventricle is less reinforced, and the enormously dilated
aorta fails as a bellows. We know that atheroma rarely engages
with the aortic orifice in such a way as to cause regurgita-
tion ; Stadler indeed makes the surprising statement that for
nine years in his clinic (8000 patients a year) he had met with
no case of aortic regurgitation due to (non-syphilitic) atheroma ;
he infers that aortic regurgitation in the elderly, if not
rheumatic, will prove by the Wa.R. to be syphilitic. But to
regard every lesion in a Wa.R. positive patient as syphilitic is
surely rash assumption. Still it is true that the effect of atheroma
is rather towards stenosis ; of syphilis to a dilapidation of the
passage.2 Apart from the incident of aneurysm, or of angina,
syphilitic aortitis which has advanced to this point, which has
broken open the gateway, forced the gates, and blocked the
sources of supply, may bring life to an end within two or three
years, as in the case of the fine powerful young man under the
care of Dr. M'llwaine (p. 179) ; whereas aortic regurgitation
due to other causes, such as bygone rheumatism, may be con-
sistent with a long survival — even of twenty years or more.
Unhappily in the syphilitic case, so covert in its approaches, only
too often we are not consulted until regurgitation is established ;
too commonly indeed the sounds of regurgitation are among the
first signs to be noted ; the worst mischief is then virtually

1 See, for example, an interesting case published by A. Morison, Lancet,
Feb. 3, 1912 ; and a paper by Fortescue Fox, Lancet, July 8, 1911, p. 73.

2 In one or two cases of my own after a few (three or four ?) years the
regurgitant murmur ceased ; the systolic continuing alone. This alteration
I guessed might be due to a contraction of peri-aortic scar tissue ; but I had
no autopsy. The patients certainly seemed to be at some better advantage.

sec. I IN SYPHILIS 177

achieved. We cannot be sure whether or no in a particular
case the coronary arteries are blocked ; but on common
experience the forecast is gloomy enough.

If regurgitation do not ensue the prospect is brighter ;
but, as we have seen, the latency of aortic syphilis deprives
us of data for its average duration. The appearance of a
regurgitant murmur gives us indeed a starting-point, but for
dissolution, not for initiation ; aortitis is an advancing lesion,
but at what rate of advance, past or future, we cannot
compute. Deneke found that of his 178 cases, rheumatism
being carefully excluded, in 124 the syphilis invaded the valve ;
and of these in 46 both aortic regurgitation and aneurysm were
present together. Until regurgitation appears however we are not
obliged to give, or to apprehend, the gravest prognosis. Saathoff,1
it is true, found that in six out of seven cases this aortitis had
led to regurgitation, but Deneke's and SaathofFs figures, if
valid for cases in sailors and dwellers about a seaport, many
of them virulent and neglected, are too high for ordinary mixed
practice. We know that a considerable proportion of cases of
aneurysm do not extend to valvular insufficiency ; and, in and
out of hospital and my own consulting rooms, I recall case after
case of aortic syphilis arrested, by nature or art, before audible
impairment of the valve.2 In one case of Hodgson's dis-
ease, long under my own observation, one in which the aortic
valve never became incompetent, though for some ten years
signs of aortic dilatation, which for all this period were obvious,
slowly increased, life was prolonged until the age of fifty years,
and for much even of this period in health and activity.
Death was by agonising seizures of laryngeal spasm. This
patient travelled much about Europe, and in Egypt ; and it
was curious to find how few of the many eminent medical
men whom, here and there, at home and abroad, he consulted,
recognised the true nature of the case. Scarcely any of them

x Saathoff, Munch, med. Wochenschr., 1906 and 1910.

2 Gruber found aneurysm in about 20 to 25 per cent of aortic syphilis,
and computed that, of the cases of aneurysm of the thoracic aorta, aortic regur-
gitation appeared sooner or later in about one-third. These proportions for
my experience seem both of them high. By the way — to digress to the
visceral arteries, such as the splenic or mesenteric — we may find in them
every stage of the formation of saccular aneurysm, from incipient slight
ulceration to deeper penetration and formation of sac with clean edges.

178 AOETITIS part ii

then seemed to be familiar with the Hodgson-Welch aorta, a
state which ultimately was fully demonstrated by necropsy. In
this case an eminent person, eminent in surgery rather than in
medicine, was saved only by chance from operating for innominate
aneurysm ! So long then as the aortic valve is competent, we
are justified in hoping for a conservation of fife for some years ;
and perhaps, by active treatment, for an arrest, or staving off,
of the affection. I cannot therefore agree with the reckoning of
a recent distinguished author that after aortic syphilis is estab-
lished, the mean duration of life is only one and three quarter
years. Unless the numbers are very large, a few swift cases
may bring down the mean to a very low figure. Such means,
without statement of extremes, are worse than useless.

When, if at all, the coronary orifices become involved we
cannot tell. But I have said that in the cases of syphilitic
aortic disease with regurgitation the prognosis is unfavourable.
Grau 1 and Stadler 2 also have rightly laid great emphasis upon
the default in this lesion of a due and stable hypertrophy of
the left ventricle ; Grau goes so far as to say boldly that if
the compensation be good the case is not lues. This maxim
corresponds with my own experience, though in a syphilitic case
now under my care a fair compensation has been attained. In
such cases the coronary arteries may have escaped ; as, on
the other hand, they are often blocked without valvular in-
competence. In regurgitation from other causes, the heart, as
we all familiarly know, grows vigorously up to its work, and, if
the reflux be not intolerably copious, will for many a year keep
up no very inadequate balance of function ; but in syphihtic
disease, as a rule, the insufficiency is not met in this definite
and energetic way. These far from uncommon cases do badly.
Although after death the parts may not indicate a large
regurgitation the heart does not rise to the occasion, or does so
imperfectly. I recollect one case in which after death the rift
proved to be quite a small one, yet the patient had succumbed
within two or three years. It may well be that in these
many cases of quicker dilapidation, as in this one, the

1 Grau, " Luetische Aortenerkrankungen," Zeitschr. f. klin. Med. Bd. Ixxii.,
1910.

2 Stadler, Die Klinik d. syphilitischen Aortenerkrankung, a valuable mono-
graph, based upon 200 cases and 150 necropsies. Jena, 1912.

sec. i IN SYPHILIS 179

coronary orifices were occluded ; I have not myself made an
adequate comparison, but the surmise seems reasonable. As
with other side vessels, the process rarely extends far on the
coronary arteries ; and if one only be blocked, myocardial
function is still maintained by anastomosis (e.g. p. 267). In
another part of this book (p. 361) I have proved, it is true,
how wonderfully a heart may hold its own even with blocked
coronaries, but under other conditions : in these cases — cases of
atheroma — no cardiac hypertrophy may be required, and probably
their mouths are closed very gradually ; moreover these changes
befall persons of an age when life and its avocations are con-
fined within a narrower and narrower circle. If in the syphilitic
cases the orifices be blocked, the myocardium will present
evidences of grave degeneration, although within the muscle
the coronary branches may be normal throughout their course.
The following case from my own notes, in which the coronary
arteries were probably blocked, may be cited here :

Male patient of about 35, seen with Dr. M'llwaine, then of
Redhill, who recognised the nature of the case, and watched it closely
throughout. Syphilitic aortitis was plain enough to the instructed
observer. Soon the valve began to suffer, and at first with a re-
markable intermittency of regurgitation, as if it depended more on
relaxation of the orifice than on destruction in the cusps. The reflux
murmur, as we both observed, went and came until seven or eight
months before his death, when it became persistent. Before this
period he improved substantially on antiluetic treatment (mercury,
etc.), was able to fish and shoot a little, and to play a quiet game of
golf. Then dyspnea set in, his legs grew puffy, and a systolic murmur
became audible at the apex also. In spite of all this he decided to
sail, with a medical attendant, for warmer seas, and on shipboard
to take complete rest. The result was better than we expected,
for with this rest and change of air, combined with digitalis and
other appropriate means, the mitral murmur vanished, and other
symptoms cleared up. But a faint aortic diastolic murmur still
persisted. He improved but for a short time ; ere long the mitral
murmur reappeared, and with it other signs and symptoms of heart
failure, not this time to be dispelled.1 (See case, p. 529.)

In the Hodgson -Welch aorta, however bulging, as in

1 I have not thought it necessary to insert other cases, although I am
somewhat rich in notes of them. They differ only in degree, and I have blended
their characters in the text.

180 AORTITIS paet ii

aneurysm, the heart is not called upon for overgrowth ; for in
neither case ordinarily, as we all agree, are the arterial pressures
raised. Stadler says that in Hodgson's disease, as in aneurysm,
if there be no valvular nor renal complication — which often of
course there is — their range is usually normal throughout. He
has found no reason to assent to the alleged great frequency of
renal disease in these cases ; x he agrees however, as from the
state of the aorta we should expect, that the pulse amplitude
is enlarged, the systolic pressure being relatively high and the
diastolic low (40-70 mm.).

In syphilitic regurgitation it may be asked if this lack of
adequate response on the part of the left ventricle may not be
due to the co-operation of a gummous lesion in the heart itself,
below the valve ? Now it is a curious result, but so it is, that
syphilis of the heart and aorta, a combination which one might
expect to be frequent, is really somewhat infrequent. The
heart substance is attacked, or the aorta is attacked, but
it does not often happen that both are invaded together.
Thus also, as we have seen (Vol. I. p. 294), the aorta may be
gravely infected while the peripheral arteries remain intact. Of
course there are many examples to the contrary ; especially in
those cases in which the infection is otherwise widespread, as
in the case I have quoted from Benda, of a woman in the
Moabit Hospital, aged only 22, which, besides a syphilitic aorta,
and much syphilis elsewhere (including, if I remember right,
the portal vein, a vessel sometimes similarly attacked both in
acquired and in congenital cases), presented also some syphil-
itic disease of the myocardium. Dr. Lauriston Shaw (Lancet,
Sept. 23, 1900), at the necropsy of a man, set. 26, who died
suddenly during apparent health, but with a history of both
strain and syphilis, found the aorta beset with " atheromatous "
patches, and an aneurysm on the right of the root of the aorta,
over the right ventricle. There was a gumma in the heart near
the apex, and a small one in the pancreas ; in all other respects
the heart and the rest of the body were healthy.

The portal vein lesions hitherto described seem to have
been rather of the intimal type ; more like atheroma with

1 Leube, Rose Bradford, and others. See chapter on Renal Disease and
Arteriosclerosis, Vol. I. p. 367.

sec. I WITH TABES AND GENERAL PAEALYSIS 181

break-up of the elastica and degenerated media ; thence follow
thrombosis and the consecutive visceral evils. The records of
Pick, and many other pathologists, contain cases of this com-
bination, though often the clinical notes are not given. But the
irregularities of distribution are endless. I remember a terrible
case of virulent syphilis, ravaging, among other parts, the
larynx, but the heart and vessels, to the best of our opinion,
were intact, and the patient made a complete recovery.

The association of this disease of the aorta with tabes was first
pointed out, I think, by Berger and Rosenbach.1 But I have
noted how frequently in aortic syphilis this lesion exists alone ;
often indeed without any accessible stigma — unless it be by
the Wa.R. test — of the parent infection. My own impression
is that the association is more common in tabes than in general
paralysis, but it may well be because I have seen more of tabes ;
palsy cases disappear into asylums, while the tabetic remain
in our general hospitals, and come to necropsy there. I find, on
comparing many published records (Chiari, Straub,2 and others),
that in tabes it may be no exaggeration to compute that some
degree of syphilitic aortitis, if duly searched for, may be found
in 40 per cent ; possibly in more. And we may surmise that
the proportion in general paralysis may be no less. Conversely,
Goldscheider,3 in 136 cases of syphilitic aorta, detected 29
of tabes ; but the symptoms were often slight, and easy to be
overlooked. Deneke 4 reported that of 173 patients with
syphilitic aortitis 40 per cent had tabes, and in one-tenth of
the rest it was suspected. By the Wa.R. 87 per cent were
positive ; 6 were dubious, and 16 negative, but of these 13
were under active specific treatment ; moreover as the staff
became more expert in the method the negative instances
were becoming fewer and fewer. In all cases of luetic aortitis, as
a matter of routine, the pupils and knee-jerks should be tested.5

1 Berger u. Rosenbach, Berlin. Iclin. Wochenschr., 1879.

2 Straub, Verhandl. d. deutsch. path. Ges., 1899.

3 Goldscheider, Wien. med. Klinilc, No. 12, 1912; quoted Epit. Brit. Med.
Journ., Aug. 10, 1912.

4 Deneke, at a meeting of the Medical Association of Hamburg in 1912 ;
quoted in the German journals about that date. See also p. 167.

5 See also Lippmann, a worker on this subject, Aortenlues, Festschr d.
allg. K'haus, Hamburg, St. Georg, 1912 ; quoted Zentralbl. f. Herz- u. Gef.-
Kranktn., Nov. 1912.

182 AOKTITIS part n

The number of these patients who admitted infection, or indeed
seemed to be aware of it, were a small fraction.

Deneke says that the death-rate of the syphilised is 68 per
cent above the normal level of insurance computation ; well may
he denounce the sequels of syphilitic infection as " ungeheure ! "
Of 83 deaths from syphilis in the Hamburg Hospital during
1909-11, 54 were due to aortitis ; the rest to other specific
lesions.

To turn now to the morbid histology of the process : we are
prepared to accept syphilis of the aorta as a peculiar lesion,
a lesion which has an origin, characters, and issues different
from those of other affections of the aorta : different from atheroma,
with which however in elderly cases it is often mingled ; and differ-
ent, though less different, from other infections of the vessel.
In histological mode the rheumatic aortitis is not unlike it, and
like it is often associated with regurgitative lesion.

We have seen that the seat of syphilis in the aorta is
curiously definite; that ordinarily, like the rheumatic poison,
but with even more constancy, it fastens upon the vessel near
to, but a little above, the semilunar valve ; or about the
mark of the ductus botalli. Welch pointed out this proclivity,
and the tendency thence to spread upwards along the trans-
verse arch, and downwards to the valve. The lower margin is
but too prone to creep to the mouths of the coronary arteries
(p. 265). Often the disease occupies the descending thoracic
portion also, and rarely may reach as far as the forks of the
gastric and renal arteries ; usually it terminates, with a
sharp limit, at the diaphragm. In some cases the innominate
is involved, but, save that occasionally it blocks their
mouths, the disease does not spread far into the side vessels.
In Jores' Case VII.1 the thoracic lesion, though characteristic,
extended to the descending aorta and cceliac axis (vide et
p. 309).

With other infections the syphilitic has these characters in
common, that it seems to invade the vessel by way of its
vasa vasorum, and to be, as Heller 2 and Chiari showed, an
inflammation ; that is, an irritative lesion with reparative

1 Jores on p. 382 of the Virchoio's Arch., 1904, paper. See also Case VIII.
2 Heller, A., Munch, med. Wochenschr. No. 50, 1899.

sec. I SYPHILITIC LESION 183

reaction ; as contrasted with the degradation of atheroma, which
is not directly due to a specific infection. A cellular hyperplasia,
with the exudation of a hyaline substance, follows the courses
of these vessels, many of which become occluded. Thus by the
vasa vasorum lues is instilled into the aortic wall ; but accord-
ingly its chief activity lies at first more in the adventitia,
where this network is abundant, and between this coat and
the media. The adventitia may become thickened by several
millimetres. The media, as in the rheumatic kind, soon follows,
and with perilous consequences ; but the intima, rarely the
seat of a primary lesion, suffers last, though it is practically
always thickened by fibrosis, and often exhibits a patchy pro-
liferation of the subendothelial tissue. About the vasa vasorum
and the adventitia the proliferative features resemble those
which Dr. Mott produced by painting the outside of a vessel with
an irritant solution, or those of vessels involved in contiguous
inflammations, or again of certain experimental infections with
bacteria. In an early phase then the vasa vasorum are the active
seat of cell proliferation ; like active changes become patent in the
outer media, and, directly or obliquely, pass more deeply into this
coat, so weakening it that it becomes less and less able to with-
stand ordinary blood pressures. Some observers, Molinari x for
example, believe that the outer elastica suffers early ;
in the first instance its injury may be due to the buckling of
the wall. These changes in the adventitia are often coarse, and
may not bear upon the face of them any syphilitic stigma,
unless here and there they form masses which may be called
gumma (Benda). About such fresh foci, in the external media and
adjacent layers, the specific spirochaeta has occasionally been
found (Reuter,2 Benda, Schmorl and others), on the whole perhaps
not infrequently ; so that the question whether this aortitis
be " parasyphilitis" and the exudative elements non-specific,
has fallen to the ground. Gruber quotes Vanzetti 3 as having
produced a characteristic aortitis in animals by direct infection
with the spirochaeta.

1 Molinari, G. (of Breslau), Schwielige Arteriosklerose u, Syphilis, Leipzig,
1904. A Dissertation for Doctorate.

2 Reuter, Zeitschr. /. Infektionskhtn. Bd. liv.

3 Vanzetti, Arch. p. le sc. med. 35, No. 24.

184 AOETITIS pakt n

My own impression is that definite gumma, such as we find in
heart or liver, is in the syphilitic aorta rare (Vol. I. p. 300). This
name can scarcely be given to the cushions on the internal aspect,
characteristic and salient as they are, unless it be on the ground
of healing by scar. Kraus would make two classes, of gummous
and diffuse aortitis ; but the difference is superficial ; " gumma "
is itself not histologically peculiar, but a concentrated focus of
proliferating fixed cells and wandering cells. Whether called
gumma or not, the phase may be ranged in the direct line of
infection. In case of doubt, all other parts — eyes, skin,
testicles, etc. — will be scrutinised for specific inscriptions. One
small circular scar on leg or arm, with sharp walls and white
and silky floor, may suffice to clinch the diagnosis 1 (see p. 210).

The aortic bulges, infiltrated and thickened as they are,
probably owe much of their outward protrusion to the yielding
of the media ; though a diffuse toxic necrosis of the muscular
and other structures, plain enough in sections of the media, is
of course not peculiar to lues ; it is well marked also in the
rheumatic kind. In the adventitia these collections of plasma and
lymphoid cells, around the vasa vasorum or radiating from them,
are often disposed to an annular distribution, as we see in the
larger cushions visible to the eye. It is said (Fukushi 2) that
new growths of elastic, as well as of connective (kollagene)
fibre, may be seen in the adventitia. But of course in the
necrotic portions the elastic fibres suffer early, lose stain, and
break up ; a perishing which may be secondary to that of
the muscular coat. Fukushi thinks that the plasma cells and
lymphocytes are so abundant as to give a specific character to
the exudation ; but I agree with Klotz 3 that similar phases
may be seen in rheumatic and other kinds of aortitis.

In the media we see lesion both spreading inwards from the
adventitia and established also in separate foci ; nests of plasma
cells attached, as it were, to the finest inward twigs of a vas
vasis. These vessels, after the first congestive and proliferative
phase, silt up, and thus entail the atrophic phenomena which
ensue upon the inflammatory ; and this more and more as time

1 See Appendix, p. 210.

2 Fukushi (of the Berlin University), Virchow's Arch. Bd. ccxi., 1913.

3 Klotz, 0., " Rheumatic Arterial Lesions," Joum. Path, and Bad. vol.
xviii. No. 2, Oct. 1913.

sec. I SYPHILITIC LESION 185

goes on. There are nevertheless, as we shall see, large areas of
healing by scar. Between these foci of active mischief may be
seen, both microscopically and by the naked eye, areas of quite
normal structure ; although, as the process extends, these normal
areas gradually merge in the universal degradation. This
" mesaortitis productiva " x is very severe in the neighbourhood
of an aneurysm. The miliary foci in the media, sometimes
called, as we have seen, a little figuratively, " miliary gumma,"
may be, indeed usually are, intensive and extensive ; so that
(passing by saccular aneurysm, with which I am not concerned)
the media buckles outwards more or less, here and there, accord-
ing to the inequalities of the distribution of the disease ; but
(aneurysm apart) these bulges are usually basin-shaped and
contain no clot, or but a pellicle. Sections of the wall show all
these processes very clearly, as in two specimens kindly sent to
us by Dr. James Mackenzie, and prepared, mounted, and drawn
in colour under Professor Woodhead's supervision.

The intima, in contrast with atherosclerosis, if not intact,
is ordinarily, besides any injury by dislocation, not much the
worse, sometimes possibly a little the better ; for it may be
thickened, even rather densely thickened, so as to line the cavity
of a hollow, or part of the cavity even of a saccular aneurysm ;
a fibrotic thickening which may have some protective value. But
occasionally, as in certain specimens which Professor Teacher
showed me recently at Glasgow, the intima may itself also become
the seat of proliferative foci quite detached from those in the
media (Vol. I. pp. 302 and 479) ; and about the intima there may
be a good deal of diffused proliferative activity of the simpler kind.

In the later phases of the luetic process, so long as atheroma
does not supervene, appears, as in inflammatory lesions, a
strong tendency to scarring, to a kind of repair by fibrosis,2
as contrasted with the fatty and calcareous perishing of athero-
sclerosis. From the adventitia inwards, and also in the media
and subintima, so widespread a fibrosis goes forward that while
at one or more spots active granulomatous change, if such it
be, is still in progress, at older spots scars are forming, with

1 This name, given by Chiari, fails to connote primary attacks on the
adventitia.

2 See Wiesner, Centralbl. f. allg. Path. u. path. Anat., Jena, 1905 ; Klotz,
0., Journ. Path, and Bact., Oct. 1907, and some ephemeral papers of my own.

186 AOETITIS paet n

puckerings, pits, and pouches ; some parts scooped out even
to translucency ; various stages of disease which give to the
Hodgson- Welch aorta its characteristic aspect. Benda says
that some of the smaller patches may form scar and heal
without deformity. It is true that in a small way scar may
appear in atherosclerosis also, but quite subordinately, not
characteristically. Indeed apart from acute infections scar is
rarely discovered.

The process of extension to the aortic valve has been minutely
examined by Dr. Sidney Martin.1 The vessels in the valve seg-
ments begin to thicken ; in the cusps, and beneath them, a general
periarteritis is set up after the fashion peculiar to syphilis. Thus
the valvular membranes themselves thicken, scar, and pucker.
The same process may be seen in the sinuses, so that here again
the machine may be much deformed ; but, if taken early, the
mischief may perhaps by specific treatment be dispersed. I may
add that, more commonly in syphilis than in atherosclerosis,
the attachment of a cusp to the wall breaks away, throwing
two limbs of the valve together.

The pulmonary artery may be attacked in like manner, but
is far less liable to the disease than the aorta ; usually it escapes,
but not always.2

I repeat that these changes and their seat give to the
Hodgson- Welch aorta within and without a peculiar aspect,3
which, in cases under middle life and uncomplicated with athero-
sclerosis, cannot be mistaken. At Leipzig, in 1912, Professor
Marchand spread out before me ten of these aortas, so recent that
they had not yet been put up in their jars. About no one of these,
to the practised eye, could there have been the slightest doubt.
Specimens may be found in almost any good museum. The arch
lies before the observer widely dilated, distorted, thickened, pitted,
pouched, puckered and scarred out of all recognition ; indeed I
have known such a specimen taken at first sight for an ulcerated
colon. In parts, as I have said, the wasted and cicatrised
wall may become so thin and pouched as to be translucent.

In the earlier stages of the aortic infection the vessel is not

1 Martin, S., Clin. Journ., June 20, 1907.

2 See Barth, H., Frankf. Z. f. Path., 1910.

3 See illustration (coloured) in Balfour's Dis. of the Heart, 3rd edition.

sec. i SYPHILITIC LESION 187

so much dilated and deformed ; if viewed from without, perhaps
scarcely at all. It is on the inner face that the more or less
annular, raised, cushion-like tumidity may be seen, lying afinger's-
breadth, or a little less or more, above the valve. It is in my
experience pink, at any rate at first, and except for its saliency,
and a certain succulence or translucency, scarcely visible above
the surrounding mucous membrane. But on the surface of the
syphilitic cushion a rough granular appearance may be perceived
(p. 262), and, when recent, its boundaries are fairly sharp. The
parts from a case of incipient aortitis which Dr. Parkes Weber
brought to my lecture on Angina Pectoris at Fitzroy Square in 1908
had these characters (p. 264). Such also was the form of Brault's
case (quoted by Letulle) already referred to. In other and
probably riper cases the wheal is said to be yellow, or yellowish
white, but to differ in form and colour from the more opaque
atheroma. Tripier * regards all gelatiniform patches, whether
associated with atheroma or not, as syphilitic. I am disposed to
say that, in translucent greyish or even pinkish tint, influenzal
or rheumatic patches, or even the acuter extensions of atheroma,
may have a like aspect. The criterion is the lack of fatty
and calcareous change, so long, that is, as atheroma may
not have supervened, a mosaic often to be seen in later stages
and later years. Besides these larger cushions, smaller ones
also, like peas or seeds, may be noted here and there upon
an otherwise normal inner surface ; these are apt to join
together so as to form the padded ring I have described. As
I shall point out in the essay on Angina Pectoris, it is of great
importance in early cases to inspect the vessel carefully from the
outside, as the adventitia and the periadventitial lymph-glands
may be thickened and dense with infiltration, but at a glance
show little that is morbid. Yet in a square centimetre, or less,
of this fibrous sheath may lie the long agony of angina pectoris.
Now how in life are we to detect this insidious but deadly
evil in time to arrest it before these vital parts, especially the
mouth and valve of the aorta, are destroyed ? If a patient is
known to be syphilitic, a close watch over this among other
vulnerable parts may enable us to infer its presence, and to scotch
it before too much harm is done ; the supreme difficulty is with

1 Tripier, Etudes anat. din., Paris, 1909.
VOL. II N

188 AOETITIS part n

persons not recognised as syphilitic, and in whom no character-
istic sign or symptom had arisen until the lesion of the aorta
had made some considerable way. Now that the spirochseta is
found in tabes and general paralysis the parasyphilitic distinction
will probably vanish ; the question will be whether or no the
specific remedies can be directed to the part diseased. That the
spirochseta is not readily found in aortitis, and not yet in the
media, is no great matter ; it is likewise scarce in periosteal
gumma. We have seen indeed that it is not easy to pronounce
upon the form of these hyperplastic deposits, as definitely
granuloma ; they may present no such criterion of specific
origin, but they are quite consistent with " tertiary " syphilitic
outbreaks elsewhere. My own opinion and experience tell
me that these aortic outbreaks are "tertiary," and in their
degrees amenable to specific medication, whether by mercury
or salvarsan. They are not, I think, very amenable to the
iodides ; more than once after large and long and ineffectual
dosing with these salts in vain, I have seen the symptoms and
signs of aortic lues recede during a subsequent course of mercurial
inunction. There is room for hope then that, if we can but detect
the disease early, we may arrest it before it does its worst.

That in some cases of aortitis we have to deal with mixed
infections is not improbable ; but on this point we have little
definite information.

Of acute aortitis as a result of lead or other mineral or
vegetable poisons, I have but scanty notes ; but I may state,
not from my own experience only, that in some plumbic cases
aortic disease may appear without renal disease. Dr. Seymour
Taylor x has published a case of plumbism with anginous
symptoms, followed by those of ruptured aortic valve.

On muscular stress as a cause of aortitis in a vessel
otherwise sound, I have little to add to what I have written
under Atherosclerosis (Vol. I. p. 205). That such stresses co-
operate with more insidious causes of aortitis — acute or chronic —
I have said already. The far greater prevalence of the Hodgson-
Welch aorta in men suggests some co-operation of bodily labour.2

1 Taylor, S., Lancet, Feb. 22, 1908.

2 See e.g. Grassmann, Munch, vied. Wochenschr., 1907 ; and Hesse, Arch. f.
Iclin. Med Bd. lxxxix., 1907.

sec. i EFFECT OF MUSCULAK EFFOET 189

I recall one case only in which mechanical stress seemed to have
originated a definite aortitis ; and in this case the strain may
have co-operated with some unrecognised infection. Later
enquiries indeed suggested a rheumatic history. The patient
was a young housemaid who, on lifting a bedstead, a weight
beyond her strength, felt a sudden severe pain and distress in
the chest, which persisted in great severity. She came several
times into the Addenbrooke's Hospital, when Dr. Lloyd Jones
called my attention to the case ; and she was once or twice
in St. Thomas's, when Dr. Hawkins kindly sent me news of
her. The signs and symptoms were those of acute aortitis, sub-
sequently becoming chronic and invading the aortic area so far
as to cause stenosis. Her crippled state, and the angina pectoris
which continually beset her, preyed upon her spirits, and after a
while engendered, not unnaturally, a fretful and wayward dis-
position, so that she was accused of hysteria and of mock
angina ; but on the main facts of the organic lesion we were all
agreed. The angina was typical and very severe. After long
suffering this young woman quite recovered her health ; but a
harsh systolic aortic murmur and a thrill, at the base, present
throughout the illness, still bear their permanent witness.

Of other agents in the causation of chronic aortitis, I may
touch so far again upon gout (Vol. I. p. 275) as to say that chemical
research fails to discover urate of soda in the aorta of gouty
bodies ; and that experimental injections of uric acid have no
effect upon the vessel : therefore the attribution of the disease
to silting up of the vasa vasis by uratic crystals is likely to
share the fate of many another ingenious guess.

On the experimental side of the subject definite results
are difficult to attain ; experiment on the generation of aortitis
by bacterial agency is obviously intricate, and in its results
equivocal. Nevertheless, some instructive work has been done.
Gilbert and Lion's successful experiments in 1888 in producing an
infective aortitis by injections of bacteria and their toxins are well
known (Vol. I. p. 285). The pneumococcus, the B. coli, Eberth's
bacillus, and pyogenic organisms, have been inoculated upon the
aorta in animals with no inconsiderable success ; a success now
sufficient to indicate to us that such microbes are capable of
engendering acute aortitis, if circumstances be favourable to

190 AOETITIS part ii

their implantation. See Jordan's case (p. 161). The case
of the horse poisoned by diphtheritic toxin (p. 164) seems to
prove, moreover, that in the absence of the microbe itself toxins
of bacterial origin may suffice to produce this inflammation. I
have already suggested that it may be more easy for toxins than
for bacteria to fasten upon a large artery.

As we pass from the acuter to more chronic modes of
aortitis we are still beset by the obscurity and incertitude which
cast their shadow over this clinical field. Thus, disease of
the ascending aorta, as distinguished from diffuse atheroma
or arteriosclerosis, receives less attention than its due ;
it may occur alone, or nearly alone, and, if its symptoms
be often ambiguous or equivocal, it is quite capable of
compassing the patient's death ; so that we shall do well to
suspect it, and to interrogate the signs of it more warily. On
two recent occasions I ventured, and ventured as it proved with
justice, to persist in a diagnosis of lesion of the ascending
aorta against the judgment of colleagues who did not so
much deny it as ignore it. Chronic disease of the ascending
aorta, without aneurysm, is far more common in middle life,
in early adult life, and even in youthful life, than we are wont
to realise, and is for the most part insidious. On the signs
and symptoms by which it is to be known I have said much
and shall say more in the essay on Angina Pectoris. When the
patches are small and few, the evidence, if any, may be wholly
indirect. Let me repeat that the name atheroma is conveni-
ently restricted to the decaying — the necrotic — phases, which
may so appear from the beginning, or may follow inflammatory
processes as indicated by the name aortitis. When inflamma-
tion or, in the particular case, repair, is predominant, we speak
of the process as aortitis ; when intimal degeneration pre-
vails we speak of it as atheroma. But in the course of chronic
aortitis and atheroma — as in the course perhaps of all chronic
maladies — tides of acute activity may, and often do, take
place ; and the uniform course of the patient's symptoms may
be disturbed by vacillations and exacerbations. Thus it is that
symptoms of angina pectoris may manifest themselves in
patients in whom the physician had recognised no more than a
gradual and less dreadful mode of decline.

sec. I EFFECT OF HIGH PKESSUBES 191

In high blood pressure with or without renal disease

we are all agreed that the higher the pressures the more the
arch of the aorta will suffer ; and that, because it bears
the first and chief brunt of the cardiac systole, the first
portion of the ascending limb of the arch, is the first
and chief seat of atheroma. The surprising thing is that
the effects are not sooner manifest (Vol. I. p. 190). Earlier
or later however, in every case of static hypertrophy of the
heart, the aortic tissue deteriorates. The vessel suffers from
the impact geometrically more and more as the blood pressure
rises, and the vessel with age loses its resilience. As we
have seen, in the chapter on Physics, if resilience fails, normal
and indeed subnormal blood pressures become relatively
excessive ; expansion becomes thumping, the machine is self-
strained, and, as this and that part of the vessel yield un-
equally, stresses become unequal. We have seen that as a pipe
becomes rigid, its movement is more abrupt ; especially at a
bend, such as the aortic arch, which at each beat is ham-
mered tangentially forward as a whole. Dilatation, in such a
state of the vessel, may possibly bring with it some slight com-
pensation in a reduction of velocity. Yet, how damaging the
heavy pulses often are, we may read in the immunity of the arch
when it is protected by aortic stenosis of the so-called pure kind
— the kind in which a big heart and a straitened aortic ring exist
without notable disease above the ring ; in these cases, as in two
of my own, the aorta, although in old age, may present little or no
sign of decay. Where, on the contrary, as in Hodgson's disease,
the heart is unimpaired, the aortic orifice open, and the vessel
itself softened, we see degradation and deformation carried to the
extreme verge of survival.

Symptoms and Diagnosis. — As the syphilitic is by far the
most common and the most grievous of the kinds of aortitis it is
more convenient and concise to begin with a description of the
symptoms of aortitis as observed in this kind. Thus we shall
best learn the clinical phases of aortitis and, by no difficult com-
parison and inference, the behaviour of the other kinds. We have
seen that, heavy as is the incidence of aortic syphilis, in not a few
cases — after the manner of the disease — the aortic outbreak

192 AOKTITIS part n

stands either alone in the arterial tree (Heller and Dohle, and
others) or with arterial disease in inaccessible parts only, as in
the heart or brain. Soft peripheral arteries are no warrant
against disease in the aorta or heart. Gruber says that "general
arteriosclerosis " comes on in the later stages of the disease ;
but we have seen that this result is not invariable, nor even
general (Vol. I. p. 295). We know too well in how many cases of
syphilitic disease the primary infection is unknown, and the
patient himself taken wholly by surprise. But, as in tabes so in
syphilis of the aorta, it seems needful to reiterate that, in cases of
which the specific origin is beyond doubt, the absence of a his-
tory of infection is a common experience, and should cause
no surprise to the physician. Here the serum reaction is in-
valuable, though of course a positive Wa.B,. does not prove
every associated affection to be luetic. A man aware of
a past infection should be wise enough to submit himself to a
thorough examination at intervals during the rest of his lif e, or
at any rate up to fifty years of age ; especially on the occurrence
of any sort of symptom of ill-health or frailty. In a subject
of tabes or general paralysis aortitis may almost be anticipated.

Of symptomatic fever it is hard to find definite and specific
records. Moreover this symptom may be merged in the fever
of a parent disease. Still, as in Dr. Windsor's case (p. 157),
the febrile curves, though not of large excursion, may be
distinct enough. Popoff x is quite clear that aortitis, like en-
docarditis, has its fever — various perhaps as its specific cause.
He has noted it, as I have done, in the syphilitic kind.

That pain, and pain having peculiar and even alarming
features, arises in disease of the aortic area — that is, of the first
portion of the ascending aorta and perhaps of the aortic orifice —
is in a sense well known ; in another sense it is ignored
or misconceived. Such is the tenacity of opinion, such are
the fetters of fixed doctrine upon plain thinking, that, as I
shall say in the essay on Angina, in the examination of cases
of angina pectoris our eyes have been too exclusively fixed upon
the coronary arteries ; the orifices and the tunics of these vessels
are scanned for atheroma, and if atheroma be found — in chronic
disease of this area they hardly escape some measure of it — the

1 Popoff, Zeitschr.f. klin. Med. Bd. lxxv., 1912.

sec. I SYMPTOMS 193

pain is held to be explained, and no fresh thought is given to the
matter. Yet the truth is that this pain, which in greater or less
degree is a predominant feature in disease of this area, is due,
nearly always neither to coronary artery nor to heart, but to
disease of the aorta, with which coronary atheroma is commonly
associated. Now it is true that a superficial internal aortitis
of the arch, even when acute, is unattended with pain, or, if
some pain be complained of, it receives little attention ; in the
aortitis of the infections pain is frequently, in some of them
generally, absent. In the aortitis of smallpox, or of typhoid
fever, we detect the evil less by pain than by physical signs, by
later consequences, or after death. In the aortitis of influenza,
or of rheumatism, pain arises in a minority of cases ; in syphilis
it may be more frequent. In atheroma of this area the
cases of pain are a small minority. There is no direct relation
then between severity of pain and the cause, the acuteness,
or the superficial range of aortitis, or atheroma ; the intensity of
the pain in certain cases is explicable, as I shall suggest, by the
depth of its penetration or thrust towards the outer invest-
ments of the vessel. In certain circumstances it is admitted
that, whatsoever pain at the heart may be, pain having peculiar
and even appalling features may arise in disease of the
aorta, especially of the suprasigmoid portion which seems
more obnoxious to infective attacks. Its characters are :
origin under the sternum, often at the junction of the first and
second thirds of the bone, and sense of constriction or compression,
as if the chest were in a vice, or the breast-bone crushed inwards
by an iron bar. And this pain may come in any degree, from
a transient sense of tightness or oppression about the upper
sternum, to utter torture. A third feature is a tendency to radiate
from the mid-sternal origin into sections of the brachial plexus,
in the first instance, of the left side, but occasionally of the right
also — rarely of the right alone. The zones of this aortic pain
may be divided into the primitive zone, and the forced zones :
the primitive zone being that of simple reference, the forced
areas those of compound reference ; these are invaded success-
ively as the irritation, or the instability of the corresponding
spinal and other segments, increases. As in a child a cutting
tooth may have a primitive area of pain in the parts about it,

194 AOETITIS part n

and thence may force sphere after sphere of inhibition, to
vomiting and even to general convulsions, so a corrosive
lesion at the first part of the aorta may cause a constricting pain
under the sternum only, or, forcing successive spheres of inhibition,
may drive to the shoulder, to the inner condyle of the humerus,
to the ring and little finger, to the neck, and so on. The pain of a
diseased aorta— angina pectoris in fact— having invaded the outer
and inner bailey, may force the very keep of life, and arrest
the heart in fatal syncope. Herein, as we shall see, lies the
peril of aortic pain to him whose heart is frail ; to him,
let us say, whose coronary arteries are occluded, or — which
by the way is far from being an equal consequence — whose
cardiac muscle is in decay. To one thus unstable at the centre
angina pectoris may be a mortal agony ; to one whose heart is
sound and perfect, or relatively sound and perfect, the agony,
if no less intense, is rarely mortal. In such cases the heart
may not quail, and the sense and apprehension of death, if
present at all, are less terrible, or indeed absent. Yet notwith-
standing, in acute aortitis, as in other agonising visceral pains,
even a sound heart may be arrested in death.

When a chronic aortitis, pursuing for the greater part a
painless course, is broken by terms of acuter activity, its own
pain may come and go with such vicissitudes ; as I shall show
in the essay on Angina (p. 426). I have seen many such cases
of intercurrent aortic pain, in acuter phases of chronic disease,
which departed for good. In acute aortitis its departure is
perhaps the rule, on condition that the heart is not degenerate.
Stadler's admission {he. cit.) that incessant anginous attacks
may be aortic, but periodical attacks coronary, cannot withstand
a moment's consideration, the difference is but one of degree ;
in the same patient we may find all degrees, from slight " steno-
cardia" to the "status anginosus." I suggest that this symptom-
atic climax depends directly not upon the acuteness of an aortitis
but, as I shall explain more fully under Angina Pectoris, upon
its penetration, on the degree of distension of the capsule of the
vessel, or of drag upon it. Dread is a criterion between aortic
and coronary disease only thus far — that a young and vigorous
heart often outbraves this omen, which seems more frequent
in old persons, or those whose heart is frail. However it

sec. i SYMPTOMS 195

is no infrequent feature of intense aortitis of infectious
origin in persons under middle age. For instance, in the re-
markable case described by Rist and Krantz x of syphilitic
aorta in a patient set. 37, when the angina was continued
and severe, the attacks were attended with sensation de mort
imminente. Yet, as regards their mouths, trunks and intra-
myocardial twigs, the coronary arteries were intact. " II y avail
done aortite sans coronarite " ; but the symptoms were angina
pectoris, typical and complete ! The kidneys were normal.
The patient died of pulmonary oedema. And in typical angina,
of elderly persons, we shall see that dread is an inconstant
symptom ; it is often less manifest in poignant cases than in
attacks which otherwise, however sinister, are less painful. If in
aortic disease, as I have suggested, and Bittorf also, the vagus
terminals may be deleted, in this chance we may find some
explanation of absences or abatements of the dread. These
remarks on aortic pain seem proper to this context, but I must
not trespass too far on the essay devoted to Angina Pectoris,
where the nature of such pain will be closely debated. Then
also I shall discuss the inconstant symptoms of local tactile
tenderness and sensibility on the chest, as described by Peter,2
and by others later.

If then the inflammation happen to light upon the invest-
ment of the aorta in such a way, or at such a rate of activity,
as to make the vessel abnormally sensitive to the pressure of the
output of blood, so sensitive as to propagate the stimulus to
the sensorium, a " stenocardial " sensation is an early symptom
(see essay on Angina Pectoris, p. 287). It is remarkable
that Deneke is almost alone in not mentioning slight angina
(" stenocardia ") as an early symptom of syphilitic aortitis.

Again, the first betrayal, if perchance it be looked for, may
be by some modification of the X-ray picture ; some yielding
of the vessel, some distortion of its contour, some darkening
of its shadow suggestive of thickening (p. 204).

Stadler says that among the early, or more indefinite, symp-
toms may be a sense of general fatigue (scheinbar neurasthe-

1 Rist et Krantz, B. et M. de la Soc. Med. des Hdp., juin 28, 1906.

2 Peter, " Exploration de la sensibilite locale des regions precordials et
preaortiques dans les maladies du coeur," France medicale, 1881.

196 AOETITIS part ii

nische Initialsymptome) ; he suggests that this debility may be
an indication of closure of the coronary mouths, but this is
probably a later extension. In some cases of my own in
which such fatigue was not noticed, or not until the mischief
was very far advanced, these vessels may have lain longer
open to the tides of the blood. I have remarked this fatigue
especially in the cases of aortitis with regurgitation, a manifesta-
tion for which there may be more than one reason ; in these
cases the coronaries are often occluded. Again, a specific
aortitis, working round the root of the aorta, may invade the
conducting tracts, as rheumatism or atheroma may do, and set
up the phenomena of heart block — this in one very interesting
case I saw and followed out. In this site periaortitis may give
rise to a friction sound. The earthy complexion and falling
hair of the syphilitic patient, in contrast with the rheumatic
type, may be notable. The pulse may be unaffected, or
simply febrile, or, in acute cases, bounding with the throbbing
aorta ; in severe cases it may intermit (vagus). In Morison's
case (loc. cit.) the vagus on one side was involved in the specific
process. The subclavian artery may be raised, vibrating, and
hammering (Vol. I. p. 395). Pressure symptoms are, of course,
late phenomena of chronic cases ; the earliest I have noted is
the rather strident " whistling " respiration on exertion which,
though by no means an initial sign, may yet long precede other
respiratory signs, and the gravest issues of the malady. This
symptom I remember especially in two syphilitic cases, neither
with aortic regurgitation. The whistling is not distressing to
the patient, at any rate not at first ; it is often more perceptible
to the bystander than to the patient himself. In two of my own
cases spasm of the glottis was so intense as to call for chloro-
form ; and in one of them for tracheotomy. The following
case is interesting in this respect :

A man, set. 44, found his neck enlarging, his face and chest puffy,
and breath short. His physician found some blueness and slight
oedema of his arms and dilated superficial veins about the neck and
chest. Yet aneurysm of the aorta or mediastinal tumor seemed
improbable. By X-rays, however, we detected dilatation of the
ascending portion and first part of the arch of the aorta, which was
pressing upon the upper vena cava, the right bronchus, and the left

sec. i SYMPTOMS 197

recurrent nerve. Syphilis was strongly denied, but a specific irido-
choroiditis banished all doubt. Under mercury and iodide of
potassium this patient made a complete recovery.

Stadler emphasises an early and insidious and more dis-
turbing dyspnea, " not obstructive but functional " ; in my
experience this has not been an early symptom, but one rather
of the stage of regurgitation, or of incipient heart failure.

We may now concentrate our attention upon three cardinal
methods of the physical diagnosis of aortitis ; that is, upon the
percussion, auscultation, and ray methods. Of the first two
methods I may speak with personal conviction, for my experience
of them is not inconsiderable ; of the last my knowledge is based
upon the demonstrations and interpretations of expert colleagues.
However, I have found these testimonies, in cases of which
I have had personal knowledge, consistent with published
records, and with each other.

The normal aorta of a young adult man should measure
5-7 cm. ; over set. 50, 8 cm. In women it is rather less.1 It is
difficult to say at what lapse of time after the initiation of
an aortitis the vessel is enlarged in both diameters — in width
and in length — and how much may be attributed to atony. It
may be that the increase in length, by tortuous displacement,
does more than the increase in width to thrust the vessel
towards the chest wall, and so to damp the vibrations of the
sternum and nearer parts of the right ribs. At first sight it would
seem that such a displacement would not come about until the
vessel were gravely affected ; but, as atony may have some
part in the expansion, this alteration need not run parallel in
degree with the lesion. Stadler (loc. cit.) has some interesting
remarks on the atonic and the destructive dilatation of the
aorta in syphilitic cases ; and again on confinement of the vessel
to narrower limits by rigidity or adhesion. These are points
on which post-mortem evidence can be only indirect ; some
evidence however there is — or so it is said — of a recession of
dilatation. For my part, in syphilis I have no recollection of this
area of dulness, once established, contracting in any appreciable

1 See study of relative diameters and areas in man and animals by Dreyer,
Ray, and Ainley Walker, with calculations of sectional area from body
surface (Proc. Royal Soc, Dec. 1912).

198 AOETITIS part n

degree ; nor have I succeeded by the methods of Abrams 1 or
Ewart (percussion on the seventh cervical spine, etc.) in bringing
about the slightest reduction of its compass. Indeed in several
cases of great alleviation under treatment I have found the area
of dulness still to abide unchanged. In rheumatic and other
aortitis on the contrary such recession generally comes about.
Ordinary atherosclerosis rarely widens the aorta so remarkably.
And as, unless in exceptional cases, the blood pressures are not
increased, we are not puzzled by fluctuations in the volumes of
the heart's chambers. Nor again do the positions of respiration
alter the percussion area of the syphilitic aorta. Of a muffling
effect on the manubrial fremitus of adhesion around the
ascending aorta I can find no note, neither in cases of my
own nor in those of others ; but the sign is worth looking for.
It is said that a corresponding area of dulness may be detected
at the 3rd-4th dorsal spines.

On the site of the area of dulness I need not dwell
minutely ; Potain, whom we have to thank for its explicit
demarcation (loc. cit.), and many later writers have described
it as the dulness " en casque " — in the form of a fireman's
helmet. If from without inwards, on many radii, the boundaries
of it be obtained by careful percussion, the area will be
found to occupy the manubrium, or at first perhaps the middle
third of it, with an adjacent area of the second rib and
third interspace, one to two finger-breadths to the right. In
one of my cases (lues) it extended fully 4 cm. to the right, and
the outline may slope up from the 4th cartilage. The dulness
about mid-manubrium is generally quite decisive, at the top
a little less. It may cross over a little to the left side, but is
never so dull there as on the right. Of the alleged corresponding
dulness in the area of the 3-4 dorsal vertebrae I can say nothing.
Dr. Sansom advised the use of the pleximeter for this mapping;
the pleximeter is useful for class teaching, but, to me at any rate,
the help of the sensibility of the under finger is indispensable.
This percussion sign, even if we cannot call it a very early one,
I have found very trustworthy.

In the normal person, unless we include spare old persons
with deteriorated vessels as relatively normal, the arch of the

1 See Brit. Med. Journ.. July 8, 1911.

sec. i SYMPTOMS 199

aorta is not to be felt in the jugular notch. Normally, it lies
2-2| cm. below; over it lie fat, and layers of connective tissue.
It may be palpated in persons wasted, or neurotic with atonic
vessels, in the subjects of Graves' disease for example, or when,
as in high pressure cases, the heart is hypertrophied. But, as
Wenkebach has demonstrated, before deciding the value of this
upper palpation the position of the diaphragm must be care-
fully ascertained. Yet even in the syphilitic aorta the vessel
is not always palpable, Stadler adduces two cases of the excep-
tion ; but, as in syphilis the vessel begins to yield near its root,
when this jugular sign occurs it is usually at a stage of the aortic
disease when we have other and surer evidence. Moreover it is
often palpable in ordinary atherosclerosis, when the subclavian
and upper arch are crooked and thickened. In some individuals
none of these conditions, however inveterate, seems to produce
it ; though radial pulse differences, due to straitened mouth,
may be present. In the younger subjects of rheumatic aortitis,
with narrow jugulum, the vessel may not be, often is not, accessible
to the finger ; in this disease, unless by atony, it is not so
much enlarged. Concerning influenzal aortitis in this respect
I have no note. In acute cases I have often found the vessel
tender to the touch (p. 427), a tenderness to be distinguished
from any discomfort of the palpation.

In this context I must allude again to the subclavian sign of
Faure (loc. cit. p. 349), Gerhardt, von Schrotter x and others ; but
in syphilitic aortitis at any rate, it is not of more than occasional
service. When the aorta is stretched and twisted, the sub-
clavian artery, as the patient depresses his right shoulder, may
be thrown up in the supraclavicular notch (Vol. I. p. 395).

Some evidence of elongation of the ascending aorta, better
than may be afforded by the subclavians, was pointed out by
Traube,2 and verified by Edgren (loc. cit.), myself, and others ;
namely, mobility of the heart's apex (Vol. I. p. 396). Undue and
even extreme mobility of the heart is seen in other maladies, as
in neurasthenia ; but by their proper features this and such
atonies can be excluded. As the patient turns from the supine
position to his left side, the heart's apex will swing outwards,

1 Von Schrotter, " Erkgn. d. Gefiisse," Nothnagel's Path. u. Ther. vol. xv.
2 Traube, Gesamte. Beitrage, Bd. iii.

200 AOKTITIS part n

until its beat may shift far outside its normal limits. From
its normal place, the heart's apex may fall away even to the
anterior axillary line. At the same time the left line of absolute
dulness moves to the left, though not to the same degree. We
may be satisfied of undue mobility even in an enlarged heart,
and by position tests we may be enabled to attribute some
extrusion of the apex to elongation of the aorta rather than to
ventricular hypertrophy. Points so nice as these, if often useful
in particular cases, cannot be reduced to rule ; but we may
remember that destructive dilatation of the arch, with loss
of its " bellows " function, might, by degrees of dyspnea or
even by pulsus alternans, simulate heart failure (?). As in
the case of aneurysm, cardiac hypertrophy has no necessary
association with aortitis, acute or chronic.

If we turn to auscultation, we shall find another sign of value,
one which should give us an earlier clue ; unfortunately it is
incapable — as yet— of objective demonstration; as yet it exists
only as an apprehension of the mind of the listener, and is
inconstant. Whether or no in future inscription of cardiac
sounds may represent it we cannot say. The sign is a
certain quality of the second sound, that which Potain
described as the bruit de tabourka,1 a phrase I have
used in teaching for many years, both in Leeds and in
Cambridge, because the customary English term, " clang-
ing second sound," is not free from objection. Clang is the
rather unhappy term of English acousticians to signify what the ?
French call timbre^ the quality by which, for example, a certain j
note on the violin differs from the same on a horn or other T
instrument. Thus the " clang " of the normal second aortic
sound would be contrasted, let us say, with an altered clang
in aortitis, especially in the syphilitic kind ; for this peculiar
quality some other term, such as " tympanic second sound,"
would be better. Tabourka sound would do, should this term
become sufficiently familiar to convey the idea. " Clang " is
of course a quality other than accentuation or pitch of sound.

However, names aside, the maxim itself is one of no little
importance, perhaps of the first importance ; of the first

1 The tabourka, an Algerian drum, made of an earthen pot with a skin
stretched over its mouth.

sec. i SYMPTOMS AND SIGNS 201

importance if it prove to be peculiar to syphilitic aortitis, and,
moreover, if not masked by some accident, as by emphysema, a
constant. No less is alleged for it already, but, if I rightly re-
member, Potain did not regard it as pertaining exclusively to
syphilis. Whether or no it be a constant is another question ;
the timbre of a sound is not always identical day by day ; in
the same person it wanes, waxes, or changes. Unfortunately, as
I have said, this criterion is a subjective one, one, so far as I know,
not as yet reduced to record ; though by acoustic delineation it
may hereafter be discerned. Personally, I am not yet prepared
to say that this tympanic second, as contrasted with other kinds
of aortitis, or even with atherosclerosis, pertains exclusively to
syphilis ; nor again that in syphilitic aortitis that it is a constant.
In incipient Bright's disease I have heard second sounds hard to
discriminate from it ; but I quite agree that it is characteristic
of this aortitis, and that the sign is a useful addition to
our means of diagnosis of the disease. I am disposed to explain
it by the muffling of the walls of the ascending aorta. In athero-
sclerosis it does not occur ordinarily, perhaps because this lesion
moves rather towards stenosis than towards valvular tension.
If the quality may be reinforced by high aortic pressure, it is not
by any means dependent upon it. On regurgitation signs I may
venture on a word of warning ; the murmur may be so faint,
so distant, and even so inconstant (see my case with Dr. Mcllvaine),
that unless, while the patient holds his breath, all possible areas,
particularly to the left of the sternum, are traversed, it may
escape the physician not well on his guard. That by recur-
rent fluid veins within the largely dilated arch itself a murmur
may be caused during cardiac diastole, I can neither affirm
nor deny ; if such a murmur may be dispelled, in luetic cases,
by specific treatment, and not return, this effect I should
attribute to some repair of the valve, or of its seat.

On the signs of regurgitation, and of heart's dimensions and
work, I need not dwell ; but Stadler says that in syphilitic
valvulitis the systolic murmur may by some considerable interval
precede the regurgitant ; and suggests further that to an expert
ear this, sharper, systolic sound may be distinguishable from the
systolic murmur of the aortitis. He adds that the peculiar
clanging second sound also may continue with its own quality

202 AOETITIS partii

after regurgitation is established. With the first distinction
I am disposed to agree ; and this interval may give us time
to push forward treatment to prevent the graver mischief :
as regards the second I regret that I have made no close
observation ; on such refinements we need more clinical verifi-
cation. Possibly Dr. Eustace Smith's " retraction murmur "
might be elicited. I may remind the reader that a useful, if
not constant, point of distinction between rheumatic and early
syphilitic aortitis would be, in this kind, the absence of signs of
mitral disease.

The physical signs of aortitis, which I have found convenient
to discuss under the syphilitic kind, are to be discerned, with
differences only of degree, in the other kinds. That aortitis
should be sought and detected in early, acute, and often
transitory modes, I am anxious again to impress upon the reader.
Surely it is a serious matter to allow an aortitis in rheumatic
fever, influenza, or other infection to escape our notice.

But there is one more physical sign, one sometimes of cardinal
importance, the chafing sound of the dry, basic pericarditis,
occasionally associated with aortitis. In all such cases therefore
the sounds of pericardial friction must be vigilantly sought
for. Thus we might detect an aortitis in rheumatic fever.
Pericarditis about the aorta may arise in two modes : first,
from the outside, invading the circumference of the aorta
embraced by it ; secondly, from within, whence aortitis may
penetrate to the investing pericardium. If the former instances
are mostly rheumatic, yet they may come of other infections ;
of Bright's disease and some other maladies. Now, whether the
pericarditis be of inner or outer origin, it is, as I shall point
out (p. 454), so likely to arouse angina pectoris that a nice
appreciation of these conditions may be of cardinal importance.
In some of these cases, as Pawinski x has demonstrated, in a
remarkable essay from which I shall quote again in the Section
on Angina, we shall see that angina pectoris is independent of
coronary disease.

In a case of pericarditis sicca, described by Auscher,2 three
attacks of classical angina pectoris occurred, one of which caused

1 Pawinski, Deutsche Arch. f. Hin. Med., Sept. 1897.
2 Auscher, Bull. Soc. Anat. Paris, fev. 1896.

sec. I SYMPTOMS AND SIGNS 203

syncope. The patient recovered, but nine months later died of
rapid phthisis. At the necropsy the effects of pericardial peri-
aortitis were discovered ; but to naked eye and microscope,
the inner aorta, heart, and coronary arteries were alike
" irre'prochabler

Enlarged veins on the chest are scarcely to be expected, apart
from aneurysm. I need not say that the state of the pupils,
retina, knee-jerks, and other ordinary tests, will not be for-
gotten. Thus in syphilis, as physical signs, we may have the
tympanic second sound, the characteristic dull patch, the rise
of the arch in the jugular notch, perhaps a rise upwards of the
right subclavian : what else have we ? for all but the first are
late indications ; long before it compassed these differences the
evil was on foot.

Well, we have one more physical method, that of radiography,
which may, probably will, give us more timely data. A good
deal of valuable work has been done on this subject, and
not without success. Vaquez and Bordet1 have recently
gone carefully over this means of diagnosis, and conclude
that by the rays, using both screen and plate pictures, upright
and recumbent, this latent mischief can be caught pretty
early, and before the valve is injured. Vaquez's paper con-
tains many careful diagrammatic outlines of such aortas, as
seen under the rays, with tables of measurements. The points of
diagnosis are that the shadow of the vessel becomes both wider
and darker; points on which Lippmann agrees. In the Hamburg
Hospital, Lippmann (loc. cit.) got positive results in 70 per cent
of 180 cases. It is important to take pictures by orthodiagraphy,
both sagittal and oblique, at angles of about 20-35 degrees.
Vaquez believes that by parallel rays (3 yards off) " an exact
and impersonal document can be obtained ; the conditions
being constant." But surely screen views in various positions
should also be taken. In Vienna, Eisler and Kreuzfuchs 2 have
come to similar conclusions ; they divide their cases into the

1 Vaquez et Bordet, Paris med., juillet 1911 ; and a book published
1913. See also Lippmann, " Rontgen-diag. d. Aortitis luetica," Arzte
Verein, Hamburg, Protok. Deutsch med. Wochenschr., Nov. 21, 1912.

2 Eisler, F., u. Kreuzfuchs, S., " Die R. Diagnose d. Aortensyphilis," Deutsche
med. Wochenschr., Oct. 30, 1913. See also Grodel, F., R. Diagnostik d. Herz- u.
Gefdsserkhn., 1913.

VOL. II O

204 AOETITIS partii

Ascending-type, the Arcus-type, and the Descending-type ; of
these the Ascending is by far the most frequent. Mediastinal
tumours, although they may oscillate with the heart's pulsation,
may often, but not always, be distinguished by the outlines, if
in the memory of the expert those of the aorta be clearly fixed
beforehand. Stadler thus demonstrated a case (congenital) in
a child aged 13. Aneurysm again presents its own distinction
of outline ; yet, as Ewald says, exclusion of aneurysm must
often be difficult, and in case of small sacs near the heart im-
possible. Vaquez and Bordet give one obscure case in which
syphilitic aortitis was clearly diagnosed by the rays, when other-
wise physical diagnosis was at fault (p. 430). The dilatation and
thickening were mostly below near the heart, as usually at the
beginning they would be, and the summit of the arch was not
pushed up ; but by the rays increase of volume, alteration of
curve, and darker shadow were apparent. Before the vessel is
enlarged the rays can give no sign, unless possibly a reduction
of the pulsations and a deepening of the shadow, indefinite
signals. It is said that under specific treatment the shadow
may be seen to lighten and the pulsations to return.

Such, and as yet so imperfect, are our physical signs of
aortitis, a malady in its syphilitic form as prevalent as it is
insidious, as stealthy as it is destructive. In cases where there
are no data, in the present or in the past, to suggest syphilis, it
is hard to see how we can be forewarned ; we shall not even be
consulted until some stenocardial sensation disposes the patient
to seek advice. Then our course is clear ; physical signs or none,
we shall use the Wa. test promptly, and, if positive, press forward
specific treatment with all speed and vigilance. Even with a
negative Wa.R.,1 if the patient's age and history be not incon-
sistent with syphilis, and if there be any percussion or ray sign,
and no counter-evidence of any other infection, such as acute
rheumatism or influenza, we must press forward the specific
therapeutic measures, anxiously watching results. It is better
in treatment, as we are wont to say of certain obscure

1 In subjects of aortic syphilis, verified as such on the post-mortem table,
as observers have of late become more and more expert, the Wa.R. is now stated
to be constantly positive ; but I presume that occasionally negative reactions,
due for instance to the use of specific remedies, may still occur.

sec. i ANEUEYSM 205

and possibly syphilitic cerebral conditions, to err on the
positive rather than on the negative side.

How far the remedial effects of salvarsan may tell in aortic
syphilis, with or without aneurysm, is a question now under
active discussion. Mechanical injuries once inflicted may be
irreparable, but some sanguine observers report under the use
of salvarsan a reduction of the skiagraphic shadow. Let us
hope they are right. Vaquez and Landry,1 who have discussed
the methods of treatment of the disease, report beneficial
results from salvarsan in the majority of their cases so treated.
Others, such as Gigaard (who has been quoted in various
journals), still rely on iodide of mercury. The impression seems
to be general that for this lesion the iodides alone are of less
value (p. 126). A close watch is to be kept for any sign of
relapse, on which treatment should be promptly resumed.

Aneurysm of the aorta, large and pre-eminent a part of
aortic disease as it is, lies outside my subject (p. 168). I will only
remind the reader how rarely it seems to arise from atheroma (Gee,
Oppolzer, Hollis, Thorburn). Atheroma is not so directly a
disease of the media, and it trends more to the floor of the arch ;
aneurysm inclines to the convex side of the arch. However, as a
secondary effect, atheroma is found largely round the edges and
bordering tracts of aneurysms, where it is to be distinguished
from any syphilitic aortitis. Those aneurysms, too small for
clinical observation unless possibly by the X-rays, which are apt
to form about the root of the vessel, are often due to aortitis.
In this area recesses are commonly found after death, especially
in or near the sinuses of Valsalva ; some of them are too shallow
to contain clot, others retain clots of nominal substance ;
others again are narrow -mouthed pouches, aneurysmal in
the saccular sense, and may rupture into the pericardium, or
compress the base of the heart. These aneurysms occasionally
give rise to signs of aortic disease, or to symptoms of angina
pectoris (p. 431). Moreover, like gumma and other lesions of
this part, they are apt, by interference with the conducting
tracts, to retard the pulse rate.

In many cases we find a general arteriosclerosis with less
eminent aortic disease, and may have moreover to discriminate
1 Vaquez et Landry, Arch, des mal. du cceur, sept. 1912.

206 ATHEROMA OF THE AORTA partii

between the anginal symptoms of aortic disease itself, secondary
cardiac discomfitures, and tabetic crises.

Atheroma of the Aorta. — The morbid anatomy of this
disease of the aorta is for the most part included in its chapter
in the essay on Arteriosclerosis (vol. i. p. 508). All the earlier
records (Morgagni,1 J. P. Frank,2 Broussais) are or may be vitiated
by the interpretation of intra-aortic post-mortem staining as an
inflammation. Virchow 3 showed that the descriptions of " false
membranes " on the inner face of the vessel were fallacious.
Laennec and Gueneau de Mussy supposed aortitis, first
perhaps described definitely by Cornil and Ranvier in 1869,4
to be, like atheroma, a degenerative process ; but Cornil and
Ranvier described the gelatiniform patches with proliferative
activity of the surrounding cells. If, anatomically speaking,
the gelatiniform patch is a character of acute aortitis, we must
not forget that this feature may be seen in active stages of
chronic atheroma. In infective aortitis these fresh patches
may be found full of microbes, especially of cocci.

We have seen now that aortitis is no uncommon event,
and that even periaortitis is not very rare, and arises under
many and various conditions. Now all diseases of the aorta,
if they pass into chronic states, tend to atheroma ; or at any
rate to a blend of inflammatory with atheromatous processes.
When ultimately syphilitic arteritis mingles with atheroma,
the two diseases co-operate to produce the expanded, bossy,
scarred, wrinkled and puckered vessel, together with the fatty
and calcareous decay of the supervenient atheroma. I have
referred to a good picture of the process in Letulle, vol. i.
p. 156. The age of the patient is of course a factor in this
transformation.

Rupture of the aorta is most commonly indirect, the rupture
being of an aneurysm, large or small. Acute perforative disease,
such as in the case of Oliver and Woodhead, is very rare ; and,
save under some striking circumstances, must be beyond
diagnosis. But rupture of an aorta, apparently sound, or in a

1 Morgagni's Twenty-sixth Letter.

2 Frank, J. P., De curandis hominum morbis, Mannheim, 1792.

3 Virchow, Pathol. Anat. vol. i., " Entziindung d. Aorta."
* See also Histol. Pathol, 1881.

sec. I RUPTURE OF THE AORTA 207

comparatively young person, as described by Morgagni more
than once,1 if an infrequent is not now a surprising event. Since
Broca published his leading paper (Bull. Soc. AnaL, 1850) many
cases have been submitted to the proof of dissection. In some
the vessel, though not diseased, has seemed thinner than
normal, as if imperfect in development. Pilliet,2 in the same
journal, added twelve cases to the list. Dr. Teacher showed
me two such specimens in Glasgow. In both the rupture was
about f inch above the valve, and no proof of disease was found.
In Dohrn's 3 case the vessel was found healthy. The rupture
was clean across the arch on its downward turn at the point
of attachment to the spine. It happened in a boy, set. 18,
who fell down 17 yards. There was no outward wound of the
chest. The tear was as if due to a forward and downward
jerk. But some cases are syphilitic ; as for instance that of a
woman (positive Wa.R.) in whom a circular rupture was dis-
covered 2 cm. above the valve.4 Here I may recall Letulle's
opinion on syphilitic atrophy. Frankel 5 gives four cases : (1)
Male, set. 68, cardio-renal disease and high pressures, and an
atheromatous aorta (see p. 303) ; (2) Male, labourer, set. 27 ;
(3) Male, set. 33, tuberculous ; and (4) Boy, set. 1| years, ill
with mild bronchitis. The accident was suddenly mortal in
all. The boy had stenosis of the isthmus. In the essay on
Angina (p. 433), I shall discuss these supra-sigmoid cases. Sir W.
Osier6 mentions one, in which from a first rupture the patient
recovered, to die a year later of a second. A drawing of
the aorta was shown. The first attack was diagnosed as
angina pectoris, and rightly so. An effort or wrench has often
determined the moment of the rift, which may not penetrate all
coats but, checked by the outermost, form a dissecting aneurysm,
as in a case by Pallasse and Roubier.7 In the same issue of
that journal cases were cited by Cairmont and others); 8 in one

i E.g. Ep. LIU. 35. 2 Pilliet, Bull. Soc. AnaL, 1889.

3 Dohrn, quoted Zentralbl. f. Herz- u. Gef.-Kranktn., Juli 1914, from Zeitschr.
f. Med.-beamte, No. 7, April 1914.

4 Quoted Zentralbl. f. Herz- u. Gef.-Kranktn., Juli 1912.
6 Frankel, Berl. klin. Wochenschr. Bd. I. p. 795, 1913.

6 Osier, Sir W., Lancet, March 26, 1910.

7 Pallasse and Roubier, Lyons mid., 1912 (quoted Arch, des mal. du coeur,
p. 600, sept. 1913).

8 Same issue of Lyons med.

208 AOETITIS part ii

of them the haemorrhage forced its way to the origin of the left
subclavian and down the abdominal aorta. The seizure began
with intense retrosternal pain passing down the left arm. The
heart was normal. Romeick x says death is often sudden, and
may be painless, though in some cases angina pectoris appears
with great severity, and generally with extreme angor (" hoch-
gradigem Angstgefuhl "). The angina he tries of course to
hook on to some supposed anterior coronary sclerosis. In
three-quarters of the cases the rupture opened into the peri-
cardium. From the aorta the issue of blood is usually more
rapid than in rupture of the heart, and survival so much the
briefer. In rupture on the plane of the arch, as distinguished
from rupture of a pouch, it is remarkable that the rent,
though usually transverse, may run lengthwise of the vessel ;
when the immediate cause would seem to be rather a dis-
tension of the vessel than the tearing away from cardiac
attachments pictured by some authors. Dr. Petch of York
published a case (Lancet, 1899), of a man, set. 56, who died
suddenly, in which the aorta had parted from the base of the
heart, and the distal end was retracted into the arch of the
vessel, and invaginated after the manner of an intussuscep-
tion. Other instances of this form are on record.

Of the treatment of aortitis, which indeed is almost altogether
that of the general disease of which it is a part, there is little
to say which will not be found in the sections on treatment of
Arteriosclerosis and of Angina Pectoris ; but, on account of the
possible enfeeblement of the heart (p. 178), I suppose that
salvarsan can be used only in persons otherwise favourably
disposed, and then with every precaution. This I am told is
Ehrlich's opinion.

Developmental deformities of the aorta, such as stenosis
of the vessel at its duct, or at the seat of the ductus botalli,2

1 Romeick, working under Marchand, Spontane Buptur d. Herzens, Inaug.
Diss. 1907.

2 Botallo is to be held in remembrance as a great surgeon ; but, so far as
modern medicine goes at any rate, we owe our knowledge of this duct to the
Bolognese anatomist, Aranzio. In ancient times it was known to Galen ; as
was the foramen ovale, etc. I may remark that the dilatation of the vessel

sec. i DEFOKMITIES OF THE AOETA 209

scarcely fall within my subject, and on them I have nothing
fresh to say. In respect of the hypoplasia studied by Virchow,
and the peculiar nephritis which the great pathologist found to
be not infrequently associated therewith, I may refer to an able
paper by Ettore Chiarruttini in the eighth number of the Clin,
med. ital. of 1900, " Le Anomalie di calibro dell' aorta in
rapporto alle nefriti e all' ipertrofia cardiaca."

Josef Burke x of Vienna published a valuable discussion of the
whole subject of aortic hypoplasia ; a discussion based upon
one hundred recorded cases. He laid stress upon this defect as
but an eminent part of a general vascular hypoplasia ; in most
cases at any rate it is an arrest of growth, and associated with
other imperfections of embryonic development ; occasionally it is
betrayed by correlative defects. Burke is of opinion however
that this explanation does not cover all cases ; there is a group
in which the hypoplasia is rather to be attributed to disease ;
sometimes an infection, sometimes a general malnutrition. In
these cases, in young persons, he found atheroma of the aorta, and
even arteriosclerosis, to be no infrequent feature, and assumed
that in them a phase of high arterial pressure had gone before.
This is not probable. Burke discussed the sex incidence of
arterial hypoplasia, and concluded that in woman ensue anaemias,
in man cardiac diseases. He entered fully into the kind and
mode of associated and secondary changes of the heart.
Among his own cases he published one of the nephritis already
mentioned ; in this case, as in others of the kind, the endocardium
and serous membranes were inflamed.

Of abdominal aortitis I shall speak in the Section on Angina
Pectoris. It may give rise to violent cramps and pains in
the abdomen, and so often simulates other lesions, such as mesen-
teric thrombosis, tabes, colics, and so forth, that a differential
diagnosis may be very difficult. To judge from the lists of cases
which now and then see the light it would seem that the necessary
discrimination is not always used. Any of the disturbances
which may stretch or irritate the sensitive mesenteric nerve

beyond the stenosis should be no matter of surprise, when we remember the
need of compensation for the " vena contracta," and of reduction of
velocity increased at the point of stricture.

1 Burke, J., Deutsche Arch. f. klin. Med., 1902.

210 AOKTITIS part II

end-organs would, so far as the pain goes, simulate abdominal
aortitis. French observers speak of " hypertension " in the
dorsalis pedis as one of the signs ; but, as I have said else-
where, in the presence of normal general pressures this is very
improbable. A contracted vessel may give indications of
resistance (Russell) wrongly ascribed to the blood pressure
(Vol. I. p. 77). To palpation the abdominal aorta may appear
much dilated, and tender to touch.

One or two cases of a congenital dilatation of the aorta are
on record. Little is known of the condition, if indeed it piove
to have any definite and independent features.

Appendix I. (p. 156). — I have seen and examined Jeeves five
years later with two colleagues. She considered herself well, goes
for walks, visits her friends, and so forth, but was avoiding laborious
work. She had a double aortic murmur, and enlarged left ventricle.
There was still a large area of dulness at the upper third, of the
sternum, and to the right of it, and a dilated aorta was palpable
in the episternal notch.

Appendix II. (p. 184). — While finally revising these pages a
respectable married woman, aged 64, came under my care in the
Addenbrooke's Hospital with aortic murmurs, direct and regurgitant,
and hypertrophied left ventricle. As in my opinion " senile ather-
oma," the diagnosis suggested, rarely issues in regurgitation, I
searched for other evidence and found upon the right leg two or three
such scars, one especially clean cut, about 6 mm. diameter, quite
typical. Owing to military pressure our clinical laboratory was
shorthanded, but Dr. Mott was so good as to apply the Wasser-Mann
test for me, with a " strongly positive " result.

SECTION IL-ANGINA PECTORIS1
CHAPTER I

INTRODUCTORY

In this secret and fell disease there is a fascination to which
no physician is a stranger, a fascination in its dramatic events
and in the riddle to be read. By angina pectoris the humble
out-patient is for the nonce lifted up into the sphere of
a Hunter or an Arnold ; over him we endeavour to bring the
old discordant and mutually destructive arguments into some
consistency, ringing again the old changes on the old bells. I too
am content to compose another tune on the old chime : still, I
have the excuse, at least to myself, of an independent endeavour,
if not, as I diffidently hope, to solve the old problems, yet at least
to elucidate them by compelling our nomenclature, our technical
terms, and our current phrases to declare themselves each for
what it is worth ; and, no longer drifting hither and thither about
the nosological field, to compel them to take up each its own
rank, and no other than its own rank, in the argument. In this
Section therefore some controversy is unavoidable ; and as I
must withstand adversaries better equipped than myself, I
fear lest what Jurine said of Parry may be said of me, " II
nous semble que M. le Docteur a moins manque d'indulgence

1 The whole argument of this section was in substance contained in a paper
read by me before the East Anglian Branch of the British Medical Association
at Yarmouth on June 2, 1894 ; and, two years later, was incorporated in my
Lane Lectures at San Francisco. It occupied a part also of my Cavendish
Lecture in 1903 ; and almost in its present shape was read at the Fitzroy Square
Offices of the Mount Vernon Hospital on January 9, 1908, or at any rate was
so written for this occasion, though in the reading much of the subsidiary proof
was necessarily omitted. It was delivered again, with some further illustra-
tive matter, before the Section of Medicine of the Association at the Belfast
Meeting in 1909. I republish it now in full, after revision.

211

212 ANGINA PECTORIS paetii

pour mi-meme que pour ses collegues." I would not forget
Harvey's saying, " Concordia res parvae crescunt, discordia
magnae dilabuntur," but I want the concord on my own side.

For concerning angina pectoris, more perhaps than any other
disease, it is of importance to be quite clear at the outset what
we are to talk about. It seems as if the perplexity of thought, so
conspicuous in its interpretation, were infecting the clinical idea
itself, dissolving it before our eyes. As in their case-records
authors become more confused the more they grow bold to assure
us, frankly or implicitly, and not without a certain complacence,
that there is no such disease ; moreover they not only disinte-
grate angina pectoris, or what was angina pectoris, but dress in
the rags of it other and alien conceptions, after a fashion which
cannot but destroy the stability of all clinical ideas whatsoever.
In an editorial article in a recent number of a leading English
medical journal, I read — -not, as might be supposed, in irony — this
concerning angina pectoris : "Its generally admitted symptoms
have no fixed pathological significance ; they may be associated
with grave organic disease of the heart and coronary arteries,
or with nothing more serious than a heavy meal, a disordered
stomach, or excessive smoking " — or, he might have added, a
squall in the nervous system. In other words, trivial and
mortal disease are much the same thing, and technical terms may
be blown about like straws in the wind. Because the pathologist
— who year by year has been drifting farther and farther from
clinical medicine — because the pathologist has been unable to
demonstrate its anatomy, therefore the physician is to dismiss
angina pectoris as a dissolving view. But not in this malady
only have we to repair clinical ideas delivered from our fore-
fathers but damaged in modern pathology.

Thus of such modern authors more than one, and these not
the least distinguished, breezily assure us that angina pectoris
is " not a disease but a symptom," a riddle over which I confess
I have not perplexed myself overmuch. For how can one dwell
on a statement so odd and so narrow when, within the very same
pages, we may read under this same title descriptions of a series,
of a many symptoms ! " Symptomatic " angina may be ; it is
no doubt the symptomatic or clinical side of some internal lesion,
as yet undetermined ; but to speak of a series as a single term

sec. ii WHAT IS A DISEASE? 213

is to confuse confusion. Other authors, fortified by the great
authority of Latham, though equally determined to deny to
angina pectoris the title of a disease, do admit that this name
signifies a " symptom-group," a phrase with which, hackneyed
as it is, there is less reason to quarrel ; under it we may conceive
some definite image. Yet for several reasons the term is inade-
quate : the word " group " fails to suggest a fairly uniform
series or dynamic procession of symptoms. When is a disease
not a disease, but a symptom-group ? One writer has told
us : he says " a symptom- group differs from a disease in
its various causation and various pathological bases," which
surely is to propound that a similar series of events can have
dissimilar causes ! If a single symptom, a cough for example, a
pain in the side, or a hemiplegia — for a symptom does not become
a disease because it is a big one — may be roughly attributable
to various causes, it is unthinkable that an array and pro-
cession of events can issue from causes in the main different.
Even within this narrow limit the acute and expert physician may
perceive that coughs, pains, and hemiplegias of several origins
are not indeed in character quite identical. Vomiting, for in-
stance, usually betrays by its behaviour the kind of causes to
which in the particular case it is due ; and as we turn from
symptoms to symptom-groups, the correlation of causes and
consequences becomes more and more inevitable. The difference
between a "symptom-group," or " syndrome," and a disease, if
one may venture to interpret other people's notions, is that a
" symptom -group " is a certain shorter chain of symptoms
common to more than one completer series — a path of inoscula-
tion. To disregard the perspective of the phenomena is to
lose the clinical idea ; thus the picture of the malady as a whole,
as in the case of angina, convincingly delivered to us by the
elder physicians, is dissolved. Is not then all this hair-splitting
between symptom-group and disease factitious ? Is it not
chercher raison ou il n'y en a pas ? Bluntly and tartly to deny
to angina pectoris the name of disease, a word which, by the
immemorial associations of thought, does signify to us a clinical
picture, a morbid process seen in perspective, makes us wonder
what is to be the content, colour, or compass of the word disease,
which in this case is declared to be fallacious ? What are the

214 ANGINA PECTORIS part II

notions now continually prompting certain able physicians to
forbid us to call angina pectoris a disease ?

To answer for them is not easy ; we may best approach it
by asking the larger question — What in any case do we properly
mean by the term Disease ? It will be strange if in the twentieth
century we find ourselves obliged to begin by protesting against
a recrudescence of the scholastic ontology which supposed disease,
and for that matter many another series of phenomena, to be
each one a thing in itself. It is nowadays disconcerting, to say the
least of it, to hear physicians of learning and experience gravely
enquiring of each other if this or that malady is a "morbid entity,"
and implying that the title " disease " is to be reserved for " mor-
bid entities " : no entity, no disease ! Thus to regard Disease
is to regard it as a thing, or an immanent principle having an
independent existence of its own, and to forget that it is merely
an abstract conception of a multitude of similar experiences in
the mind of a skilled observer. The judicious Latham was not
very intelligible when he spoke of angina as not " a disease
sui generis, but a series of symptoms " : for, clinically speaking,
what is any disease but a series of symptoms recurring with
fair uniformity ? Let us understand at once that angina pectoris,
like typhoid fever or pneumonia, pretends to no " entity " ; that
the name signifies a general idea of a process which takes place
in certain sick men, never repeating itself identically — no two
cases ever were identical, — but recurring with a measure of
uniformity sufficient to make it possible and useful to construct
for ourselves an abstract idea of it. Objectively, we may com-
pare it to the photographic method of the superposition of many
images of somewhat similar men, by which a " compound photo-
graph " is constructed ; a picture not of any thing in itself, but
an abstract notion of a certain group of approximate variations.
Thus a certain disease, angina let us say, is a compound im-
pression of the anginous phenomena severally observed in
Johnson, Thompson, Wilkinson and others, and by the minds of
Heberden and of his successors fused into an ideal picture, and
by them communicated to us. The individual patient is in-
deed a thing, an entity if we please, but he cannot be named
Angina pectoris ; this name signifies a general idea or concept,
of which he is but a particular and a partial instance.

sec. ii WHAT IS A DISEASE? 215

Now unless by comparison and revision we bring such in-
dividual notions into a common form, we can never agree, even
to differ ; for these mental concepts, or Diseases — Measles, for
instance, Epilepsy, Appendicitis, and so forth — are no smooth
and rounded images of fixed evolution ; nor are they even
definitely logical categories, within which all the individual
instances of J. and T. and W., etc., can be accurately fitted ; all
" diseases," as is the case with all categories in biology, overflow
each other, interpenetrate each other, and borrow each other's
characters in ways which are those of nature rather than of logic.
I have often said, figuratively, that, by the stepping-stones of
borderland cases, one may walk from any one disease round the
whole continent of morbid principalities and return dryshod to
the starting-point. The title of Disease, then, is not to be with-
held from a process, which on the whole is fairly consistent,
merely because a few equivocal instances may refuse for a while
to come in. Were this objection allowed, no classification in noso-
logy could be maintained ; for in all its classes aberrant instances
occur abundantly. Notwithstanding, if in a large majority of
cases we note that a morbid process recurs with fair consistency,
if we are to reason of it, and if we are to compare it with other
series, we must form a concept of it, and our concept must have
a name. When Latham says epigrammatically, " We are sure
that [angina pectoris] is an assemblage of symptoms ; we are
not sure what it is as a disease," the point, if there be a point,
is soon blunted ; for the same may be said of epilepsy, or gout,
or asthma, yet who but a pedant would deny to any of these the
name of a disease ?

By a " disease," then, we mean no " entity," no " real "
existence ; we mean but our concept of a certain recurrent series
of morbid events in many living bodies ; and our distinction of
any morbid process as a" disease," and by a name or label, is,
at most but a matter of convenience. If in respect of a certain
series of events, positive and negative, by the general consent of
competent persons it is agreed that the recurrence is sufficiently
uniform to make a concept, and to justify a label, we label it ;
but, this done, such labels must not be shuffled. If at times,
when we are diverted by the infinite mutability and continuity
of nature, and are dwelling rather on the transitions and inoscula-

216 ANGINA PECTOEIS pakt n

tions of her processes than on her uniformities, if under such
impressions we begin to think that the examples classed under
the label of angina pectoris, or under any other such label, prove
too irregular in manifestation, too capricious, too eccentric to
be fused into a type, then the indisposition to trim such cases
into a category, and to depict and to label a general concept of
them, is put upon proper ground, the ground of inconvenience.
In my opinion however, an opinion I believe based upon good
historical doctrine, the process named by Heberden in 1772
" Angina pectoris," is, in comparison with other morbid series,
even with the most definite of them, a remarkably consistent
one ; and its characters even peculiarly distinct and impressive.
An able American physician, who hesitated to allow to angina
the place of a disease, admitted nevertheless that, " clinically
speaking, angina is an important and strongly individualised
disorder, with striking characteristics, and a clinical history
peculiarly its own ! " Why, what more than this can we as
clinical physicians want for the recognition of any disease, or to
justify any name in nosology ?

I submit therefore that our examples of angina pectoris
have common and characteristic features such as to enable us
to form a general concept of it, and to attach to the idea a
label or name. And, for the series it has represented from
Heberden's day to our own, the name of Angina pectoris is a
convenient one, for happily it commits us to no doctrine.

Although Heberden rightly enjoys the place of godfather of
the disease, as he was the first to publish a formal description of
the series and to name it, yet more than once the disease had
been incidentally adumbrated before ; 1 as by Morgagni,2 by

1 Med. Trans, vols. ii. and iii. The history of angina is not dealt with in
these pages ; it is compendiously given by Gibson in a lecture published in the
Edinburgh Medical Journal of July 1902; but it is fair to say that although
Heberden named the disease and gave by far the better description of it, yet
the first precise discernment and description of it was in a letter by Rougnon
to Lorry, published at Besangon by J. P. Charmet in 1768. Pawinski (Zeitschr.
f. Jclin. Med. lxx. 3-4) says the disease was described by Baillon in the sixteenth
century. Still, the conception of angina pectoris may be said to belong to
England. Heberden's description was published five months later, it is true,
but it was so acute and comprehensive that, while later authors have tried
their best to confuse it, they have found little to add to it.

2 The most apt instance cited by Morgagni is in the 26th chapter (xxvi. 31) ;
but he makes interesting allusions to the disease in several passages.

sec. ii HISTOEY OF THE CONCEPT 217

Willis 1 under the general head of Asthma convulsivum ; by E. A.
Miiller 2 as Asthma occultum siccum — asthma was confounded
with angina by our forefathers as scarlet fever and measles, and as
typhoid and typhus, were confounded, and as cardiac dyspnea and
asthma are confused to-day — and by Hoffmann (in his Medicina
Consultatoria, early eighteenth century) as Prsecordial asthma.
Hoffmann's3 example was a definite case of the disease.
Senac, under the head of heart diseases, speaks of attacks of
pain, " Cujus paroxysm! summe procellosi majorem incutiebunt
terrorem " ; moreover of a certain patient " pectoris anxietate
molestissima laborabat." Morgagni first described the brachial
numbness and the aortic lesion. By writers such as these the
series was gradually defined and named, and so the matter
stood until, in our own generation, alien processes were
stuffed into this clinical conception, whereby the standard
idea has been blurred and the attention of the student dis-
concerted. This muddling of standard clinical concepts is a
new temper, and to be seen in other clinical fields. Thus
into Epilepsy certain loose thinkers are thrusting series of
other kinds, syphilitic or ursemic for instance, merely because,
although of alien nature, they are attended by convulsion ;
into Asthma, as I have said, any paroxysmal dyspnea : and
so again under the labels chorea, chlorosis, etc., diseases
alien in nature are intruded. To rest content with our patterns
would be a contrary error ; we must always be revising them,
winnowing the casual from the primary and cardinal phenomena,
and detecting deeper and deeper affinities. Moreover some names
and types of recent mintage, such as neurasthenia or rheumatoid
arthritis, which have been long under criticism, may on good
grounds be called again and again into question, and certain
particulars redistributed. But when one of the most distin-
guished of living physicians writes as follows, " One may still

1 On p. 541 col. a of the edn. of Willis in my possession ( Venet., 1708), the
case is " Senex perhonorificus, multis magnisque titulis insignitus, iisdem
omnibus major," who complained of a paroxysmal pain at midsternum — attacks
often at night — without dyspnea (" sine quavis tamen dyspnoea ") " or other
sign of asthma." For these reasons the case was regarded as exceptional ;
asthma Willis attributed to spasm of the muscular tissue of the bronchi, and
of it dyspnea is an essential or primary feature.

2 Op., Geneva, 1736, p. 439.

3 Hoffmann, Op. Omnia, Geneva, 1753.

218 ANGINA PECTOEIS pakt n

read of angina pectoris as a separate and fatal affection of the
heart, instead of its being regarded as a painful incidence of
varied significance that may occur in the course of a wide range
of functional and organic diseases of the cardio- vascular system,"
do we not perceive that there is a danger in looseness of
speculation as well as in tightness of definition ?

In a roving quest the eye is too readily caught by prominent
phenomena or analogies which may have no deep significance,
while the inward affinities of things are overlooked. Thus if to
call a whale a fish be consistent with good poetry, it is certainly
inconsistent with good science. So, speaking generally, it
has been of late with angina pectoris : instead of penetrating
to its deeper affinities, dwelling upon these, comparing them
with the deeper affinities of similar processes, and classifying
them severally by the profounder likenesses, too often the
eye of the modern physician is so caught by shallow analogies,
by taking and superficial semblances, that incongruous groups
or heaps are thrown together with a shovel. For instance, in a
recent interesting article, the writer, studying the anaemia of
tuberculosis and demonstrating truly its deeper qualities, con-
trasts them with the deeper qualities of chlorosis, so as to illus-
trate their profound dissimilarity; and yet in conclusion he allows
himself to name this ansemia " tuberculous chlorosis " ; that is,
he continues on superficial likeness to classify together processes
which it was the purpose, or at any rate the purport, of his article
to contrast and divide on lines of intimate difference. If
such is to be our way of naming, all nomenclature, all classifica-
tions indeed, must come to confusion ; and the laborious differ-
entiating work of clinical medicine, from the time of Hippocrates
to this day, will be brought to nought.

Still, dismissing all these distractions of meaning, the reluct-
ance of modern teachers to concede to angina pectoris the
title of a Disease is not quite accounted for ; there must be some
grounds, good or indifferent, for the demur. If indeed it were
true that angina pectoris is " only a symptom," this denial to an
unattached phenomenon of full recognition as a disease would
be justifiable. One symptom — a toothache, for instance — may
enter into many a clinical series, and be a criterion or a constant
of none. When I am told that hemiplegia is a " symptom-

sec. ii ITS UNIFOKMITY AND TITLE 219

group," and yet not a disease, I regard it as neither : I have
said that a symptom does not become a " symptom-group "
because it is a big one ; hemiplegia is but a symptomatic event
in the course of several diseases, such as granular kidney,
hyperpiesia, epilepsy, poliomyelitis, and so on. As I have said, it
may be regarded as a few terms common to several diseases ;
two or more having, for a short distance, what railway men call
"running powers " over the same line. But if, as I shall argue,
and as we shall all have to admit, angina pectoris be not a
symptom but a complete morbid series — that is to say, from
beginning to end a fairly uniform association and succession of
many symptoms positive and negative, and if by the word Disease
we mean such a series, — and what more by it can the physician
mean ? — then angina pectoris occupies its place in our minds as
a characteristic clinical concept, and our convenience dictates
for it a particular label. Yet notwithstanding, as this reluctance
so to accept it continues, an excuse may be found in the
shifting explanations of the pathology of the anginous process.
It is true we are not yet agreed upon the pathology of this
disease, whether static or dynamic ; but are we not still more
ignorant of the pathology of Chorea, of Epilepsy, of Pneumonia,
and of many another series to which, without a breath of
dissent, we attribute uniformity enough to justify definite titles as
Diseases ? And is not angina pectoris as consistent a series as
any of these ? The books, only too unanimous in their con-
sistency, copying one from another both errors and truths,
endow it with even more uniformity than by nature it has. For
instance the text-books, almost without exception, state that
the pain in angina pectoris is " precordial " ; whereas in the
vast majority of cases it is in the upper sternal area : precordial
pain in angina is rare, and generally incidental.

Does it not seem then incredible that a series of events so
grave, so complex, so complete, and so fairly uniform should
consist now in one chain of causes, now in another and widely
different chain ? Surely we must concede that as a clinical
series approaches uniformity its causes must also be approxi-
mately uniform. Caution in accepting any alleged chain of
causes as that on which angina pectoris depends is a scientific
suspension of judgment ; but eagerly to contend that so signal an

VOL. II P

220 ANGINA PECTORIS part n

evolution of peculiar and menacing features may be caused now
by this set of antecedents, and now by that or the other widely
different set, is surely not suspension of judgment, but a suspen-
sion of thought itself ? Dr. Colbeck well expresses the opinion,
which he kindly attributes to me, that if the title of angina
pectoris be used to include a variety of symptom-groups which,
although they may present a superficial clinical resemblance,
yet in their etiological and pathological relations differ widely
and fundamentally, all definite use of names comes to an end.1
No, angina pectoris, as it has its peculiar features and march,
must have its own independent and definite pathological basis
and interpretation.

1 Colbeck, "Angina pectoris," Lancet, March 21, 1903.

CHAPTER II

SIMULATIONS OF ANGINA PECTOEIS

Mock Anginas. — Let us then, if we are to understand this
disease, determine to repudiate what I have called classification
with the shovel, and, discarding superficial resemblances belong-
ing to other and widely different issues, return to classification
by intimate affinity. Let us dismiss from co-ordinate classifica-
tion all " pseudo-anginas " and other echoes, which from this
point of view are will-o'-the-wisps.1 I cannot undertake to
describe all the phantoms, whether genuine nerve storms or fanci-
ful, and even ephemeral phenomena, which have been piled upon,
and so overlain, the conception of angina pectoris as to hide
from us its austerer features. Elaborated tables are dressed
up, as it were for students' examinations, of the marks of dis-
tinction between false anginas and the true ; tables of which the
valuable lesson is not their resemblances but their polar estrange-
ments. And meanwhile, not invisible to the eye of the discerning
physician, through all this crowd of competitive disorders — com-
plaints " which," as Broadbent with playful exaggeration used
to say, " never interfere with a pleasant engagement " — the pale
horse of the mortal disease takes its inexorable way. The
appearance in these dreadful lists of unsubstantial functional
disorders seems fantastic. I do not say that none of the
mock anginas is grievous, some of them if not very alarming
are distressing enough and importunate enough ; nor do I assert

1 Dr. R. 0. Moon and some other writers (Clin. Journ., March 12, 1913)
call the mock angina, which Dr. Moon fully recognises as false, "Angina minor,"
which unfortunately signifies a process of milder degree but of the same nature.
But with much else that is useful in diagnosis he does not fail to repudiate
the pseudo-anginas. I still call " stenocardial oppression " (p. 287) A. minor,
because, though milder in degree, it is of the same nature.

221

222 ANGINA PECTOEIS part n

that from them nothing is to be learned for the interpretation of
some secondary phenomena of angina pectoris ; but to confound
these alien series with angina pectoris itself, and to give them
this solemn name, even with a difference, seems to smack of
the ingenuity of scholastic logic rather than of that discernment
of premises and origins which is born of scientific method. For
when we essay to compare the mock anginas with angina pectoris,
as in the world of practice we see it and them, they are manifest
as fakes. As a student of cardioarterial disease, towards whom
there has been a drift of cases of this kind, I do not hesitate to say
that a physician of experience should not feel more than a passing
doubt concerning any one of these illegitimate claimants. And as
a name Pseudo-angina will never do ; no category can be founded
upon negation. Sir William Go wers, whose insight into the deeper
relations of disease is so highly esteemed among us, has swept
out of our way the mock anginas, with the other more important
of this kind of comparatively trivial maladies, by putting them
into a family of their own, under the significant title of Vaso-
vagal Disorders.1 There let them stay, while in the meantime
we may learn from them new lessons in pathological kinships.

Still it is of such primary importance to realise precisely what we
are to discuss that I must be forgiven if I insist even a little longer
upon this purging of the subject. If the reader will devote
a few hours to a perusal of the older writers on angina pectoris,
of the authors of the end of the eighteenth and beginning of the
nineteenth centuries, with their truer sense of clinical form, as
he returns to modern medical writings he will note with some
bewilderment that he is leaving the solid ground of the
natural history of disease for the quagmire of clinical
sophistry. Heberden, Jenner, Fothergill, to name but a few
of the more familiar authors of the eighteenth century, not only
kept a watchful eye upon the patient, but kept also a due sense
of the relative values of the facts, an appreciation of the facts
that matter ; whereas the more rolling and speculative eye of
the modern professor is apt to wander. Accordingly all these
observers take for granted the truth that in every case of angina
pectoris there is some grave lesion, and that in the very few
necropsies published as negative some such lesion had been over-
1 Gowers, Sir W., Lancet, June 8, 1907.

sec. ii VIEWS OF OLDER PHYSICIANS 223

looked. That angina pectoris is a definite organic disease of the
utmost gravity our forefathers never forgot ; accordingly, in
this seriousness, they charted its symptoms and learnt its signals
the more accurately, and were not easily carried out of their
course by mirage. Our forefathers had to hug the shore ; we who
fetch a wider compass are tempted to sail out of our bearings.
In making their diagnoses of angina they weighed not only this
feature and that, but the whole series to which they belonged,
and the issues to which they tended. And, in the next genera-
tion, Latham thus sagaciously mistrusted the notion of a mere
functional, or " nervous," angina pectoris. He named the counter-
feit angina — angina notha ; but it is better both for doctor
and patient to avoid for it the name angina altogether. These
observers were not beguiled by such equivocal phenomena as
palpitations, arrhythmias, pantings, nervous flusters and crises,
and other spectres of the mist ; and, guided by pilots so sagacious,
the reader feels secure of their evidence and their judgment, so
far as they go. The extraordinary acuteness of Morgagni was
here again not at fault ; after speaking of high arterial pressure
as a plenitude in which the arteries could neither be more dis-
tended nor contract upon their content, he says there is a pressure
of another kind :1 "at another time we may perceive (a different
land of plenitude) the coats of the arteries contracted by the
nerves, which is especially apt to occur in hysterical patients, the
arteries being then reduced to mere filaments, so far, indeed, that
in some regions the pulses are suppressed, and these parts turn cold
while other parts remain warm." He adds that these phenomena
may supervene in graver maladies also. It is with a different
apprehension, with a sense of equivocation, that we follow the
erratic course of some essayists on angina of our own day, who
drift in " unaccountable diagonals between truth and falsehood "
— between, in this instance, angina pectoris and the masquerades
of it which, as Dr. James Mackenzie well says, are only " cloaks
for our ignorance" ; ignorance the less venial as those forefathers,
who saw at least as much of gusty nerves as we do, had left

1 Morgagni, De sedibus, lib. xxiv. c. 12, "alias ob arteriarum tunicas, ab nervis
contractas, ut in hystericis praesertim contingit, cum arterias ad tenuis filamenti
modum redactas percipimus, imo et pulsus certis in partibus supprimuntur,
unde tunc illae, reliquis calentibus, figent."

224 ANGINA PECTOEIS paet n

their charts behind them for our guidance. It has been well said,
on another matter, that " the continual use of a nomenclature
in which essential distinctions are ignored closes the mind to the
very existence of those distinctions."

Lartigue 1 is claimed by French writers as the first influential
physician to fog the picture of angina by throwing these cross
lights upon it ; but Forbes had fogged it before him.2 Forbes
declared that in about 50 per cent of cases of angina there
was no organic disease, and that in the rest it was associated
with all manner of organic cardiac and aortic lesions. To
Landois (1863) belongs, it is said, the doubtful credit of having
dragged the vasomotor red herring, and invented the misleading
title of Angina vasomotoria, or reflectoria. Walshe was tempted
to follow ; but it is to Nothnagel 3 chiefly that we owe the tran-
scendent confusions of recent authors. No wonder the descrip-
tions of angina vasomotoria are various and inconsistent ; that
for example, as Dr. Mackenzie says in his work on " The Pulse,"
the descriptions of Sir E. Powell and Nothnagel bear no mutual
resemblance. How far Nothnagel had wandered, and wander-
ing led others astray, I did not myself fully comprehend till
I consulted the article on Angina pectoris — or on the ghost of
it — in von Ziemssen's Encyclopcedia. This article, guaranteed
as it is by a distinguished name, can scarcely be acquitted
nevertheless of perversity, and even of levity ; for surely
it is levity to confuse the squalls — nervose Angstzustdnde —
of unstable " neurotics," mostly women, with the assault of
one of the fiercest and most searching afflictions which can
fall upon steadfast and resolute men. It is scarcely credible
that in this Encyclopedia under Diseases of the Circulation
angina pectoris has found no place ! After long search I
discovered it at last elsewhere, under the fanciful headline of
" Vasomotor and Trophic Neuroses," and placed between such
strange bedfellows as Progressive Muscular Atrophy on the one
side, and Graves' Disease on the other. Could professorial
pedantry be more extravagant ! unless, indeed, it be surpassed
in this very article by a comparison of the pain of angina with

1 Lartigue, Mem. sur I'angine de la, poitrine, Paris, 1846.

2 Forbes, Cyclop. Pract. Med., 1832.

3 Nothnagel, Deutsche Arch. f. klin. Med., 1867.

sec. ii SOME MODERN NOTIONS 225

that of colic, of " hysteralgia," or of heartburn (" cardialgia ") !
But the most egregious example of this eccentricity which I have
noted is the description, by a well-known modern physician, of a
case of " angina pectoris originating in the clitoris ! " Such is
the exorbitance to which by looseness of language we may fly ;
for surely to confound spasms, throbs, and vapours such as these
with an affliction so awful as angina pectoris, is, I may reiterate,
to lose sense of the relative value of facts, to ignore in the stream
of function the facts that matter, and to take analogies and
shallow semblances for natural affinities.1 The vasomotor de-
rangements which form the staple of the lapses which, after
Sir William Gowers, we will call Vaso-vagai Disorders, are, it is
true, no uncommon accompaniments of true angina, as they are
of other paroxysmal irritations of afferent nerves, and vexations
of corresponding spinal segments. One claim to consistency
indeed that encyclopaedic article can make in its scarcely veiled
grudge against certain unconformable facts of the very disease
which is its nominal subject ; namely, of angina pectoris
itself.

Against such fantasies naked sense is an unequal adversary,
so it is a matter of regret rather than surprise that some con-
temporary, and not inconsiderable, English writers on this
subject have been so influenced by them as in their turn to
admit under the title of Angina pectoris a like medley of
heterogeneous disorders. Even Gibson was bold enough to opine
" That true angina pectoris results from reflex, vasomotor,
neurasthenic and hysterical causes is now beyond the region of
doubt ! " But if we are to place " true angina pectoris . . .
beyond the region of doubt," we must begin by stripping the
" true " idea of false conceits. What would my lamented
friend have said of me had I classified functional and organic
hemiplegia together, or put hysterical convulsions with epilepsy !

Now the vasomotor phenomena of angina may be discriminated

1 Pal's brilliant tract, seductive on a first perusal, is so largely hypothetical
that it does not gain on further acquaintance, but loses rather. Many of the
cases quoted are of dubious diagnosis ; and we are often left in doubt whether
rises of pressure were cause, effect, or correlation. Indeed one begins to doubt
if it contains more than in a pedestrian fashion we knew before. Why for
claudication is any spasm necessary ? The condition is one of reduced potential ;
depleted stores, often due to damaged vessels.

226 ANGINA PECTORIS pakt n

as (a) the Secondary or Concomitant, and (6) the Accessory ; of
primary importance there is none (p. 283). The Secondary sym-
ptoms are the fringe of the case, and may not concern the patient
very much, if at all. We all know the pale face and cold ex-
tremities of renal colic ; nay, every man who, when he is hurt,
flushes or turns pale is familiar with this vasomotor sequence of
pain. By various repeated or severe irritations of sensory areas
we may call forth secondary vasomotor disturbances, almost at
will. The Accessory, those which consist in such intercurrent con-
tingencies as chill or emotion, if they may determine the moment
of an attack, no more constitute it than the detonator constitutes
the torpedo ; but of these epi phenomena I shall say more presently
(see p. 340). Thus Dr. Morison agrees with me that in this way
a rise of blood pressure may be the consequence of an attack of
angina, as at other times it may be a proximate and determining
cause of it. For instance, on another disease, an author, whose
book lies on my table, writes as follows : " On rubbing the pain-
ful area the pulse became very small, the face ashen, and sweat
arose in the hands and axillse." We all know how commonly
an aching in the areas of the 6th to the 8th dorsal nerve on the
left side is associated with states of debility and vasomotor
disturbance ; and not in women only. So long ago as 1870,
at the meeting of the British Medical Association at Newcastle,
I commented upon cases such as this : "A young woman com-
plain s of tingling, numbness and weight in the left arm and leg. She
fears paralysis. She has also pains radiating about the brachial
plexus, including the intercosto-humeral branch. When the pain
is severe, arise also heats and chills, flushings, strange visceral
sensations. On enquiry we find she has lately been confined,
is suckling a big boy, is menstruating, and at the same time has
been troubled with diarrhoea and want of appetite. We note
also characteristic tender points in the usual places, especially
in the submammary intercostal area — a part from which such
disturbances often take their rise, and where in this case the
severer attacks begin ; indeed she is never free from aching in
this place." It was then more necessary than it is now to point
out the distinctions between these cases and organic disease,
whether cerebral or cardio-aortic ; and are we to turn back to
such confusions ! A large proportion of the cases of " false

sec. ii VASOMOTOR STORMS 227

angina " under my notice have been associated with a more or
less severe intercostal pain of this kind.

The paths then by which pains are propagated outwards
may serve also for the inward penetration of external influences.
Barie records such cases, and we may witness good examples
of it every day. But — and this is an interesting reflection on
my view of angina pectoris — while by radiations apparently from
without inwards we often find that the heart is vexed, in anginal
attacks, in which the aorta is usually the commencing term of
the series, as a rule it is not. Thus in severe penetrating intercostal
neuralgia, for instance, the heart is often much disturbed (see
p. 227 et seq.) ; wherein lies one of the sources of a gratuitous con-
fusion between such cases and angina : * gratuitous because cardiac
disturbance is not a character of angina. Yet, if intercostal
neuralgia be eminently capable of producing vaso-vagal storms,
it is by no means alone in this capacity. Some years ago I saw
in consultation a lady afflicted with a suppurative disease in the
pelvis for which severe surgery had compassed but a partial
relief ; she was weak and emaciated, and suffered from attacks
of violent but apyrexial pain in the right pelvis. One of these
attacks I witnessed on my visit — it began with a general vaso-
motor constriction, pain under the left breast, cardiac turbulence,
panting, and much agitation. Vasodilatation and sweat suc-
ceeded the spasms. Many of the attacks consisted only in the
intercostal pain, pain which in extreme attacks radiated into the
brachial plexus. But the whole aspect of this side of her case was
" neurotic." In many such cases there is no pain. Not long ago
a lady had " one of her attacks " in my consulting room. As I
was feeling her radial pulse, the artery, as Morgagni remarked,
rather suddenly shrank to a thread, and then ceased to be per-
ceptible. Tension rose high in the larger vessels ; the breast
and heart became oppressed and the respiration panting ; but
there was no pain. Such attacks often depend on urogenital,
abdominal, or other visceral lesions or dislocations, or even on
carious teeth.

1 The signal of caution is never absent from the medical path. While
writing these lines I recall Frantzel's remarkable story of Jules Ferry, who
died of angina after a wound of an intercostal nerve. The record as it stands,
and so the diagnosis (Herzkrankheiten, p. 224), are however ambiguous.

228 ANGINA PECTOKIS part n

In the following case again the vaso-vagal symptoms became
detached from the pain :

Miss E., set. 48 — a pallid blinking spare woman. Dysmenorrhea
till menopause three and a half years ago. Ardent temperament and
full of active and useful works. Has had domestic trials and nursing
cares for some time, but worse last two years ; pains in intercostal
and brachial nerve areas. Violent pain, precisely in region of cardiac
apex, radiates into left arm — "in the bone"- — she indicates the whole
thickness of the arm, especially the outside aspect. Also in shoulder
blades and down the back ; never in the neck or face, but may reach
the occiput. With the pain she becomes cold all over, and prostrated,
and thus remains for 5-6 hours ; then the circulation " begins to
move again," and warmth returns, followed by flushes and profuse
sweating. But during the last few months the pain has wholly ceased,
and only the vasomotor symptoms persist. The attacks are relieved
by nitrites. Physical examination, etc., wholly negative, except
some small patches of anaesthesia, and slight contractures. These
used to be far worse, especially at the catamenial periods. I find
no note of the visual fields.

In one of his cases of this kind von Basch found in the con-
strictive phase that the blood pressure rose to 170 and 200 ; a few
minutes later it fell back to normal.1 Pain or no pain, to call such
functional vacillations as these by any name even distantly
suggestive of angina pectoris is surely chimerical. Yet Sir Richard
Powell,2 whom, as one of the most eminent of living authorities on
this subject, I cannot pass over, says : " In a large proportion of
cases angina is an entirely functional disorder, the main feature of
which is sudden increase of blood pressure, and a corresponding
call on cardiac effort. . . . The vasomotory are the most in-
tense forms of angina. ... In many cases angina pectoris
is dependent upon a disorderly action of the vasomotor nerves,
and is associated with a sound heart. In many other cases
we have a similar mechanism but cardiac disease in the back-
ground (" Secondary Cardiac Angina "). . . . In numerically
a comparatively small, although very important, group the
anginal failure is due primarily to Cardiac disease ; Syncopal
angina or primary cardiac angina." I cannot but regard this

1 This record may have depended in part upon resistance of the tight
arterial coat. (See Vol. I. p. 72.)

2 Powell, R. D., Lancet, June 29. 1901.

sec. ii VASOMOTOR STORMS 229

comparison as one of superficial, not deep, resemblances, of
analogies not of homologies or of affinities.

Again, of the so-called " vasomotor " angina let me select
another even more interesting example :

Mrs. X., patient of Dr. Mallins of Watton, set. 52 ; seen November
1910 ; menopause over five years ago, without serious trouble. As
on my visit she lies in bed, about midday, has the aspect of health
both mental and bodily. A very intelligent, capable woman. No
specific signs of hysteria. No globus. Plantar reflex, ovarian and
cutaneous sensitiveness, etc., normal. Tendon jerks not excessive.
In her past history the only relevant event is of rheumatic
fever many years ago ; without however any cardiac effects —
as verified by Dr. Mallins, by Dr. Mitchell Bruce (whom she
had consulted a year before), and now by myself. She leads a
happy and placid life, and has had no worries. She tells me
that, as she converses with me (about 1.30 p.m.), she feels quite
well ; but almost daily " about tea - time " attacks come on of
a kind which, for a few years past, have increased upon her both
in degree and frequency. As she fives at some distance from Dr.
Mallins, the attacks have not been witnessed — not at any rate in their
full course — by an expert eye ; but she gives a clear description of
them. Rather suddenly (as in Nothnagel's cases) she turns cold,
very cold if out of bed, but in bed — where she has been staying for
a few days as an experiment — with a less severe chill, a general cool-
ness all over the surface of the body. About the same time she feels
a " huskiness " in the throat (larynx ?) (no cough or expectoration
at any stage), and the respiration becomes faster and faster until
she is panting — in and out, not with a fixed chest — at a great rate ;
rapid shallow breaths. Meanwhile an oppressive weight gathers
upon the upper chest almost to suffocation — she sweeps her hand
over the whole breadth of the upper thorax above the breasts,
and a pain arising " at the heart " strikes up the anterior left axillary
line, but never enters the arm ; of this she is sure, though it is prone
to run up more or less into the neck and about the left shoulder
(phrenic ?). Still the chief seat is " at the heart," and up the anterior
axillary line. In answer to the question, " Where is your heart ? "
she points precisely to a spot in the seventh space about the size of
a florin, well below the heart's apex and abutting upon the left costal
arch. This spot, always tender to touch, during the attack is ex-
tremely painful, with a continuous acute pain. After an attack the
touch of the stethoscope on the spot is for some hours intolerable.
On investigation I found another definite tender spot also about the
issue of the seventh thoracic nerve close to the spine ; of this tender

230 ANGINA PECTOEIS part n

spot she was aware, but it had not annoyed her so much as the anterior
spot. During the chilly stage of the attack, besides the oppression
and panting, she has an alarming sense of cessation of the heart's
action. On being reminded that in health we ought not to be aware
of the heart's action, she adds that the suffering is not negative, but
" as if in stopping the heart gathered itself into a heavy ball." The
temperature is normal throughout. Concerning any changes of
complexion during the attacks there was no definite testimony.

After a while of this chill and oppression— perhaps twenty to thirty
minutes, perhaps less, for in suffering time seems interminable — she
flushes all over, the arteries begin to throb, and she tingles and burns
with returning tides of hot blood bounding through the vessels ; a
stinging pulsating heat, uncomfortable enough but almost welcome
in the rapid solution of the oppression at the chest, and of the panting.
The attacks are followed by a sense of great prostration or exhaustion ;
but after a night's rest she feels quite well again.

At the time of my visit no dulness was to be detected about
the arch of the aorta ; the subclavian and other accessible arteries
were soft, or impalpable ; the blood pressure was rather below than
above the normal ; the artery was not then small or wiry. The
heart was free from signs of disease, and betrayed no abnormality
of stresses or of rhythm. The spleen was not enlarged.

This patient, in the exercise of self-control and common sense,
had done her best to avoid apprehension of the attacks. She
had often persuaded herself that the attack of the afternoon
would not — should not — return ; but in vain : determined,
convinced, even preoccupied as she might have been against it,
in spite of herself she was seized. She cannot think that auto-
suggestion has any great part in the return ; or that therapeutic
suggestion would prevent it. The only possible toxic cause
Dr. Mallins and I could suspect was a " rheumatic " tendency,
of late years hanging about her in the form of " fibrositis " ;
especially in the fibrous structures of the knees and ankles. At
the time of my visit, when she had been some days in bed, there
was nothing to detect except a creaking left knee ; though when
about, and in damp weather, these parts were wont to swell.
We had no hesitation in recognising her seizures as the " vaso-
motor angina " of Nothnagel and others. The patient said
that the initial disorder was the chill, the next " huskiness " ;
then rapidly ensued the oppression at the upper chest and the
panting. This oppression, described as very severe, may have

sec. ii MOCK ANGINA 231

a/

been due to high tension of the aorta consequent upon extensive /
areas of vasoconstriction ; and in a diffuse bulbar discharge the
heart may also have been involved directly.

After emphatically reassuring the patient, we prescribed the
administration of atropine in doses of T^th of a grain twice a day.
Ten days later Dr. Mallins wrote : "On the next morning she
began the atropine ; and on and from that day the attacks were
reduced to quite miniature affairs, which, on the fifth day there-
after, disappeared altogether. This relief was at the cost of
intense dryness of the mouth ; so that I have reduced the dose
to once in the day." To re-educate the vasomotor system,
the practice of a simple hydrotherapeutical method was also
recommended ; but these measures — the season being winter —
had scarcely been begun, and could not have had much effect
in the first mitigation and final banishment of the seizures. But
I may add that we had applied a small blister on the back, over
the place of exit of the seventh dorsal nerve.

Now, taking these phenomena at face value, do such
characters resemble angina pectoris even superficially ? Have we
any more reason to call these cases angina pectoris than to call the
well-known throbbing of the abdominal aorta in women angina
abdominis, or aneurysm ? The so-called " heart pain," present
in many, if not in all, of these cases, the sense of distension of
the whole upper chest, often with submammary pain and intense
local hyperesthesia, are neither in seat nor kind like the pain of
angina ; the breathing, far from being held as in angina, is pant-
ing ; the bodily state is not awe-stricken, but restless and agitated.
Upon this contrast Huchard repeatedly and emphatically insisted.
That angina pectoris, like any other painful disorder, may be
accompanied by vasomotor disturbance, is true ; so epilepsy may
be, so may be migraine, so ague, and so on ; while, on the other
hand, angina pectoris may be, and indeed often is, quite free
from these epiphenomena.

We have, all of us, a plenty of such cases in our notebooks,
so I forbear to narrate many of them. Before Huchard's
book was published, Peyer of Zurich 1 and other authors had
demonstrated the differential features of these mock anginas.

1 Peyer, Wiener med. Presse, Juni 16—26 and Aug. 2, 1892 ; very interesting
papers.

232 ANGINA PECTOKIS part n

In Peyer's practice many cases had been in males, often in
anxious overworked students. In some cases he noticed the
periodicity, as in Dr. Mallins' case ; though more usually
the attacks were irregular in recurrence, or were subcontinuous
with exacerbations. Attacks sometimes came on in the night,
e.g. 2 a.m. In young men seminal emissions and frequent mic-
turitions were often present. Peyer also laid stress upon the
diffused oppression of the upper front of the chest, upon the
submammary seat of the lancinating pain, and upon the cardiac
sympathy — palpitations, throbbings, and clutchings, as if the
heart were too big ; all, as he points out, being, like the dyspnea,
features differential from angina pectoris. In such patients the
whole history and bearings of the case are distinctive. And yet
Gilles de la Tourette x proposes the pulse as a criterion ! After
saying that in the neurotic kind " rien ne manque au tableau,"
he offers as our guide that in the true angina the pulse is " small,
miserable and even intermittent," but in the neurotic kind "ample,
full, and regular." The difference between " ample " and " plein "
is not obvious ; and his diagnostic points of angina suggest that
the learned author will command most attention in his own field.
Curschmann 2 again, an accomplished physician whose death we
are regretting, wrote likewise that in pseudo - angina all the
symptoms of the genuine cases occur ("alle Symptome wie bei
echter Angina Pectoris " !). To prove this he quoted rapidity of
the pulse, palpitation, pain at the heart, and sense of oppression
to the degree of losing one's self (" Vernichtungsgefuhl ") ; none
of them characters of angina, in which, by the way, the mind
is generally only too clear. He added that in vaso-vagal
attacks the pulse never disappears from the wrist. Twice
at least in such cases I have felt the pulse slowly diminish
till it became impalpable, and the patient " far off," or tran-
siently unconscious (p. 227). I may observe that in many of
them the crimping of the vessels seems, at any rate in large
part, to be musculo - cutaneous. Conversely, in his argu-
ment against Huchard, Curschmann describes cases of " Vaso-
motor angina," of which three were fatal, and after death
presented coronary arteriosclerosis, to prove not that, like the

1 G. de la Tourette, Stats neurastheniques, Paris, 1898, p. 23.
2 Curschmann, Lehrbuch d. Nervenkr., 1909, p. 832.

sec. ii MOCK ANGINA 233

rest of us, lie made mistakes in diagnosis, but that pseudo-
angina and true angina are the same disease ! Upon the
symptoms of these fatal cases he was judiciously silent.
Weintraud, although writing in Eulenburg's Lehrbuch,1 speaks
with far more clinical discernment, not being a " nerve-
specialist." So far, in his opinion, are the vaso-vagal attacks
from " presenting all the symptoms of the genuine angina " that
he draws a clear contrast between the two maladies, and points
out that " the spurious form is merely a nervous malady
which has nothing whatever to do with heart disease."
Gallavardin 2 first classifies the mock with the true form, and
then labours to show how profoundly they differ ! Neusser
(loc. cit. on p. 303), though the very inventor, I believe, of
the coronary cramp conjecture about true angina, if he does
not discard these false anginas, says frankly, against his com-
patriots, that " The majority of these forms have only in few
features any similarity to true stenocardia." Shall we not then
agree with Dr. James Mackenzie that " Pseudo-angina pectoris is
a useless and misleading term ; and it is time it was dropped out
of medical literature " 3 (author's own italics) ?

Some writers thrust these counterfeits upon angina because
of alleged intermediate instances. Now, although I have said
that by intermediate cases one may step from any one disease of
our nosology to any other, yet it is contrary to experience,
at any rate to mine, to say that between these nervous storms
and angina pectoris transitional cases are frequent and equivocal.
The pain is different, the pulse is different, the panting is different,
the behaviour is different, the storm is different, the duration
is different, the causes are different, the issue is different.

This case, I suppose, would be styled transitional or ambigu-
ous ; of a lady of middle age, whose case a short time before had
been diagnosed by an eminent London physician as angina pec-
toris. As he found her to be the subject also of " fatty heart," I
assume that he regarded the case as angina in the proper sense,
or at least as one of the " dilemma " cases. But, from an angina
point of view, I was surprised to find that an intense orthopnea

1 Ed. 1905, ii. 325.

2 Gallavardin, Mai. du cceur, 1908.
3 Mackenzie, Jas., Heart Diseases, p. 52.

234 ANGINA PECTOEIS part n

was a part of the attacks, and one of these fortunately took place
during my visit. Had my distinguished friend realised this feature,
which presumably he did not witness, I think he would have
hesitated in his opinion ; for although a " fatty heart " may be
curiously negative as to its signs (see p. 46, etc.), with such dyspnea
other evidences of cardiac failure should have become manifest.
But there was no lung crepitation, no tenderness of liver, no
cyanosis, no fulness of cervical veins ; and, save for some accelera-
tion, the cardiac sounds and rhythm were normal. As the patient
in her respiratory strife seemed to pay no heed to us, I said
in a low voice to my colleague how odd it was that the alae nasi
were not distended. The nurse, of whom afterwards we made
some further enquiries in another room, dropped the remark that
as we left the bedroom the patient had asked her what was meant
by the alae nasi ? On our return the alae nasi were working
actively ! We plumped for hysteria, and treated the case
accordingly ; recovery was rapid and complete, and in a few
weeks the lady was shopping in London, on foot. But as
another example of the more ambiguous kind of cases, I will
allude to the following instance :

Male I saw in consultation on suspicion of angina pectoris. The
patient, a man of calm temperament, had suffered pain in his left
arm, and from time to time from certain faints or confusions of sense.
We were able however to detect the tender points usual in brachial
neuritis, and the reactions in him were peculiarly ready, for to press
on a certain point of the hand " made him feel queer," and he begged
me to refrain, for a sharp and unexpected pressure there had " more
than once made him faint right off." But I will not digress into
a fuller story of this very interesting case of brachial neuritis with
a good deal of vasomotor disturbance, which in some respects
simulated angina. Of angina there was no evidence.

But I will not multiply illustrations of the vasomotor
concomitants of irritation of sensory tracts, for almost any day
we may find cases upon which to test and study them.

It seems probable that in all such cases the first vascular
oscillation, however transient it may be, is constrictive, with a
relative rise of central pressure ; although in some a dilatation
with falling pressures quickly becomes dominant. Even in
typhoid, or other visceral, perforation it is stated that a

sec. ii MOCK ANGINA 235

transitory rise of pressure precedes the substantial fall ; and
in chronic diarrheas, such as sprue, just before a large evacua-
tion the pressure is found to rise sharply for the moment,
and after the discharge to fall below the mean. And when
constrictions occur suddenly over large areas, and are far
more persistent, however free the organs may be from static
disease, this exaltation of pressures often causes intense dis-
comfort ; and, as pressures vacillate, faintnesses, oppressions,
pantings even to orthopnea, throbbings, palpitations, flushes,
and other agitations, appear in sundry degrees and combina-
tions. Intercostal neuralgia occurs usually in women, or fragile
men ; and in them, as the attacks are multiplied, vasomotor
stability is more and more readily broken down. But, so
long as heart and blood vessels preserve their normal struc-
ture, these faintnesses, palpitations, gaspings, stiflings, bodily
agitations, hyperesthesias, and psychical commotions are as
wholly unlike the ruthless grip of angina pectoris as their
frantic alarms are unlike its silent passion.

It is curious, as in the case last quoted, to see how often
in these patients pressure upon the tender spots will excite or
exacerbate the vasomotory seizures. The general condition of
such patients also, the story of the case, and the tests of Weir
Mitchell's or other "antineurotic" treatment, confirm a diagnosis
which should very rarely present any real difficulty. Hase-
broek's cases x of so-called " Angina pectoris," cured by such
methods, were assuredly no more than phantoms of this sort.
Let me reiterate that it is notable in the spurious attacks
how obviously the heart is upset ; we note palpitations,
arrhythmias, sudden stoppages and accelerations, and so on,
which are not characters of angina pectoris. In the neurotic
cases the labile medullary centres seem to act more as an
aggregate ; respiratory, cardiac, and vasomotor balances vacillat-
ing more in unison, as they do in the ailments of children,
whose centres are less stable and independent. It is remark-
able that, in the bulbar area, the intense afference of angina
seems more contained, especially if the attacks be infrequent ;
for in many cases vasomotor sympathy, far from being
ascendant, is insignificant. In angina, as in migraine, a dis-
1 Hasebroek, Deutsche Arch. f. Iclin. Med. Bd. lxxxvi.

VOL. II Q

236 ANGINA PECTORIS part n

order often classed on superficial analogy with angina,1 the
secondary vasomotor phenomena, if afterwards expansive, are
also at first constrictive ; so that in angina some areas of the
surface of the body — especially the face and left arm — turn
pale. We shall see that although generally in angina the face
turns pallid, and the radial artery shrinks, this is not always
so ; the face may be flushed from the outset, and the artery
expanded {vide p. 341). As however I have surmised already,
even in these cases of migraine and angina some transient
moment of constriction may precede, but so transiently as to
escape observation. Indeed in this way vasoconstriction often
becomes an active part of angina : a movement or an emotion
raises arterial pressure, by this the sore parts are annoyed and,
the medullary centres being irritated, pressures may rise more
and more, and a vicious circle be established until by nitrites
pressures are reduced, or by morphia the centres blocked.

On the other hand, no waves of constriction, not even the
vasomotor convulsion of ague, will call forth angina in a patient
free from the local lesion proper to it.

Such then are the neuralgic, neurotic, and vaso-vagal symp-
toms which, often engaging in outbreaks of their own, may occur
also as secondary, or by-symptoms, of angina pectoris, as of any
other irritation ; but to exalt them to the rank of essential
characters of this disease is a vagary avoided by the earlier
observers, who knew them well enough. Yet in recent times, so
widely have these superficial features imposed themselves upon
teachers and taught, that when a year ago in a certain examina-
tion candidates were asked to describe angina pectoris, nearly all
of them covered sheets of paper with descriptions of its spurious
mimicries ; some of them, indeed, losing themselves so far in the
fog as to avoid the material part of the answer. And can we
wonder at it when one of their distinguished teachers writes as
follows : " Nothnagel established the fact (!) 2 that the charac-
teristic phenomena of the condition are capable of being produced
by functional conditions as well as by organic changes. It is

1 The link, if any, between migraine and angina is atherosclerosis, which
in the migrainous is often premature.

2 The writer probably meant a conclusion, general statement, principle,
maxim, or law, inferred from alleged facts. To take opinions for facts has not
yet ceased to be one of the banes of science.

sec. ii MOCK ANGINA 237

now universally admitted that angina may be true or false,"
i.e. that the case may be angina — always a menacing, too often
a mortal disease — or may be something else, and trivial ! As
Artemus Ward said of the gorillas, " they are supposed to be
human bein's to some extent, though they are not allowed to
have a vote."

However this random thinking may now be left without
further comment ; though the false implications in the descrip-
tion of angina pectoris as the " graver variety of the disease "
are so misleading as to be hard to excuse. The pale horse and
his rider are not of these phantoms. How are we to complain
that students never learn to think when, too often, they are
exercised in analysis as slight as this ? What, I repeat, should
we think of a lecturer who threw together into the same class
and under the same name the functional hemiplegias of hysteria
and the hemiplegias due to cerebral disease ! yet this is no forced
comparison. Let us then hear less of pseudo- angina and more
of pseudo-diagnosis. For happily we have many teachers more
clear-headed ; such as Edgren, who says plainly that he regards
most at any rate of Nothnagel's cases of vasomotor angina as
spurious ; and Neuburger of Frankfort,1 who, speaking from the
vantage of an extraordinary experience (143 cases with 38
necropsies, most of them by Weigert), warns us against mis-
taking for functional nervous disturbances a malady which
" always rests on an organic basis " ; and Dr. Norman Moore,
who says : 2 " Angina pectoris is generally associated with disease
of the aortic valve ; it is always associated with some degenera-
tion of the heart." If in this last clause we shall find matter for
controversy, the soundness of his clinical judgment amid so
much froth is reassuring.

Certain sagacious physicians, who can see that " crises des
nerfs " are a ghastly masquerade for angina pectoris, yet who are
deceived by some superficial resemblances in these several pro-
cesses, have surmised that the " real disease may arise out of the
false one." Now, in the first place, we must not forget that in
some cases of angina pectoris, especially in women, the agony of
severe and repeated attacks may drive the sufferer into hysterical

1 Neuburger, Deutsche med. Wochenschr., Juni 13, 1901,
2 Moore, Norman, Clin. Journ., Oct. 19, 1907.

238 ANGINA PECTOKIS part n

distress. So it was with the housemaid, under Dr. Hawkins
and myself (p. 189), whose attack of chronic aortitis was so
severe that the poor girl was driven to distraction. She became
wayward : at one time unruly, passionate, and rebellious ; at
another, tearful and melancholy ; and small blame to her. But
her case, both in its active and ultimate stages, was far too un-
equivocal to permit us to suppose that the disease, whose agonies
had put her thus beside herself, consisted in these scenes of
shattered nerves. And there are certain far more unhappy illus-
trations of such an error, as when in a recent essay on the subject
it was apparent to me that in a collection of cases, mostly of
"pseudo- angina," the author had included two which were clearly
cases of > minor angina pectoris (so-called " stenocardia "). Yet
the whole collection was classed as " hysteria " or " neurosis,"
and the author seems scarcely to have been taken aback by the
sudden death of one of his two patients, for imperturbably he set
down this incident as " secondary." Even among Sir William
Osier's cases of " pseudo-angina," I suspect more than one was
the genuine disease.

I have said that for a constructive review of " vaso- vagal dis-
orders" we have the advantage of Sir William Go wers' perspicuous
and practical essay; but in enquiring if the false may issue in
the true, we must discern how far these several series of pheno-
mena may be incidentally associated. In my experience, there
have been two chief groups of these cases, the syncopic and the
agitative ; in the former group we may guess that dilatation
in the splanchnic and other large areas is predominant, in
the latter, constriction. And of such oscillations are those
Secondary and Accessory Vasomotor Symptoms of angina pec-
toris (p. 226), symptoms which it has in common with other
kinds of paroxysmal pain, yet which are its epiphenomena, not
of its essential nature. And we shall admit that accessory vaso-
motor symptoms, if common epiphenomena of many irrita-
tions of large afferent nerves, and if standing in no direct
affinity to angina, yet often play a considerable part in determin-
ing the moments of its assaults. Although then the accessory
and the secondary processes may be in nature alike, or even
identical, it is a part of a careful diagnosis to discriminate the
Accessory symptoms — often accessory before the fact — from the

sec. ii MOCK v. TRUE ANGINA 239

Secondary, or fringe, symptoms. For instance, as vasomotor
oscillations may, as we have seen, be a product of angina — as
of migraine, or other painful paroxysm, and so in comparison
with the angina itself such riders be negligible ; yet if, under
an emotion, or a chill, or other such cause — as in a case of
Broadbent's the vasoconstriction of a malarial seizure — this
oscillation precede the anginal attack, by raising intra-aortic
pressure it may stand in immediate causal relation to it.
And often such vasomotor causes are as efficient as is muscular
effort ; so that the patient, whose attack to-day is determined
by walking up an incline, to-morrow may suffer by the draught
of a cold wind upon his skin, by a contact with cold bed-sheets,
by the cutaneous vasoconstriction of digestion, by the influence
of good or bad news, or some other annoyance. But to con-
found these proximate causes of an attack of the disease with
the disease itself is not only an error, but a dangerous error.

Thus however it is that some discerning physicians still cling
to the idea of an affinity between vaso- vagal attacks and angina ;
they fear lest the one, alien, even trivial, as in the first
instance it may have been, may end, notwithstanding, in
the other and graver malady. Even Balfour was tempted to
regard false angina as a sort of immature or preliminary form
of angina pectoris. In my experience I have never found reason
to suspect, nor facts to suggest, any such concatenation. The cases
of angina I have seen in younger persons have all originated in
the specific infections — especially in syphilis, rheumatic fever, and
influenza ; atheroma pertains to later life. But of atheroma
it may be surmised that in a life of continual vasomotor insta-
bility, due to turmoil or stress of mind, the aorta or heart may
in time become strained ; or that such an instability prevalent
in certain persons, however easy their circumstances, may lead
at length to cardiovascular deterioration. Yes ; such a chain
of causes is easily imagined ; but, before it can be taken
seriously, we must have more evidence of it than at present
we possess. The difference is not one of issues only, but also of
processes. In 1877 I wrote a paper to suggest that " granular
kidney " may arise from mental vexation over long periods of
years, and the opinion has since received general acceptation,
perhaps substantial proof ; but my notion was, and is, that such

240 ANGINA PECTOEIS part n

stresses act rather by obscure perversions of metabolism than by
the continual labouring of the arteries by incessant vasomotor
or vacillatory tides. So in the essay on Arteriosclerosis in this
book, I have discussed mental anxiety as a cause of Hyperpiesia
without renal disease ; now hyperpiesia may be no doubt a direct
cause of atheroma, and so a contributory cause both of angina,
as a disease, and, incidentally, of its several attacks ; but this
long insidious process is scarcely what is meant by the teachers
to whom I refer. Their eyes are fixed, as their descriptions
declare, upon the more or less immediate transition of some of the
multiform vasomotor storms of the kind and character of "pseudo-
angina " — I say " multiform," for the descriptions of various
observers, as for example of Nothnagel, of Douglas Powell, of
Gowers, or of myself, differ widely — into another kind, the kind
of angina pectoris ; the inference being that those storms ought
therefore to be interpreted as potential angina, the one being
prone to merge into the other. This is the opinion which I regard
as erroneous and deceptive. All the alleged cases of conversion
of pseudo-angina into genuine angina which I have seen, or read of,
were a development, not of a " true " out of a " false " angina,
but of a true out of a false diagnosis ; the cases, if at any time
angina, were of this nature from the beginning (vide p. 241).
At the same time I do not contest the opinion of Sir Richard
Douglas Powell, whose experience in these maladies is very large,
that in finance, politics, and other spheres of intense nervous
strain, arterial tension may range high, and be favourable to
arterial lesions ; and that, prior to angina, such vexations may
favour severe vasomotor oscillations, such as to undermine the
blood vessels. This is no unreasonable speculation, but it is
concerned surely, not with vasomotor angina, which does not
beset such persons, but with the engendering of angina proper
by way of subverted nutrition and atherosclerosis.1 For my
own part, of the scores and scores of cases of pseudo-angina
which I have seen, or of which I have heard or read, I cannot
remember one which ended in angina proper.

The pains and distresses consequent upon too liberal doses
of thyroid extract in myxoedema have been compared to angina.

1 For an analysis of these subtler causes see also Dr. Mitchell Bruce's
Lumleian Lectures for 1911, and Vol. I. p. 236 of this work.

sec. ii MOCK v. TKUE ANGINA 241

Suffocative feelings and pantings there are, but the pains are
widespread, and occupy arms, legs, and trunk. One such case
I recall vividly ; the pain and distress were bad enough, but a
comparison with angina could only be fanciful.

But to return from such speculations, full of interest as they
may be, and to emphasise the responsibility which lies upon us
all to beware of the grave, and possibly calamitous, error of mis-
taking angina pectoris for a nervous squall, I will illustrate this
error again by brief allusions to three, out of more cases on
my notes, in which it was not avoided ; and also to one recorded
by Sir James Goodhart. I will take them from the list of women,
as with them it is that we are more apt to be led astray.

Mrs. C. was a very highly strung woman, full of life and social
accomplishments. Her sister had suffered for two or three years
from vaso- vagal attacks and irregularities of the heart, but she herself
had enjoyed excellent health. After the menopause she got too fat,
though her energy and vivacity suffered little diminution. Keeping
a generous table for her friends she probably lived, from a physio-
logical point of view, rather too well. When about 55 years of
age she began to suffer from " liver," and from " oppressions,"
especially on walking up inclines. In a woman of her temperament
and offhand, unselfish way of describing her symptoms, what more
natural than to attribute them to " pseudo-angina " ; and this the
clearer as her nerves had been shaken by more than one heavy
trial. And such was the opinion of more than one physician. But
at length this arrest or pain at mid and upper sternum made it
almost impossible for her to walk far uphill ; the pain was not in
itself severe, but she was aware of an imperious arrest and an in-
describable warning. I found her arterial pressures very high, the
pulse sustained, and the heart's apex an inch or more out to the left.
On slight exertion a faint systolic murmur was brought out at the
base of the heart ; and the second sound was noisy, right up to the
apex. The aortic dulness extended 3 cm. to the right, and the vessel
in the suprasternal notch thumped against the finger. The urine,
repeatedly examined, was of full value, and contained neither
albumen nor casts.

Her case thus proved to be no " pseudo " anything, but a very
real something ; namely, angina minor and hyperpiesia. For two
years we kept the malady at bay, and happily the angina never
rose to the major form ; indeed, as her state deteriorated,
which was by way of cardiac defeat under the high pressures,

242 ANGINA PECTOKIS part ii

the oppression abated ; and before her death, in the ordinary
course of cardiac dilatation, it had disappeared.

The second case was in a lady, Mrs. K., of similar social position,
but of placid temper, and, on the whole, fortunate in the events of
her life. She likewise, about the same age, found herself checked
by a substernal compression on walking uphill, but was assured again
and again that her case was a " pseudo-angina." Her symptoms
however, when I saw her, were in site and kind like those of Mrs. C,
but her blood pressures were more amenable to treatment. For
various periods she was under Dr. Koberts of Harrogate, who kept
long charts of her blood pressures under several methods of treat-
ment. In her case a course of high frequency currents certainly
seemed, more than once, to effect an abiding reduction of the
arterial pressures, so that the symptoms were alleviated. Thus by
one method or another, of which a rigid diet was always a part, the
angina minor disappeared for a while, and for two or three years she
remained fairly well ; but the angina returned, at first in the same
minor form when ascending hills, but later in a severe and classical
form, especially in the left arm. She died in an attack. (See p.
110.)

It is surprising how long this minor form, especially in hyper-
piesia, may dog a patient without advancing to a fatal stage.

The third case was of a lady also in later middle life, left by
the death of her husband with the anxious charges of a young family
and a large estate. Her case was one of those I cited in my paper
to the Hunterian Society in January 1895. Though a woman of great
parts and energy, she could not be called neurotic in any morbid
sense ; but she was perhaps gouty in person, certainly she came of
a gouty stock. She, likewise, was " pulled up " one day on walking
up hill by angina minor, and likewise was assured it was " angina
spuria." I saw her after she had felt repeated arrests of the
kind, and found her arterial pressures too high. There were no
signs of renal disease. For a long time diet, nitrites, and other
appropriate means were successful in warding off, mitigating, and
perhaps arresting the hyperpiesia and angina ; but, unhappily,
before many more years had passed, she succumbed to a rapidly
growing uterine carcinoma.

These are three instances, out of many which I could cite from
my own records, of angina minor, a malady far from uncommon,
which were interpreted as " pseudo-angina."

The next illustration of the danger of thus paltering with

sec. ii MOCK v. TRUE ANGINA 243

diagnosis in matters so serious, I have taken from a lecture
by Sir James Goodhart : x

Male, set. 60, consulted " a physician in town, who said he was
suffering from pseudo-angina." At a later date he saw another
well-known physician, who also, I suspect from motives of humanity,
called it a " false angina." But the case proved then and after-
wards to be only too genuine.

And another reported by Dr. Core :

Female, aet. 48. Recurrent attacks of intense pain in the chest
radiating down the left arm ; considered to be " pseudo-angina."
However arteries " stiff " and aortic second sound reinforced.
Systolic aortic murmur. No history of rheumatism. Blood pressures
during stay in hospital 190-200. A few months after discharge
died of cerebral haemorrhage. (This case was probably not syphilitic ;
in syphilis the arterial pressures are usually moderate, and death not
by ordinary cerebral haemorrhage. — C. A.)

Bureau 2 well says : "Above all it is when aortitis occurs in a
youngish woman that the mistake may be made " (of regarding
it as mock angina). He quotes a case from Bucquoy,3 in which,
after some hours of distress interpreted as " globus," the patient
suddenly had a typical seizure of angina pectoris and died in it.

Humanitarian motives do not justify deliberate deception ;
however I suspect that these sadly erroneous opinions were given
in good faith, and fell in with the fashion of confusing angina
pectoris with nervous squalls. But this kind of plausible or
irresolute diagnosis is doing more harm than we realise.

Of angina pectoris as an alleged event of Graves' disease I
know nothing. I have seen nothing more than oppression with
palpitation, " point de cote," and pains about the chest and
arms not characteristic of angina proper.

1 " On Angina Pectoris," Clin. Journ., April 4, 1894.

2 Bureau, Aortites aigues, These de Paris, 1893.

3 Bucquoy (quoted Bureau), " Clin, sur l'aortite aigue," Journ. de med. et
de chirurg. prat., 1882.

CHAPTER III

TOBACCO ANGINA

Tobacco Angina, if this name is to be received, is a curious
and rather rare affection. It was recognised first, I think, by
Beau,1 who described eight cases. I have seen only three well-
marked cases : in two of these the attacks were mild ; in the
third they were of intense violence. But even this patient had
scarcely the aspect of angina pectoris ; it was not a state of
awe-stricken arrest, but a strife. The patient, a strong man of
middle life, but presenting some signs of arteriosclerosis, had
an attack in my presence : he writhed in a passion of distress ;
by his wrestling with the invisible foe the sofa on which he
was lying was partly overturned, so that from the back of
it he rolled on the floor. It was difficult to get him to
say exactly, even after the attack, where the pain was, or if it
were pain, or some other distress, which made him frantic ; but
it seemed certainly to be a thoracic, and apparently a cardiac
oppression, and, taken alone, reminded me of the agony of a clot
in the heart. There was no more dyspnea than the muscular
effort would naturally produce ; there was physical alarm, but
perhaps not the peculiar angor animi. The attack lasted some
three or four minutes. To note the behaviour of the heart
during the height of the seizure was impossible ; but as it
declined, the action was rapid and irregular. Moreover in the
tranquil intervals more or less arrhythmia continued, an
arrhythmia having the common characters of tobacco heart.
The well - marked premature systoles, the palpitation, the
agitation, and the audible characters of the heart, suggested

1 Beau, Arch. gen. de med., 1862.
244

sec. ii TOBACCO ANGINA 245

tobacco ; so that I took upon me, too confidently perhaps, to
assure the patient, who had some knowledge of medicine, that
his fears of angina pectoris were unfounded. He was a very
persistent smoker of strong cigars, and on restriction of this
habit the symptoms abated.

Cases of tobacco-poisoning which, if in the intermittent returns
and the kind of distress they fall far short of such anginoid
attacks as that just described, yet have somewhat similar
features, are not very uncommon. For a fuller description of
these cases, which may simulate degrees of angina pectoris,
I may refer the reader to the section on Tobacco Heart in my
chapter on " Functional Diseases of the Heart " in Allbutt and
Rolleston's System. But here I may dwell for a moment on
these lighter simulations, for their signs may be more equivocal
than those of the violent seizures. Indeed in the minor cases
there is not rarely a sternal or " substernal " oppression such as
to arrest or deter the patient as he ascends a hill, or at least to
dispose him to stop. Many years ago a medical friend of mine,
now in excellent health, but who had then been smoking too
many cigarettes, told me that in walking up a hill a tight, con-
stricting pain would catch him across the mid-chest. If he
stopped it passed off. The tobacco was discarded, and with it the
pain departed. But, on reflection, and speaking as a physician,
he said he could not have distinguished the pain from a slight
angina pectoris. Dr. Mitchell Bruce says that in tobacco
cases the pain occasionally passes into the left arm ; this I
have not observed in cases wholly free from suspicion of true
angina. (Dr. Bruce lays no stress on tobacco as a cause of
arteriosclerosis.) In a few moments, often with some inter-
mittence of the heart and an eructation of wind, the attack
passes away ; but this it may do in true angina. As the attacks
may very suddenly appear, so when the poison is laid aside they
soon vanish ; still, in a man of middle age with arteries no
longer at their best, the diagnosis might for a time have to
be held in suspense. Dr. Bruce therefore, while warning us
lest we pronounce a case, which is but tobacco-poisoning, to
be genuine angina pectoris, quotes a case in a man, set. 60,
who, after some ominous stenocardia — such as I have described
above — had a " fearful pain of the chest, and down the left arm,

246 ANGINA PECTORIS part n

cold sweats, and a sense that his last hour had come " ; yet on
dropping his tobacco he recovered. It is not quite clear that in
this elderly man the case did not partake of the nature of genuine
angina, attacks of which may have been determined in an athero-
matous aorta by the vasoconstrictive effects of tobacco on the
intra-aortic pressures. Or, if it be true, as alleged, that the use
of tobacco leads to arterial disease (vide Arteriosclerosis, Vol. I.
p. 250), it may provoke aortic lesions out of which angina pec-
toris may arise. In a gentleman, set. 53, who called upon me not
long ago not for angina but for cardiac oppression, arrhythmia,
and palpitation due to tobacco, I found the systolic pressure was
fully 160. No peripheral atheroma was palpable.

The genuine spectral horror or awe of angina I have never
observed in mere tobacco angina, but reasonable alarm only.
The vertigo, so frequent in tobacco excess, is often in part a
cause of the alarm. Dr. Lloyd Jones of Cambridge kindly
permits me to say that he has had not a few attacks of tobacco
angina, attacks which at first he supposed to belong to the genuine
disease. Some of the attacks were severe but, after no little
anxiety in respect of them, he became convinced that they
were due to increases of his generally moderate allowance of
tobacco ; as for instance during a holiday or on a long rail-
way journey. Dr. Jones thinks that in his case the attacks
were attended with sharp rises of blood pressure ; at any rate
they were always promptly relieved by a whiff of amyl nitrite.

But some of these tobacco cases simulate rather the false than
the genuine angina.

Male, age about 45, brought to me by Dr. Poignand of Walsham
le Willows, smoked strong cigars all day, and indulged freely also in
food and drink. He had become subject to " syncopic attacks " of
long and alarming duration. A persistent, not paroxysmal, aching
pain was seated in the left chest between the third and the seventh
ribs. The pain was independent of exertion. In the definite seizures
the pulse disappeared ; near them, or in less severe attacks, it would
run up to 160. By strict obedience to our directions the patient
completely recovered ; but four months elapsed before any definite
amendment could be relied upon.

It so happened that, after writing these words, a gentleman,
set. 40, who had suffered from attacks of this kind, called

sec. ii TOBACCO ANGINA 247

upon me again for an opinion. He had dropped his tobacco (forty
cigarettes a day !) for just four months, but still was com-
plaining a little. However, except an occasional extra-systole, I
could find nothing wrong with heart, arterial tree, or blood
pressures.

Edgren records two cases of severe tobacco angina, and says
that they are very different (sehr verschieden) from the genuine
disease. And perhaps some cases by other writers, recorded as
" vasomotor angina " and so forth, may be recognised by the
wary reader as pertaining to tobacco. That wearisome importun-
ate submammary ache, not anginous, is often notable in tobacco
cases. Von Basch witnessed, and promptly diagnosed, one
severe case of the kind in a woman ; in women, at any rate in
England, I am thankful to say, this cause might well escape our
suspicion. An arrhythmia, independent of the attacks, may
serve as a note of distinction ; and, what is rare in angina
pectoris, the patient will complain of this cardiac irregularity
and palpitation independently of the attacks.

Huchard asserted that tobacco angina was caused by con-
striction of the coronary arteries, being, as it were, a sketch of
genuine angina ; a postulate which, to less adventurous thinkers,
seems to be a mere guess, and an unlikely one ; for, as we shall see
subsequently (p. 356), it is inconsistent with what is known of
the physiology of these vessels. A kind of " pseudo-angina " it
may be, probably is.

A case commented upon by Mouriquand and Bouchat 1 well
illustrates the occasional difficulty of detecting the true nature
of particular cases :

Male, set. 54. Sudden seizure of angina pectoris. Previous health
good. No alcohol. No rheumatism. Syphilis denied, and no sign
of it found. But a very heavy smoker — thirty to forty cigarettes
a day as well as several cigars. Cardiac signs practically negative.
P.M. — Heart practically normal, aortic valve healthy. On ascending
aorta several gelatiniform patches. Orifices of coronary arteries
obliterated by such patches, but orifice of right coronary artery just
visible.

Now, as on microscopic examination these patches proved
to be a certain typical subinflammatory disease of the vessel,
1 Mouriquand and Bouchat, Arch, des mal. du cosur, oct. 12, 1912.

248 ANGINA PECTOEIS pakt n

especially of the media, and to differ from the degenerative
characters of arteriosclerosis, they unhesitatingly and no doubt
truly recorded the case as syphilitic, and not due to tobacco.
The authors consider that the attribution of genuine angina to
tobacco is unproven. I also believe that many cases of true
angina, infective cases for example ending in recovery, are
erroneously put down to tobacco.

CHAPTER IV

CAUSES OF ANGINA PECTORIS

A. Remoter Causes. — Age. — Angina is by no means un-
known in the aged and decayed, but its greater prevalence is at a
somewhat earlier stage, in the years of senescence ; in senectus,
not in senium. However, no general rule can for the present
be accepted, as our statistics are vitiated by arbitrary or pro-
miscuous collection of cases. Angina in its typical manifesta-
tions is far from unknown in young persons. Heberden refers
to a case in a boy of 12 (due, probably, to rheumatic fever
or other infection) (see Aortitis, p. 150) ; his " Unknown "
was only set. 46 (syphilis ?). Fothergill publishes two typical
cases beginning at the ages of 25 and 30 respectively (probably
syphilitic). One patient died, the other recovered. He com-
ments on this recovery as in his experience unique. One of
Allan Burns' patients suffered from angina during the age period
36 to 40. He died of cardiac dropsy, and probably the whole
morbid series was syphilitic. I have notes of at least three
cases in adolescence — two in senior schoolboys, one in an under-
graduate ; all three were cases of rheumatic fever with aortic
disease, and all, so far as the angina was concerned, ended in
recovery. I have seen also two definite cases in children, the
younger one a case of rheumatic pericarditis (also with re-
covery) ; and the late Dr. Gibson showed before the Medico-
Chirurgical Society, in March 1903, a child, the subject of angina
and aortic valvular disease of rheumatic origin. Dr. Hugh
Stewart 1 has published a case of angina pectoris (with aortic
and other valvular disease) in a boy set. 7 ; the angina

* Stewart^ Hugh, Edinburgh Medical Journal, June 1906.
249

250 ANGINA PECTOEIS paet n

came on towards the conclusion of a severe rheumatic fever —
first indefinitely, then in frequent and " typical attacks."
There was no cyanosis, no dyspnea ; but sudden pallor,
pain, arrest, and anxiety. Such was the older child of my
two, a girl set. 12|, whom I saw in private consultation.
At the end of an attack of rheumatic fever she also com-
plained of intense retrosternal pain and constriction, the pain
radiating in the usual way down the left arm. During a
partial recovery she died suddenly in an attack. Unfortunately,
no necropsy could be obtained. These cases in young persons
with sound hearts generally end in recovery, so far as the
angina is concerned ; and thus they fail to appear as such in
the Registrar-General's Reports ; so it is also with many of the
syphilitic and most of the influenzal cases.

The many syphilitic cases fall for the most part between the
ages of 40 and 50 ; but not very rarely between 25 and 35. Sir
William Osier1 publishes a case in a man set. 24, whose primary
infection was nine years before. Neuburger (loc. cit.) includes
two cases (in males) of set. 31 and 37. In middle life cases of
angina largely increase in number, the period of greatest fre-
quency being from set. 55-65. Seneca's first attack was at the
age of 60. I have notes of two patients in extreme old age, viz.
83 and 90 respectively ; the second case is mentioned p. 514.

Osier, of 40 cases, had 4 under set. 40 ; 13 between set.
40 and 50, 13 between set. 60 and 70, and 9 between 70 and 80.
He gives the age periods for larger numbers as follows : Under
30 years, 9 cases ; 30-40 years, 41 cases ; 40-50 years, 59 cases ;
50-60 years, 81 cases ; 60-70 years, 62 cases ; 70-80 years, 13
cases ; above the age of 80, 3 cases.

Station of Life. — It may be true, on the whole, that the disease
falls rather upon the upper classes, but I have not found it so
rare in hospitals as is commonly supposed ; such a distribution
of the disease may be apparent only, and governed by the chances
of individual practice, the prevalence of syphilis, and so on. The
same remark is made concerning gout, that it is a disease of the
easy and intellectual classes. Now both gout and angina not
infrequently, though by no means always in either case (Vol. I.
p. 273), are associated with high arterial pressures; and the persons
1 Osier, W., Lumleian Lectures.

sec. ii CAUSES 251

of whom we are speaking, as a class are sedentary and
consume larger quantities of the richer foods. However we must
first be sure of our facts, for Samberger,1 of 73 cases in the
Policlinic of Prague (1895-98), says " all these patients belonged
to the class of poor working people."

Sex.— The comparative rarity in women seems to be un-
questionable, although statistical reports scarcely bear out an
extreme disproportion (see also section Aortitis, p. 172). Heberden
thinks he saw in all about 100 cases, of which only 3 were in
women. In Husband's 237 collected cases women were in the
proportion of 1 to 60. Sir John Forbes, for his Cyclopcedia of
Practical Medicine, collected 88 cases, of which 8 were in women.
Osier in his 40 cases saw 1 woman only ; these fractions, to
judge by my own experience, are too small. Consultations on
behalf of heads of families are more frequent, and in the case
of men of distinction are demanded also in respect of the
public. Burwinkel,2 in a collection of 117 cases, found the
women to the men as 1:7; of Neuburger's own 143 cases
118 were male, 25 female. I have seen many cases in women ;
I recall at once, as I write, ten or a dozen of the most typical
in kind and degree. Certainly angina minor (" stenocardia "),
often met with in the course of Hyperpiesia, is by no means
very rare in women. So of Samberger's 73 cases, about one-
third were in women. Of this difference of sexual susceptibility
no very definite account has been given, for women also have
coronary arteries ; it may be surmised that the causes lie,
in some measure at least, in the smaller incidence of syphilis
and gout on women, and perhaps in the protection of the
thoracic aorta from physical strain. Were angina pectoris " of
the nature of neurosis," it would on the contrary be more
prevalent in women. The neurotic crises confused with angina,
a disease with which, as we have seen, they have nothing in
common, neither in nature nor symptoms, do fall chiefly upon
women, and feminine men.

Heredity is of course not a " Cause " ; paradoxically it might
be called the absence of causation, an apparent severance of

1 Samberger, Bohemian Arch, of Clin. Medicine, vol. i. fasc. i. 1899, quoted
Epit. Brit. Med. Journ., June 17, 1899.

2 Burwinkel, Deutsche med. Wochenschr., April 5, 1906.

VOL. II R

252 ANGINA PECTOKIS part n

the chain of causation ; but the detachment of the individual
from the stem is no very radical schism in a continuous growth.
Heredity is then the cause of a quality in the offspring only after
the manner in which the finger may be regarded as the cause of
the finger-nail. Moreover there is too much contingency in its
causation (infections and habits) to make transmission apparent.
Nevertheless a proclivity to angina may run in families ;
such examples are not infrequent. I think Robert Hamilton x
was the first to notice this reappearance. Neuburger, in 20
of his 143 cases, found a history of angina in blood kindred.
It is often stated that it is usual in angina pectoris to find a
hereditary tendency to irritability of the nervous system. This
notion, which in my opinion is baseless, has probably arisen out
of erroneous diagnosis.

Season. — Heberden concluded that angina has no periods of
seasonal prevalence, and subsequent teachers have agreed with
him.

B. Proximate Causes. — Whatsoever the nature and seat of
angina pectoris, I must insist that its causes have much in
common with those which determine arterial disease generally.
These causes I have set forth so far at length in my essays on
Arteriosclerosis and Aortitis, that here I have only to indicate
their special bearing upon this peculiar appanage of arterial
disease ; and for this purpose we may consider five chiefly : (1)
the strain of bodily labour ; (2) the strain of high blood pressures ;
(3) mental and emotional causes ; (4) infections ; (5) some of the
obscurer causes of atherosclerosis.

1. Bodily labour, so far as we can discriminate its effects,
seems, taken alone, to be no very fruitful parent of angina.
Though not a few cases are recorded in forgemen and other
Anakim, in many of whom probably the angina was syphilitic,
for it was often associated with aneurysm (vide p. 188), Sir
Richard Douglas Powell hesitates to regard physical stresses as
frequent causes of angina ; and Dr. Colbeck concludes that,
infections apart, it is far from common in blacksmiths, navvies,
and other such labourers (see however case of Bartholmes,
p. 366). Gibson, on the contrary, did " not doubt that
many of those whose avocations lead them to physical overstress
1 Hamilton, R., Med. Comm., 1780, vol. ix. p. 307.

sec. ii CAUSES 253

are liable to angina pectoris " ; and he added that in his
experience of the prevalence of the disease in the hospitals of
" districts where hard mechanical occupation is the rule, angina
pectoris is far from uncommon amongst working people." *
This important opinion may need the qualification that, like
general paralysis, this prevalence among labourers is urban
rather than rural ; it prevails where syphilis prevails. In my
experience, infectious cases, as of rheumatism or syphilis,
omitted, its incidence upon the labouring classes in Leeds was
not remarkably high. Indeed in my own notes I find but one
case in which labour may have been the chief cause ; and, as
the patient was a soldier, it is not unlikely that there also
syphilis entered into the causation.

T. B., set. 26, had been exposed on service to exceptionally heavy
labour. He was the subject of severe angina pectoris in its classical
form, including dread. He answered questions frankly, but neither
in the history nor present signs were traces of rheumatic fever or
of syphilis to be verified. The first attack was certainly produced
immediately under severe bodily effort ; and since this event he had
been liable to seizures on slighter efforts, so that he was unable to
follow even light employments. Wa.R. not tried.

A similar causation was supposed in the young housemaid
under Dr. Hawkins and myself (p. 189).

It is surprising indeed that not more cases of angina are
attributable to single violent efforts. If such were the case with
T. B. and the housemaid, yet in the vast majority of recorded
cases, if the moment of the first attack were determined by effort it
was by an effort comparatively slight — such as an ascent of no very
steep acclivity, a walk against a wind, or the wielding of a weapon
no more formidable than a fishing-rod or golf club. And in
many of these cases, if the first declaration of the evil were thus
called forth, on close enquiry it proved that the crisis had been
preceded by some warnings ; as by transient oppression in the form
of angina minor — a momentary tightness under the breast bone,
or a vague and transitory sense of arrest — sensations obscurely
ominous of what was incubating within. One gentleman indeed,
a resident in Halifax, did tell me his first attack was as a bolt
from the blue, while after a hard day's sport he was bicycling
1 Gibson, G. A., Diseases of Heart and Aorta, p. 763.

254 ANGINA PECTOEIS part n

home up a steep hill, in happy rivalry with his sons and daughters ;
and Latham, unaware of the infections, thought " some con-
siderable effort " started the disease in the majority of his cases.
When disease has corroded the intima and media, some rather
greater effort produces a rise of pressure which the old coats no
longer resist ; it forces the media, and the strain, reaching the
adventitia, tugs upon it as abdominal tensions stretch the
mesentery (Vol. I. p. 447 and II. 194). Dr. Mackenzie 1 de-
scribes a case in a builder, set. 48, in whom a first attack of
angina reached its maximum two hours after a violent bodily
strain. We know that an apparently normal aorta may split
(see p. 206), and a split might not be immediately mortal ; but it
is more probable that, in such cases as that of Dr. Mackenzie,
the strain took effect at a spot of pre-existing syphilitic or athero-
matous disease. In one of Broadbent's cases (pp. 301, 302) the
initiation of angina was traumatic ; a severe crush of the chest
gave rise to distressing attacks of angina and a double aortic
murmur : we know that many an aneurysm has been thus
determined, though syphilis is at work more frequently than we
have been wont to suppose.

That the moments of the several seizures are often determined
by effort, even by effort of mind or emotion, we know only
too well ; so well indeed that there is a notion abroad —
one which more than once has been mentioned to me in dis-
cussing a diagnosis — that attacks are always so determined.
Huchard countenanced this erroneous notion. Yet from
Heberden himself we have learned that attacks may occur
during sleep, often during rest. Diderot died of angina, and
a very severe attack is recorded which awoke him from sleep.
Such nocturnal accesses may be in obedience to secret tides
of blood pressure ; 2 and we shall remember that an apoplexy
not infrequently occurs during sleep. In an old gentle-
man suffering from angina, since dead, whom I saw with Mr.
Atkinson of Saffron Walden in the autumn of 1911, the attacks,
which were many, had generally occurred between 2 and 3 a.m.
A nocturnal attack, which may be quite as severe as at other

1 Mackenzie, Jas., Brit. Med. Journ., June 30, 1906.

2 See Dr. Ewart, Lancet, Sept. 15, 1906, who suggests fatigue toxins ; and
Dr. Gordon of Exeter, Lancet, August 7, 1909.

sec. ii CAUSES 255

hours, and is aggravated by its untimeliness, makes one point of
diagnosis from mock angina ; but tobacco seizures, whether
anginoid or of cardiac disorder, do sometimes occur at ghostly
hours. One such case I well remember.

2. The Strain of continuously High Blood Pressure. — It is not
necessary then to assume that, for injury of the vessels about
the heart, pressures must have run for some years continuously
at excessive heights ; though of course we might expect this
to be no rare experience. In not a few persons, probably
in the majority of cases, atheroma becomes established in the
aorta-coronary area, not so much because the blood pressures
had been positively excessive, as because these parts, whether
by original structure or by the insidious influence of some un-
recognised toxic or other morbid process, were vulnerable.
However, the belief is prevalent that angina pectoris is correlated
with excessive bl6od pressures. Although in Hyperpiesia it is
true, as we should expect, that high pressures coinciding with
vascular disease result in a larger proportion of anginal co-
incidence, yet even if we lump Hyperpiesia and Bright's disease
together, we shall find angina mentioned in but a small minority
of these two classes. Sir James Goodhart (loc. cit.) observes
how commonly " the extremest arterial high tension may be
quite free from pain." Given however a defective aorta, the
intercurrence of high pressures is likely to promote angina, or to
aggravate it. Moreover, angina is, for the greater part, a disease
of the elderly, in whom pressures naturally rule a little higher.
Notwithstanding, moderate pressures are quite consistent with
angina, and are not infrequent in it, as Vaquez, and even Pal,
have carefully noted in not a few cases -,1 Dr. Mackenzie,
as we shall see, has verified this conclusion. For instance, in
my many syphilitic cases I have found moderate pressures to
be the rule. KaufTmann 2 says that pain (with the normal
heart) raises the minute volume, the blood pressure, and the
heart's work ; thus the arterial pressures may be driven up only
during the attack itself, to subside during the tranquil intervals.
For obvious reasons the blood pressure can rarely be taken
during a severe attack ; but in a certain elderly lady two of us

1 See, e.g., B. and M. Soc, Med. des hop., juin 28, 1906, p. 663.
3 Kauffinann, Zeitschr. f. exp. Pathol, u. Therap. Bd. xii., April 24, 1913.

256 ANGINA PECTORIS part n

found the systolic pressures during attacks to be 166-180 ; in
the intervals only 140. The difference may have been wholly
emotional. Dr. Morison in one case (a man set. 73) found the
pressure during an attack to be 140-145 (pulse 84 mm.). Drs.
Mackenzie and Price informed me, in a private letter, that (in
a case of syphilitic aortitis verified post-mortem) the systolic
pressure, ordinarily 120, rose during an attack to 140. I
have notes of some families of which certain members were the
subj ects of hyperpiesia , others of angina pectoris. On the contrary,
in another case of mine we found during an attack that the
pressure fell to 120, indicating not so much vasodilatation as
cardiac inhibition ; for, after relief of the pain by antipyrine, the
pressure rose again to 140. If however the aortic pressure
falls low, anginal attacks may and usually do cease ; though
Huchard's assertion that " L'angine de poitrine ne peut plus
se produire chez un malade en etat d'hypotension arterielle "
betrays his besetting incaution. An interesting example of this
sequence is reported by Dr. Bruce Porter 1 in a case of angina
pectoris with aortic disease. The patient was a man, set. 43, in
whom, during a gradual progress of heart failure, the attacks
did not cease until the systolic pressures had fallen to about
100 mm. In another case, of Dr. Morison's (a man set. 32),
during the attack " a musical murmur " (of aortic regurgitation)
was almost hushed ; yet the attack was relieved by nitrites.
Records during attacks are too scanty to justify any general
conclusion, but we may take it that there is no direct relation
between arterial pressures and angina.

3. Mental and Emotional Causes. — He is a happy man who in
middle and later life can look back upon a many years without
strife and disappointment; not a few patients of angina have
no doubt been worn down by such trials. On the other hand,
many happy and thriving country gentlemen, and successful pro-
fessional men and tradesmen, suddenly seized by angina, have
no grave record of the kind, nor look back upon any " neurotic "
family history ; so that if, as I have supposed under Arterio-
sclerosis, certain cases may have been engendered by such cares,
these in my experience have not been widely efficient, nor formed
a characteristic source of angina. The great stress laid by some
1 Porter, Bruce, Brit. Med. Journ., Nov. 21, 1904.

sec. ii CAUSES 257

physicians upon business cares and excitements indicates the
sphere of their practice among the wealthier commercial folk,
who are prone to eat and drink too much. And may not such
attributions as " domestic worries " and " infelicities " some-
times cover a secret syphilis ? For other causes of atheroma,
and so incidentally of angina, I may refer my readers to my
essay on the causes of Arteriosclerosis (p. 148).

4. Infections : Gout. — Our gluttonous and bibulous ancestors,
to judge by the records of their physicians, seem to have been
subject to terrible conflicts which were lumped indiscriminately
together under the conjectural titles of Gout at the Heart, at the
Stomach, or at the Diaphragm (Butter). Fothergill held the
gouty hypothesis, and Materia arthritica retropulsa was Hoff-
mann's explanatory title for Angina. Some of these cases
seem to have been angina, others the dyspnea of ursemia or
hyperpiesis, others turbulent cardiac arrhythmia, gastric
fermentation and colic, and so forth. The description of
such cases by Sydenham, by Heberden, and by many other
authors in the eighteenth and early nineteenth centuries, are full
of interesting matter. If we claim more discernment, we have
not yet the data for an analysis and redistribution of the terms
of all their series ; but from general impressions we gather a sub-
stantial remnant of evidence in favour of some long association
between gout and angina pectoris. Butter (I.e. p. 304), Eisner,1
and Hoffmann convinced themselves of a causal bond between
angina and gout, or some kind of " arthritism " ; and, as Eisner
was the first herald of angina in Germany, so this arthritic hypo-
thesis of the disease gained a strong foothold in that country.
Wichmann 2 however warned his countrymen that coincidence is
not necessarily causation ; he remarked that itch might occur in a
syphilitic patient, yet stand in no causal relation to this cachexia
(p. 192). In his not very important tract on Angina Butter
supposes angina to be diaphragmatic gout ; and Erasmus
Darwin was of a like opinion. Wall said, " Angina et podagra
alternatim per intervalla segrum vexant " ; Canstatt said the
same ; Forbes agreed, but put plethora — or rather gorging and
tippling — in the first place, as contributing to a common sub-

1 Eisner, AbJiandlung ilber Brustbraune, Konigsberg, 1778.
2 Wichmann, Ideen zur Diagnostik, Hannover, 1797.

258 ANGINA PECTOEIS part n

stratum of disease. " Plethora " was often in the mouths of our
forefathers, who generally meant by it what recent writers mean
by " high tension." At the present day, Ebstein, in his work on
Gout (1906),1 says, a little paradoxically, that angina pectoris is,
as it were, an attack of gout ; his meaning seems to be that
angina pectoris is a play of this irritant humour upon the nerves
of the heart, so that angina appears to him " lediglich auf nervoser
Basis zu beruhen " (p. 256) : on what nerves he does not state.
In 194 cases of gout he found 72 with cardiac troubles, and 97 (!)
with angina pectoris. He admits that in subjects of angina
there is often no history of frank gout, but he reads many of
them nevertheless as of gouty stock. More particularly, he says
angina is apt to appear in the glycosuric gouty ; but, as even
Ebstein is foggy in his diagnosis of angina, and evidently was
led astray more than once by cases of the spurious disease, and in
other cases by paroxysmal dyspnea, we cannot lay much stress
on his calculations. Certainly they are not borne out by
ordinary experience. I cannot say that I have found angina more
common in gouty glycosurics than in other elderly men with
underlying arterial degradations. So far as I am aware, the most
valuable personal observations on gout and aortic disease are con-
tained in Dr. Mitchell Bruce's Lettsomian and Lumleian Lectures
(1901 and 1911), to which again and again I have to acknowledge
my debt. On this part of the subject he says,2 " One-fourth of all
cases of " gouty heart " have pains of anginal character, and often
pronounced angina." In twelve out of twenty-nine .of his cases
of gouty heart a systolic murmur was heard in the aortic area,
conducted into the carotids — a sign of deterioration of the aortic
arch and valve. This statement confirms the opinions of
Sir Dyce Duckworth, of Dr. Norman Moore, and indeed
of Murchison, on the earlier incidence of disease of the
arteries, especially in the aortic area, in persons actually
gouty or of gouty habit (Vol. I. p. 273). As an extreme
instance, Dr. Bruce relates the history of a patient, who
before the age of 20 had suffered from gout, both articular and
irregular, and in whom, at this precocious age, angina pectoris
supervened. Could we have a stronger suggestion than is

1 See also Berl. klin. Wochenschr., June 24, 1895.
2 Bruce, Mitchell, Lancet, May 23, 1901.

sec. ii CAUSES 259

offered to us by this prevalence of angina in the ill-defined group
of gouty persons, of the origin of angina, not in the heart — for the
heart in these cases, some of which are cases of high arterial
pressure, is, until strained or very atheromatous, if abnormal,
abnormally strong — but in the aorta, and especially in that part
of it which abuts upon its valve. If this atheroma occlude the
coronary orifices, or so invade their trunks as to cut off the
more direct blood-supply to the heart, making it thus less able
to evade inhibition, then the angina becomes more than a painful
malady, it becomes a treacherous menace to life. Among the
more interesting records of the older physicians are those cases
in which anginiform states gave way to podagrous seizures, and
conversely. Dr. Gayford kindly sent me the notes of such a
case, which ran as follows :

Male, set. 68, engaged in large commercial affairs. In spring
" could not shake off a cold," and frequently had recurrences of
pain and tightness across the chest ; these would pull him up while
walking, and might seize him even while lying quietly in bed. The
pain would extend to the left shoulder, and at times down the left
arm. The heart at such times was most irregular, often 120, with
a cantering rhythm. The pulse was not hard, and the radial artery
was in fair condition. There was no murmur, but the heart's action
was tumultuous. Trinitine relieved these states. At other times
a rapid cardiac rate would set in, without pain — when the pulse
would be small and soft. On November 21, " had an attack of heart
failure ; pulse uncountable, jugulars distended and throbbing
violently " ; but then he was seized, for the first time, by gout
frankly in the foot, and on its appearance all the cardiac disturbance
ceased. The pulse became regular, at a rate of 60, and the relief so
far has proved permanent. Previous treatment addressed to gastric
disorder had done some good. (Compare case, p. 503.)

This most interesting case suggested to me that the goutypoison
which affected the heart so turbulently, not after the manner
of angina, might have attacked the aorta after the transient
fashion of gouty inflammations. I may mention here another
case, to which I shall refer again under Diagnosis, in which an
elderly man of almost unbroken health and activity had a slight
attack of gout, which was followed by epigastric, and even slight
thoracic oppressions, which seemed to differ from slight angina
only in the cardiac arrhythmia associated with them. In him
also after a few weeks' treatment the attacks wholly disappeared,

260 ANGINA PECTORIS pakt n

and he recovered his former bodily activity. If then it seems
probable that gout, both as favouring arterial decay, and again
by some more instant irritation, may take a considerable place
in the causation of angina, we shall remember that authors
on angina have for the most part written from experience of
the wealthier classes in whom many other causes are at work.
Diagnosis may be at fault. And we must not forget that even
among the wealthy not a few anginous patients are of spare and
temperate habit, with no signs or likelihood of gout.

If, as I shall argue, in the majority of cases angina pectoris be
due to an "atheromatous" process of a senile kind, penetrating
more deeply than usual in the suprasigmoid section of the aorta,
a process scarcely to be called infectious in a definite use of the
word, yet a considerable minority of cases, a number rapidly
gaining recognition under modern clinical analysis, and entering
into a class most significant in respect of the pathology of the
disease, arise under the corrosive effects upon this part of
acuter and more specific infectious poisons. As we have seen
in the section on Aortitis, Flexner and other pathologists have
found, besides the syphilitic spirochaeta, other specific microbes
in aortitis, lying within the tissues, either unmixed or
associated with septic streptococci. Boinet also has found
in such conditions the microbes of erysipelas, of rheumatic
fever (Poynton), and of influenza ; in some cases grafted
upon or turning into atheroma. Sir William Osier,1 though
he speaks sceptically on the clinical side, yet admits (p.
430) the frequency of infective foci of arterial degeneration,
as in scarlet fever, measles, diphtheria, influenza, smallpox,
and typhoid ; foci recognisable on necropsy as patches in
the aorta and larger arteries, or as sclerosis of smaller vessels.
By one observer, quoted by him, such evidence was found in
the bodies of 80 out of 300 children who had died of acute infec-
tions. But of all these infections the most active, definite, and
frequent cause of angina is syphilis ; after syphilis come
influenza and rheumatic fever, and, if we allow for the
irregular prevalence of influenza, in this order. But of these

1 Article on Diseases of Arteries in Osier and Macrae, Syst. Med. vol. iv.
c. 10.

sec. ii CAUSES 261

infections I have written at length in the chapters Arterio-
sclerosis (Vol. I. p. 282) and Aortitis (p. 148).

The incidence of syphilis upon the aorta, and especially upon
its suprasigmoid part is at a far higher rate than that of in-
fluenza, even during its epidemic periods. Burwinkel in his study
(he. cit.) of 117 cases, put the causes of angina in the following
order : (1) syphilis ; (2) obesity, diabetes, and gout ; (3) aortic
disease ; (4) influenza and malaria ; (5) heredity. Many cases
of angina, apparently syphilitic, may be picked out of the
records of the older writers. I must content myself with a
few, such as this from Morgagni (Ep. iv. 22 ; see also Ep.
xvi.), who emphasised lues as a cause of arterial disease :

Male, set. 43. " Valde anxius," laid hand " on sternum." Died
suddenly. P.M. Semilunar valve harder than normal. First
portion of arch of aorta, as seen from outside, bulging non secus ac
si in tuber um modo quadamtenus hie illic assurgeret. Inside, super-
ficies rugosa.

We may compare this with Hodgson's, Welch's, Wilks', and
later descriptions. His case of a woman who on the least
effort suffered from pain in the upper part of the chest and left
arm, who died suddenly in a paroxysm, and whose aorta was
atheromatous, was probably syphilitic, as her age was only 42.1
Lancisi 2 fully recognised the syphilitic or " Gallic " aneurysm ;
e.g. as follows :

Male, set. 45. " Habitus carnosi, vitae omnino libertinae nimirum,
Dianse, Neptuno, ac Veneri frequenter indulgens, ex qua postrema
pluris contraxit luis stigmata," etc. Again, an " egregius cithareedus,
qui ex impuro concubitu non semel in pudendis vulneratus." In both
of these patients aneurysm followed.

In another paragraph, unfortunately on speculative grounds,
or misled by the abuse of it in syphilis, he includes mercury as
a cause of aneurysm, and deprecates its use ; "in nullo Aneurys-
mate, etiamsi a lue gallico profecto." Senac quotes from Portal,
" Cadaver syphilitici . . . aorta supra cor valde dilatata."
Syphilitic aneurysm we all know, diffuse syphilitic disease of
the arch we know, but syphilitic angina pectoris, depending

1 See also Parkes Weber's case, pp. 187 and 264.
2 Lancisi, De motu cordis et aneurysmatibus, Napoli, 1738.

262 ANGINA PECTOEIS part n

upon syphilitic lesion of the supersigmoid and sigmoid area,
has not received the general and prompt recognition which
its frequency and urgent importance demands.1 My friend of
old days Lockhart Clarke 2 described an unmistakable case of
syphilitic angina pectoris in which the aorta just above the
aortic valve presented a raised convex transverse eminence
with a somewhat rough surface (p. 187). It " consisted chiefly
of fibrous tissue without any appearance of atheroma." The
orifices of the coronary arteries were occluded. Sir William
Osier (in Lumleian Led.) said syphilis was not concerned in
any one of his cases, which surprised me. May it not have
been a factor in his case of the woman, set. 37, cited later in
the same lecture ? Dr. Mitchell Bruce 3 said that in his experi-
ence angina was nearly three times more frequent in the
syphilitic than in any other degenerations of the root of the aorta
(italics mine). From my own experience in England I must
regard its recognition as of pressing importance ; for this kind
of angina, if not promptly curable, is fairly amenable to specific
remedies. Bouchard, at the Meeting of the British Medical
Association in 1908, said that of 261 consecutive cases of syphilis
12 (more than 5 per cent) had angina pectoris ; while of 3739
consecutive cases of all kinds, its incidence was 71 (i.e. under 2
per cent) ; but of these 38 showed signs of aortic disease. In 7
of the syphilitic cases an aortic regurgitant murmur disappeared
under active specific treatment (cf. case p. 179).4 And not only
is due vigilance called for in overt cases of angina which
may have a syphilitic origin, but no less in slighter cases of
stenocardia (angina minor), cases which may be so slight as to
escape the serious attention of patient or physician, but yet
may be no less significant of the same baleful poison, and no
less perilous. As Mitchell Bruce says, a transient and equivocal

1 The pioneers in this pathological research were of course Wilks (in 1863) and
Welch. Hodgson may not have perceived that the gross disease of the aorta
which he so well described was syphilitic. He scarcely says so. Among later
tracts on the subject, are those of Heller, " Syph. Aortitis," Verhandlungen d.
deuUch. path. Gesellsch., 1900, Bd. ii. ; of Doehle, Deutsche Arch. f. Iclin. Med.
Bd. lv. p. 190, a most important article ; and of Saathoff, — also of the Kiel
School, — Munch, med. Wochenschr., 1906, No. 42 (see p. 168 et seq.).

2 Clarke, L., St. George's Hosp. Rpts., 1866.

3 Bruce, M., in his third Lumleian Lecture.

1 See Lancet, Aug. 8, 1908 A more than usually lucky percentage.

sec. ii CAUSES 263

sense of substernal constriction may to the wise be a hint of
an initial stage of syphilitic aortitis which, in later stages, may,
and too often does, proceed, if not to overt angina, yet to
extensive deformation of the vessel, to impairment of its valve,
or to the establishment of saccular aneurysm.1 Unfortunately,
when syphilis attacks the valvular area it is too often with the
result of insufficiency ; syphilis rarely produces obstruction only,
as atheroma does. Let us take a lesson from the following
records of this accurate clinician. Of 28 cases from his own
private notes of cardiovascular disease with a history of
syphilis, Dr. Mitchell Bruce 2 found double aortic disease in 9 ;
and practically all the rest presented that tone of the aortic
second sound, which signifies degeneration in this area, while
" apical murmurs were relatively uncommon." Two-thirds of
them presented sclerosed radial arteries. " Pain of anginal type
was a prominent complaint in half the cases " (italics mine). Was
it in fear of the orthodox coronarians that the learned author did
not allow himself the use of the plain name of angina pectoris ?
He joined Dr. Mott in the warning that all this is imperfectly
realised. In a case of syphilitic cardiovascular disease in a
man, set. 42, published by Sir Thomas Barlow,3 attacks of
angina pectoris set in, and persisted intermittently till death,
two years later : at the necropsy was found syphilitic infil-
tration in the wall of the left ventricle, and " around the
aortic orifice " ; there was also in this area a small unruptured
aneurysm. It is remarkable that in this case the infection
had occurred only three years before ; we shall see that the
primary disease is usually farther back in time, even 20 years
being no unusual interval ; though, as I have said before, we
must not forget that in their confessions patients are tempted
to push the sin, if such were its origin, as far back into the past
as may be plausible. Three at least of my cases of typical
angina of syphilitic nature occurred in physicians infected in

1 See paragraphs on Angina and Aneurysm, p. 205, in the section in this
work on Aortitis (my Cavendish Lecture of 1903) ; also Mitchell Bruce, Lancet,
July 8, 1911, p. 74, an article in which he reinforces his lesson with added
materials.

2 Lettsomian Lecture for 1901 ; in substance repeated with more facts in
Lumleian Lecture for 1911. (Lancet, July 15, 1911.)

3 Barlow, T., Trans. Pathol. Soc, 1877.

264 ANGINA PECTOEIS part n

the course of their duty. One of them, whom Dr. J. Mackenzie
will remember, was a lady. I recall at this moment only two
cases in married women of syphilitic angina definitely due to
marital infection. In Bruce's cases the average interval between
infection and aortic symptoms was 25 years ; with a maximum
of 54 years and a minimum of 5 years. I have quoted his
maxim that syphilitic aortitis may exist, and progress slowly
and latently for years, "as a rule, in the form of presternal
oppression on exertion" before declaring itself (italics mine).
The following remarkable and crucial case was very kindly
communicated to me by Dr. Sidney Phillips : 1

Male, set. 34, syphilis in 1885. Never had rheumatism. Entered
St. Mary's, October 31, 1895. Had had four attacks of angina
pectoris, radiating especially into the throat. He had on these
occasions " to crawl home." There was a diastolic murmur at the
right base. On mercury and potassium iodide he made some im-
provement ; but on December 23 he had a very violent seizure,
and two days later died suddenly. P.M. Gumma projecting into
the lumen of aorta immediately behind the valve ; none of the cusps
involved, nor independently diseased. There was about J of an inch
space between the margin of the growth and that of the cusps.

I will quote also the following case in a private letter from
Dr. Rolleston : 2

Male, set. 27. In-patient, more than once, for angina pectoris
(supposed to be "functional " !) ; last admission on October 8, 1890.
Systolic apex murmur. The patient died suddenly after dinner
on October 9. P.M. Ventricles dilated. Aortic orifice stenosed
by extensive disease of the aorta (presumably syphilitic) immediately
above the valve, which was thickened and could scarcely have closed
properly. In this case, it is true, there was stenosis (see p. 263).

As it often happens, the orifices of the coronary arteries
were in this case almost obliterated ; these arteries being
themselves otherwise normal. On the evening when this
lecture was delivered in Fitzroy Square Dr. Parkes Weber
had happily secured the heart and aorta from a fatal case of
syphilitic angina (Female, set. 42). 3 The specimen presented

1 Letter dated Jan. 20, 1906.

2 Letter to me, July 23, 1907.

3 This case was published by Dr. Weber, Proc. Roy. Soc. Med., April 1908.

sec. ii CAUSES 265

the usual cushion-like protrusion of suprasigmoid luetic aortitis,
and the process had advanced to occlusion of the coronary
orifices (p. 182). I ventured to turn the case to my own
purpose by paraphrasing Dr. Weber's interpretation ; namely,
that to the occlusion of the coronaries was due, not the
patient's angina, but her death from angina ; the source of
the angina itself being the aortitis. Disease of any kind in the
suprasigmoid part of the aorta is of course prone to invade
the coronary orifices, and this condition it is which brings about,
not the angina, but the mortal issue of it ; yet many, or most,
published records of angina are useless for my present research,
because the pathologist, content with the discovery of coronary
disease, or of gumma of the myocardium, gives little or no heed
to the aorta. However in not a few crucial autopsies after
angina we have clear evidence that the coronaries had escaped ;
as we shall see presently. But I am anticipating.

If our sight could penetrate the chest during life, we should
recognise cases of angina without coronary implication more
frequently ; for, as most of the syphilitic and other infectious
cases are in comparatively young persons, the disease in them
is often not mortal ; at any rate not by anginal inhibition,
though only too often death ensues indirectly by way of
aneurysm or of aortic regurgitation. Here however is a case in
a male, eet. 60, a patient of Dr. Mathewman of Bromley :

Infection " 25-30 years ago." For five years (in the secondary
stage) persistent skilful treatment. Accessible arteries normal.
Systolic murmur at base, and altered second sound. Systolic
pressure 140. Has had " pulsus alternans " for a long time ; showed
us a tracing of it by Dr. Newton Pitt taken lJf. months before. This
persists. No dilatation of heart. No Stokes-Adams symptoms.
Angina pectoris in typical form, but not very severe in degree, and
abating.

In syphilitic, as in other infectious cases, pressures do not
as a rule run high ; the patients are for the most part under
middle age. But in the following patient, set. 50, sent by Dr.
Eve of Hull, Hyperpiesia and Angina were in co-operation.

He had lived generously, plenty of wine, etc. No tobacco. Some
years ago specific infection, non-suppurating bubo. Wife had

266 ANGINA PECTOEIS paet n

miscarriages. Had careful antisyphilitic treatment. Two years
ago, walking after partridges, pain in left forearm ; it continued as
lie walked for an hour or more, but did not pull him up. Soon how-
ever the pain did begin to arrest him, even on the slightest ascent ;
and it extended up inner arm to shoulder, and crossed the sternum
about the manubrial joint. Did not mention dread. Arteries rather
thick. Systolic blood pressures about 200. (Eve and myself, 190 and
200.) No definite signs of renal disease, though a trace of albumin
had been detected occasionally. No casts. First cardiac sound with
faint murmur at base. Aortic dulness, at manubrium and to right
of it, very definite. The general treatment (besides the specific)
had been rigid dietary and laxatives (Eve).

It is therefore of the utmost practical importance, in examin-
ing a case of angina pectoris, especially in a patient not obviously
a subject of senile atheroma, to search for any note of old syphilis ;
a characteristic scar, however tiny, or mark on limb, eye, or
pharynx ; pupils insensible to light ; a premature general arterio-
sclerosis, a reaction to Wassermann's test, and so forth. In all
cases of angina under the age of 60, in which evidence of syphilis
is not patent, the Wassermann test should be applied.1 I have
said that syphilitic aortitis is in my experience not always
accompanied by a general arteriosclerosis ; Dr. Mitchell Bruce
found this in one-third only of his cases of cardiac syphilis ; he
puts it " that syphilis of the organs of the circulation is a
locally distributed disease." Dr. Mott's experience is to the
same effect.2 Even if, with the angina, nephritis high-blood
pressure and arteriosclerosis seem to complete a diagnosis of
Bright's disease, we must not forget that recent researches 3 have
suggested that nephritis is one of the consequences of syphilis,
so that this subtle infection may still lie at the bottom of the
case, and be a proper object of the treatment. Again and again
it has forced itself upon my mind that symptoms interpreted
as thoracic or cardiac crises of tabes, were sometimes those of a
coincident angina pectoris engendered by the same poison ; a
distinction not to be regarded as a mere clinical refinement,
because a vigorous specific treatment, if bootless in respect of
the tabes, may not only dissipate the angina, but also prevent

1 See Jacobaeus, Deutsche Arch. f. klin. Med. Bd. cii., 1911.

2 My own experience, essay on Arteriosclerosis (Vol. I. p. 295, etc.

8 Sir John Rose Bradford, and others.

sec. ii CAUSES 267

extension of the mischief to the aortic valve (p. 176). How latent
the aortic disease may be is illustrated by this case of Dr.
Morison's,1 which I give in summary :

Male, set. 32, Angina (" typical ") one month. Physical signs
negative. No abnormal sign about the base of the heart. Urine
normal. Died in an intense and protracted seizure. P.M. Typical
Hodgson's aorta, which had " nearly occluded the orifice of one
coronary artery." Myocardium " perfectly healthy " (italics mine).
"Aortic valve normal; cardiac plexus normal" (vide p. 362).

Among many other cases of syphilitic angina on record, I wish
to refer to two, very similar, published by the late Professor
Dieulafoy ; 2 for the one which ended in recovery was verified, if
I may say so, by the second which was mortal ; in this instance
again after death suprasigmoid aortitis only was found. Dieu-
lafoy was compelled to admit that disease in this spot can set
up angina pectoris without any implication of the coronaries.

In the number of cases, no inconsiderable number, in which
life was not forfeited, we may guess that the disease did not
invade the aortic cusps, nor block the coronary arteries ; or
that specific treatment was adopted in such good time that any
such exudation was dissolved ; or again that these vessels, if
blocked wholly or partially at their orifices, were still permeable,
or could accept blood from other connections. If in cases with
aortic regurgitation sudden death occurs, it may be impossible to
say whether death were due to the aortic or to the coronary
disease, or to both. I have already insisted (p. 21) that extreme
stenosis or occlusion of the coronary orifices is not inconsistent
with an apparently normal myocardium ; though, if with closed
coronary orifices fife and a fair integrity of the heart are
to be spared, the process, as we have seen in the chapter on
Cardiosclerosis (p. 23), must be very slow. It seems at first
sight that syphilitic aortitis would go too quickly for such
accommodation, yet I have seen some recoveries from severe
syphilitic aortitis, in which specific treatment had not been very
prompt, or not very systematic. The misfortune is that too often
a permanent aortic regurgitation is established (p. 182) ; usually,

1 Morison, A., Cardiac Pain, p. 35.
2 Dieulafoy, Traite, etc., 15th ed. pp. 983-984.

VOL. II

268 ANGINA PECTOEIS part n

says Tripier,1 with separation of the cusps from each other at
the points of attachment (p. 186). This I also have observed.

Even after recovery from syphilitic angina, we must warn
the patient, as in other forms of syphilis, against a relapse of
the malady. This misfortune was painfully impressed upon me
in the case of a gentleman who, at about set. 45, was under my
care in 1906 for more than a year, during which period we got rid
of the angina, and of all signs of active syphilis. But in 1910 a
recrudescence of the angina set in with a faint aortic regurgitant
murmur. The patient then came under the care of Dr. Evans
of Lowestoft, with whom I corresponded. In spite of energetic
specific treatment he died, and with suffocative symptoms which
Dr. Evans attributed either to latent aneurysmal pressure on one
bronchus, or to mediastinal syphilis.

I have suggested that in some of these cases the swelling might
not have invaded the mouths of the coronary arteries, or had
receded from them. As, during a comparatively acute aortitis,
the process is extending to the valve, the second sound, as
we have seen (p. 200), is apt to alter in a peculiar way (" bruit
de tabourka "), different from that of atherous conditions.
When the valve is touched, incompetency, with a double aortic
murmur, soon appears ; an order which Dr. Mitchell Bruce is
right in contrasting with that of ordinary — " gouty or senile "
— atheroma, in which the murmur is usually systolic only.

Tuberculosis has not much to do with angina pectoris ; but
here I must cite a remarkable case of an old phthisical patient
quoted by Dr. Ewart from Perez, a case of mediastino-pericar-
ditis in which " Perez' sign " was heard. The case has been
commented upon by Ewart,2 Powell, Fowler, and others. The
patient suffered from " excruciating, in fact anginal, pain."
There was " no reasonable doubt that inflammatory adhesions
of a chronic tuberculous nature were present in the anterior
mediastinum." (For Malarious Aortitis, see p. 165.)

Influenza. — The severe epidemic at the end of the nineteenth
century brought more into light the occasional attacks of this
infection upon the aorta ; and if, fortunately, in proportion
to the diffusion of the disease itself, and even perhaps to some

1 Tripier, Eludes anatomo-cliniques, Paris, 1909.

2 Ewart, W., Brit. Med. Journ., April 6, 1912.

sec. ii CAUSES 269

latent degrees of influenzal aortitis, angina pectoris is rare, yet
the absolute number of recorded cases of this dangerous sequel
is far from inconsiderable. This sequel I have discussed in the
chapter on Aortitis (p. 163), and will here touch only upon its
connections with angina.

Influenza was regarded by Gibson as the chief of the infectious
causes of angina ; but, in this infection, as in rheumatism, the
attacks of angina are often attributed, as apparently by Gibson
himself,1 to a myocarditis with painful stretching of a weakened
ventricle. Yet in diphtheria, although myocardial softening
and dilatation are recognised phases of the disease, angina, if not
unknown,2 is very rare. The attacks, Gibson adds, resemble
in the closest manner true angina (italics mine) ; . . . though he
" could not but conclude that the cause of these symptoms was
some nervous disorder, and not a true angina pectoris." And,
as I have said elsewhere, Sir William Osier's and Dr. Shadwell's
records of " spurious angina " in influenza, justifiable as their
diagnoses may seem, do not exclude the genuine disease as no
very rare sequel. Sansom's papers on this subject,3 of which I
made free use in my Cavendish Lecture, were at the time of their
publication the most important exposition of this interesting sub-
ject, and one the more impartial, as Sansom was at first beset by
the reigning opinion that the attacks, typical as they were, could
not be angina pectoris because his first cases were not mortal,
and because the heart seemed " perfectly normal." Then how-
ever came two mortal cases, and in them patches of subacute
suprasigmoid aortitis were revealed ; so that in his subsequent
experience of such cases, whether mortal or not, Sansom accepted
with more confidence the aortic origin of the angina. He de-
scribed the morbid histology of three cases of aortitis, but they
presented little to distinguish them from acute aortitis arising from
other causes. On March 7, 1908, Dr. Finney of Dublin wrote to me
to ask the question, " Have you met with fatal angina after in-
fluenza, with a weak dilated left ventricle ? One of my patients
died in this condition, and another is now (in peril). . . . There

1 Gibson, G. A., Disease of the Heart and Aorta, p. 764.

2 See Aortitis, p. 164.

3 Sansom, E., Trans. Med. Chirurg. Society, 1894 (following a paper two
years before) ; and Hunterian Lecture of 1899 on " The Effects of Influenza upon
the Heart and Circulation " (Lancet, Oct. 21, 1899).

270 ANGINA PECTOEIS part n

was no valvular lesion in either case." Merklen again testifies
that angina pectoris follows " la grippe . . . assez souvent." x
Marmorstein, in a remarkable article, " Des aortites grippales," 2
gives, as a chief symptom of this aortitis, " douleurs avec carac-
tere angoissante et retrosternale." Furthermore, we are now
aware that not myocarditis only but endocarditis and pericarditis
also may arise in this disease.3 Sir William Osier, who in his text-
book * says " a number of cases of angina pectoris have followed
influenza," in another place 5 narrates the case of Chief-Justice
X., who in the winter of 1893 had a severe attack of influenza.
During convalescence he felt pain in the chest on ascending
hills — attacks of angina, which became more importunate and
even severe. With some intervals of relief in the summer season,
the angina hung about him, and in the winter gained upon him.
He died in an attack. The patient, says the author, always
insisted that the influenza was the cause of the angina. In the
same place the author records another case, the sequel of in-
fluenza, which ended in recovery. It observed the usual areas
of radiation, and the attacks were so horrible that the patient
feared a respite lest he should have to go through the suffering
again ! That, notwithstanding phenomena so unequivocal, my
distinguished colleague should have placed this case in the
category of " pseudo-angina " is to me incomprehensible.

Curtice and Watson of Philadelphia 6 have discussed " The
Action of the Influenza Poison on the Heart," and collected
about 70 cases of influenzal angina pectoris. Some of these are
of rather doubtful interpretation, but they confirm the maxim
which I had proposed before, that when influenzal or other
angina occurs in young and vigorous patients the large majority
of them recover. They found that influenzal angina might
be as severe as that due to any other cause ; in some there is the
peculiar dread, especially in the elderly cases, which indeed were
often mortal. They give some interesting records of their own ;
one in a youth set. 18. An important case, narrated by Rendu,
will be found in the chapter on Diagnosis (p. 498). Dr. Guthrie

1 Merklen, P., " Endo-arteritis bei Influenza," reference mislaid.

2 Marmorstein, " Des aortites grippales," Rev. de mid., 10 mars 1908.

3 E.g. Flexner, S., Penn. M. Bull. xv. 1902-3. * Edition of 1905, p. 893.
6 Osier, W., Angina Pectoris, p. 29.

6 Curtice and Watson, Internal. Med. Mag., January 1893.

sec. ii CAUSES 271

Rankin 1 has reported a case, in a lady, set. 48. During conval-
escence she felt for the first time " discomfort referable to her
heart, and went through paroxysmal attacks of precordial pain
. . . suggestive of angina pectoris. The aorta was beating in the
episternal notch, and its throbbings were unpleasantly manifest "
(italics mine). She had a great dread of these anginal attacks,
which, however, were relieved by vasodilators. There was no
suspicion of syphilis. As the lady recovered, we cannot on the
data before us be sure of the genuineness of this case, especially as
the phrase " prsecordial pain " is now used so equivocally ; but at
any rate the illness seems to have been very grave. Dr. Rankin
likewise seems to have based a diagnosis of " pseudo-angina "
on the fact of recovery ; but I must reiterate that in persons
whose hearts are sound, recovery from infective angina pectoris is„
the rule, if a rule with too many exceptions. A sad instance of
such an exception occurred in the case of a Kentish physician,
set. 40, of sound constitution, who after influenza was attacked
by angina pectoris. While at work in his surgery, so violent
an attack seized him that he died in less than an hour. Yet
if he had crawled back into life, and ultimately survived, no
protestations would have*saved him from the imputation of
a " mere neurosis." Frankel, in the fourth edition of Eulen-
berg, reports a fatal case of influenzal angina in a man set. 50,
who had presented no previous signs of cardiovascular defect.
No autopsy is mentioned. Dr. Samuel West 2 says that " at-
tacks of cardiac failure, which we now recognise as a rare sequel
to influenza, were in earlier epidemics more frequent " ; and he
refers to cases in his own experience of " sudden feeble irregular
heart, and imminent peril of death, or actual death " ; symptoms,
by the way, which, as we have seen, are not those of angina —
unless any cardiac dissolution may be thrown into angina, — but
with these he describes also some cases " of anginal form, often
having the same character as true angina (italics mine), and radiat-
ing in a similar way, or with increasing feelings of tightness or
oppression, associated with a sense of cardiac syncope." Here
again I declare that if the cases have the same characters and
issues as angina, characters in which a physician of Dr. West's

1 Rankin, Guthrie, Practitioner, May 1904.
2 West, S., Practitioner, Jan. 1907 (Influenza Number).

272 ANGINA PECTOEIS part n

experience and ability can read no difference, the refusal to
admit them into the category of angina becomes, in a Euclidean
sense, absurd.

As in the more familiar modes of angina, the vasomotor
symptoms which may accompany it are secondary. For instance,
during an attack of influenzal angina, in a case in which aortitis
was verified after death, Sansom noted that " the radial artery
contracted, and the mucous membranes became pallid ; the
vessels then dilated, and the face and lips flushed " ; tides which
may attend upon the irritation of any afferent nerves. In the
behaviour of this or that case fallacy may lie ; but when again
and again these cases are agonising, perilous, and even mortal ;
when, concerning such a case, a medical colleague in his letter to
me says that it is one of "pseudo-angina," although, he adds, "the
attacks were extremely like those of true angina, and are induced
by slight exertion" ; and when in not a few necropsies an under-
lying acute aortitis has been demonstrated,1 and yet, notwith-
standing these agonies and these perils and these findings, an
accomplished physician of the day writes, of the sequels of
influenza, that " various cardiac neuroses (italics mine), such as
bradycardia, tachycardia, and angina (!) are only too commonly
the result of this disease," and when his disciples take upon
themselves the grave responsibility of assuring such patients,
and the friends of such patients, that the symptoms are those
only of a mock angina pectoris — a mere nervous storm — does
not equivocation become worse than " absurd " ?

On the contrary, Sir Richard Douglas Powell,2 whose opinion
on these subjects carries great weight, testifies that he has seen
" toward the decline of an attack of influenza, acute anginal
seizures ; no cardiac lesion, yet severe anginal cramps of the
heart." Of my own experience let me recall the striking case
which I saw with Dr. Humphry (Aortitis, p. 163) : and to it I
will add the following brief summary of a case which, during the
last influenza epidemic, I saw with Messrs. Hartley and Agnew
of Bishop Stortford :

Mr. T., set. 63 ; attack of influenza with pyrexia for a few days —
highest recorded temperature about 102°. The fever had not long

1 See Cavendish Lecture, p. 163.
2 Powell, Sir R. D., Practitioner, loc. cit.

sec. ii CAUSES 273

fallen, when one evening about 10 p.m. he had a violent attack of
angina, and a slight systolic aortic murmur appeared. I saw him on
the fourth day thereafter. The aortic murmur was now quite loud,
and the angina pectoris had passed into the status anginosus ; though
the agony had been palliated by nitrites, morphia injections, and
absolute rest. By such expedients for ten days the malady was
scotched, and after this time gradually disappeared. He never
had any dyspnea, and the pulse, save rises of rate now and then
under pain to 88-90, was normal throughout. The pain was sub-
sternal, and radiated down the left arm, especially to one spot on
the inner aspect of the upper arm a little above the elbow.

Now three weeks before this influenza, Mr. T. had been carefully
examined for a large life insurance, and accepted at ordinary
rates. Had the systolic murmur been there, it could not have
escaped observation, as it was loud over a large area. I noted
also a definite extension of dulness to percussion on the
manubrium and two fingers' breadth to the right of it.

Cooper x has described a case of perforating aortitis in which
" there was no evidence of syphilis or injury, but a probable
history of influenza shortly before the aortic symptoms. The
aorta was adherent to the oesophagus, left lung, and pleura. In
the aorta was a round well-defined hole about an inch in dia-
meter. It appeared to be " a circumscribed aortitis."

In influenza arteritis may likewise befall other vessels.
Edmond Fort 2 records 6 deaths in 15 cases of this kind. The
arteritis is not dissimilar from that of other infectious diseases.
It frequently occurs during convalescence, and is most frequent
in the arteries of the leg, generally on one side ; but it may be
bilateral. Gangrene may ensue. The pain may be so severe
as to demand the injection of morphine.

Of malaria as a cause of angina, I know nothing. (But see
Aortitis, p. 165.) It is confidently alleged as a cause by some
authors, as by Le Roy de Mericourt and Laveran. However,
men on travel, or foreign service, are apt to pick up other
infections beside malaria.

From a recent article (I think by a Russian physician, but

1 Cooper, R., Lancet, Feb. 21, 1914.

2 Fort, E., These de Paris, 1901. Summary in Epit. Brit. Med. Journal
of that year.

274 ANGINA PECTOKIS pakt ii

I have lost the reference) I learn that in convalescence from
plague anginal seizures may appear (Aortitis ?).

Rheumatic aortitis is more frequent than is generally supposed.
Being usually superficial it is often painless. In the pages of
careful clinical observers we may note here and there, as, e.g.
of Merklen,1 " violente douleur retrosternale avec oppression " ;
indeed he accepts angina as a rare event in aortic rheumatism ;
but his attention is so riveted on the heart that the significance of
the sign is unheeded. However, as on this event and its con-
nection with angina pectoris I have written already at sufficient
length in the section on Aortitis, I must be content here
with little more than a reference to it (p. 150). But I
may repeat that Dr. Carey Coombs,2 in his researches into
rheumatic myocarditis, states that " aortitis is usually present "
(italics mine) at the root of the aorta which " microscopically
proves to be inflammatory " (p. 159). It is proper to add that
he detected also arteritis of the coronary arteries. I have
mentioned Dr. Hugh Stewart's 3 report of a case of angina
pectoris in a boy, aged 7, suffering from severe rheumatic
aortitis ; the pain came on suddenly with pallor and anxiety.
Also (p. 158) a case of the same combination in an under-
graduate under the care of Dr. Christian Simpson, one of the
most excruciating cases (for the time) of angina I have ever
witnessed ; and I have seen since another case, not so severe
but typical enough, in a girl aged 12|. Dr. Simpson's patient
made a complete recovery, save for an aortic regurgitant
murmur. He was ordained, and undertook full work as a
curate near London. About ten years later he died suddenly.
And I would again remind the reader of the very interesting
case of angina minor in a young man suffering from acute
rheumatism, under the care of Dr. Windsor of Royston, to
which I have referred in the section on Aortitis (p. 157).

Dr. Poynton4 narrates two very interesting cases of " acute
inflammation of the aorta, associated with profound myocardial
disease." I must permit myself to transcribe the introductory
paragraph :

1 Merklen, Lemons, 1908, p. 172, as quotation from " Freund " ; no more
accurate reference given.

2 Coombs, Carey, loc. cit. p. 159 ; and Quart. Journ. Med.

3 Stewart, Hugh, loc. cit. p. 154. 4 Poynton, Lancet, May 20, 1899.

sec. ii CAUSES 275

" Cases are recorded from time to time in which, with or without
angina, death occurs quite suddenly, and in which the necropsy
reveals a condition of inflammation at the base of the aorta, unusually
acute in its character and remarkably localised in its distribution.
In these cases the aortic valves may be thickened by chronic in-
flammation, and yet they may nevertheless be quite competent,
and neither during life nor after death can aortic regurgitation be
demonstrated and brought forward as an explanation of the sudden
cardiac failure. The area of the aorta which is so gravely and
severely diseased is the one from which the coronary vessels arise,
and it is a natural suggestion that the heart-wall has suffered in its
nutrition either from a narrowing of the lumen of one or both of these
arteries, or that the vessels have shared in the same acute process,
and their ramifications have become occluded as a result. A refer-
ence to the literature upon this subject proves that such may be the
case in some instances, but in the two cases which are recorded
below I do not think that such an explanation is tenable. In neither
of these two cases were the orifices of the coronary vessels certainly
diminished in size, nor were their walls visibly diseased ; and micro-
scopic examination of the heart-wall showed that their ramifications
were not occluded. In both cases the cardiac wall was examined
with especial care, and in both the changes found were widespread
and severe, and of a nature analogous to that found in the aorta. It
is difficult to escape from the conviction that there had been a
common antecedent cause which had thus injured these two organs
which anatomically and physiologically are so closely associated.
The changes in the aorta were obtrusive, but in the first of the re-
corded cases those in the heart- wall might macroscopically have been
easily overlooked ; yet in both cases I should suppose the sudden
death depended far more upon these less obtrusive signs in the heart
than they did upon the striking changes in the vessel- wall. The
question of the etiology of this condition is one of great difficulty,
and it will perhaps be the most rational course to record the two
cases with the necropsies and microscopy before allusion is made to
their causation."

Of the first of these cases Dr. Poynton gives the full clinical
notes ; from these I will quote but this sentence : " Dr. Cheadle
saw her during this attack, and considered it to be one of true
angina." After death the aorta in its first two inches appeared
to be the seat of an acute, supervening upon a more chronic,
inflammation. The branches were not affected. The orifices of
the coronary arteries were open, the walls of both vessels were
macroscopically healthy, and (in a number of sections) no occlu-

276 ANGINA PECTORIS part n

sions were detected. No micro-organisms were detected in heart
or aorta. Of the second case no clinical history was obtained.
The death in both was ascribed by Dr. Poynton wholly to the
lesion of the myocardium, in my opinion an incomplete conclu-
sion. Later, Poynton and Paine 1 say of these cases : " The end
is usually quite sudden, and the necropsy shows as its most strik-
ing feature an acute inflammation of the aorta." Among my
own notes I find the following case (here much abbreviated) :

Miss H., set. 47. At the age of 18 had rheumatic fever, " and
with it, and for a short time afterwards, had angina pectoris."
This information she gave me unasked, and said the diagnosis was
made without hesitation by two eminent physicians. (The neurotic
notions were not then in vogue.) The angina had never returned,
but heart symptoms had been coming on of late. She has now a
dilated heart and a mitral murmur with the usual signs of oedema,
etc.

It is, perhaps, a matter of surprise that angina pectoris does
not more frequently accompany malignant endocarditis, a process
which is often engrafted upon the aorta from its valve, or arises
there independently. Still there are not a few such cases on
record, and two at least have fallen under my own eye. The case
quoted from Dr. Morison (p. 301) as of dextral radiation was one
of malignant endocarditis.2 A good description of this incidence
is given in Charcot and Bouchard's System of Medicine (ed. 1 893)
by Dr. Andre Petit. He says an ulcerative aortitis, consisting
in an extension of the infectious process to the aorta from the
endocardium, presents symptoms coincident with those of the
endocarditis ; 3 but sometimes manifests itself by crises of aortic
pain of a pseudo-anginous (!) character, radiating into the back
and shoulders, sometimes by seizures of true angina pectoris ("par
acces de veritable angor pectoris "), a fanciful distinction ; indeed
he adds, " In some cases an appreciable dilatation of the first
portion of this vessel can be demonstrated." Passing over the
inconsistency of this writer's inferences, I can testify to the
truth of his description ; and that after death the inflammation
may be verified as a propagation of the infectious process from

1 Poynton and Paine, Researches on Rheumatism, 8vo, 1913, p. 67.

2 From information kindly sent to me by Dr. Morison in a private letter.

3 Vide Aortitis, p. 161.

sec. ii CAUSES 277

the valves and orifice to the tube of the aorta. In such cases
the coronary orifices may not be involved. As regards the in-
consistency of diagnosis, even Dr. Stengel surely entangles him-
self in a like distraction of meaning when, as if using the very
phrase of Petit,1 he says that aortitis gives rise to " spurious
angina " ; yet describes the pain as substernal, radiating to
the shoulder, etc. "... without the involvement of the heart
muscle, so often seen in true angina." " These patients," he
adds, " are especially liable to painful attacks on any physical
exertion." Just so ; then where during fife is the criterion of
spuriousness ? Of what use to the traveller is a signpost invis-
ible while on his journey; or to clinical medicine a diagnosis which
cannot be made till the patient is dead ! It is not quite clear
indeed what that is in which the heart muscle in " true angina "
is found " involved " ; my friend Dr. Stengel cannot mean that
in this malady the disease of the heart muscle is a pathological
criterion or correlation of true angina, for, if so, why " often " ?
Either myocardial disease is essential to angina or it is not ;
Dr. Stengel's words imply that it is not, which is true. In death
from angina pectoris the state of the heart, whether normal or
abnormal, is not a constant.

Surely all this pseudonymous hair-splitting does not tend to
edification, for in rheumatic, influenzal, and other infectious
forms of aortitis the angina is generally attributed not to a false
but to an organic lesion ; namely, to a myocarditis accompany-
ing the aortic disease. Sir J. W. Moore,2 for instance, and
Frantzel 3 likewise, have attributed attacks of angina pectoris to
the weakness and dilatation of the heart, consequent upon the
acute infection. Is it not sufficient, on the other hand, to
point out that in certain infections, such as diphtheria and
typhoid, which seem very rarely to touch the aorta, but do com-
monly poison the heart's muscle, angina occurs not " often,"
but indeed very rarely, and from the cardiac disease never ?

Dr. Parkes Weber asked me why angina was not an invariable
effect of, say, syphilitic aortitis. Well, as we shall see, much
depends on the rate, the intensity, and the precise seat of the

1 Loc. cit. p. 31.

2 Moore, Sir J. W., Dublin Med. Journal, 1890.

3 Frantzel, Varies, d. Kranh. d. Herzens, 1889.

278 ANGINA PECTORIS part ii

lesion. The aortitis may be too superficial ; or the afferent end-
ings may be destroyed so gradually that pain may be averted or
slighted, or some readjustment brought about. I may ask in
my turn why angina does not occur in all (or in most) cases where
the coronary arteries are occluded ? This inconsistency Dr.
Weber admits in the Pathological Transactions, 1906, where he
gives an explanation he did not offer to me.

CHAPTER V

SYMPTOMS

As in the introductory sections of this essay I have divested
angina pectoris, or shown how to divest it, of the false
draperies which of late have been the fashion, now let us attempt
to delineate its features in their true austerity. Angina pectoris
has been too often and too admirably described to need any new
portrayal : x I propose first to discuss its symptoms so far only
as may be necessary to illustrate my theme ; next, to make a
similar selection from its morbid anatomy ; then, upon the facts
thus reconsidered, to erect my own hypothesis, and, finally, to
deduce therefrom what may be relevant concerning diagnosis
and treatment. Although we decline to recognise phantom
anginas, yet angina pectoris itself, often in typical, often in
larval or fractional, forms, presents to us, as do all other dis-
eases, symptoms and by-symptoms, main symptoms and fringe
symptoms, symptoms essential and symptoms incidental. Let
us begin by distinguishing the essential symptoms, those which
are cardinal and crucial, and consider the subordinate symptoms
afterwards. In the first place, then : —
A. Cardinal and crucial symptoms are :

(i.) Peculiar and startling pain, usually sternal in seat
but, as it forces its path into contiguous segments

1 I have skimmed through Hippocrates, Celsus, Aretaeus, parts of Galen,
Rufus, Oribasius, etc., and failed to discover any definite record of the disease ;
therefore I have omitted a historical section from this essay. Seneca's well-
known case however seems unquestionably genuine (p. 319). The name
" morbus cardiacus " covered a heterogeneous lot of cases ; probably angina
pectoris was among them. Here and there one comes across remedies for pain
in the chest evidently very severe and alarming. Scribonius Largus speaks of
this pain and of a secret remedy which he could not obtain till the death
of him who held it ; then it was published and dedicated to Tiberius.

279

280 ANGINA PECTOEIS paet n

of the spinal centres, above and below the last
cervical and upper thoracic circuit, spreading thence
into widening areas — into the left arm, or right
arm, or both arms, the neck, and parts even
still more distant, and frequently attended, or
alternated, with paresthetic sensations ; sometimes
traversing the segmental centres from sensory to
motor tracts, to set up paresis or cramp of corre-
sponding muscles, or even an atrophy of them.

(ii.) Arrest or restraint, brief but imperious, of respiration ;
and more or less of all muscular activity.

(iii.) Sense of impending death, not constant but in many
cases appal ling ; often, even in slight or incipient
cases, an organic dread or sense of ill - omen, as
contrasted with rational apprehension.

B. Accidental or subsidiary features, not crucial nor cardinal: —
(i.) High arterial pressure ; sometimes primary, some-
times secondary, often altogether absent, even
from typical cases.

(ii.) Atheroma, or other general arterial disease,
(iii.) Vasomotor disorders, such as are seen in other painful
or alarming conditions ; polyuria, sweats, saliva-
tion, etc.
(iv.) Restlessness, belchings, tremor, dyspnea (in com-
plicated cases),
(v.) Some discomposure, be it more or less, of the heart's

rhythms or energy,
(vi.) Sudden death, by cardiac inhibition.

C. Aberrant or larval cases ; in which, for example, the pain
may for a while remain peripheral, as in a finger, or in one or
both hands ; or, very rarely, without pain, as a sense of sudden
arrest and dread ; or, again, in which the pain is felt in the
epigastrium, or about the apex of the heart, or below it in
the course of the seventh, eighth, or ninth thoracic nerve, or
even still lower in the abdomen.

Pain. — By common consent we shall begin with the
pain ; and this in angina is not mere weight, oppression,
or aching about the heart. The recent laxity in defining
the seat of the pain counts for much in the prevalence of

sec. ii THE PAIN 281

erroneous opinion concerning the nature of angina pectoris ;
or rather the common fault is not so much a lack of pre-
cision as a certain precision of error. In one of the examina-
tions for the Membership of the College of Physicians, a test of
candidates of comparatively ripe clinical experience, in answer
to a question — not of my setting — on angina pectoris, I found
in every answer the pain described as " precordial." Gibson
said the pain " is often confined within the precordia " ;
though he himself had shown that it would be truer to say that
it never is. In only one of his own diagrams did this area even
partake of the pain, and this was in a complicated case with
double aortic murmurs and a dilated heart.1 Now strictly the
" praecordia " are the diaphragm and parts about it ; and its
metonymic significations have been less in the direction of the
heart than of the upper abdominal viscera — the liver, spleen,
stomach. " Leni praecordia mulso dilueris melius." Thus we
read severally of " pectus, cor, et praecordia." 2 By " angustia
praecordiorum" the older writers meant, not angina — which may
have been hinted at as an " insultus ferox," etc. — but the sub-
mammary depressing ache of chronic heart-disease. However,
what our text-books and their readers intend by the word, as
indeed they are wont alternatively to say, is " the submammary
cardiac region," " at the heart," etc. Romberg uses the words
" Herzgegend " and " Herzschmerz," plainly meaning the sub-
mammary area ; Eichhorst says the chief symptom (Haupt-
symptom) of angina pectoris is " Herzschmerz " ; and Dr. Byrom
Bramwell, no less an authority, defines angina pectoris as " A
paroxysm characterised by pain in the region of the heart."3 In a
well-known modern English treatise the pain is described in like
manner, as seated " at the heart," the words " in regione cordis "
being added later, apparently as a quotation ; and, a few lines

1 Gibson, G. A., Fig. 9, p. 20 (Edin. Med. Journ. loc. tit.), and Diseases
of Heart.

2 Celsus uses " praecordia " rarely of the thoracic, generally of the abdominal
cavity ; for Pliny the word means viscera (" exta"). When Persius said of
Horace " circum praecordia ludit," he was not referring to the submammary
or any unilateral spot. If we agree to .transfer the meaning of " praecordia "
to the area of the heart, we must be quite clear as to our use. Or we might
introduce the word " pericordia," which, in this sense, occurs here and there
in ancient medical writings.

3 Bramwell, Byrom, Brit. Med. Journ., Jan. 15, 1910.

282 ANGINA PECTOKIS paet n

farther on, the author explains, with no notion of inconsistency,
that the sternum is squeezed or crushed back to the spine
as if with a vice. A medical friend of mine, in introducing to
me a patient suffering from angina, said " his precordial pain
is terrible " ; whereupon, by way of justifying his physician, the
patient rubbed and patted the upper part of his sternum. A
physician, writing from a foreign watering - place in high repute,
refers the pain in a certain case of angina to " the region of
the heart," yet in the very next sentence speaks of it as seated
in the " upper third of the sternum, and the second and third
intercostal spaces, radiating to the left arm and back." The
better early authors, on the other hand, are consistent in speak-
ing of the sternal, or substernal seat of the pain ; the phrase
" heart pain " is a modern blunder derived, not from the observa-
tion of nature, but from preconception ; for it is remarkable that
in all the vagaries of its distribution its rarest flight is to the
submammary area. Now, by the tyranny of words, this false
turn of phrase, biassed no doubt by the only too real sense of
peril at the heart, has contributed more than we suppose to the
stiff-necked assumption- — for a sheer assumption it is — that the
seat of angina pectoris — of the pain, that is, not of the death —
is in the heart, and to the laboured ingenuity with which this
interpretation is dressed up. A cardiac angina there may be,
but we shall see that to distinguish it needs far more discrimina-
tion than is usually devoted to the problem.

For the clinical facts let us first consult Heberden : of the
pain this leading authority writes : x " Sedes ejus est modo suprema
pars, modo media, modo ima ossis sterni ; non raro tamen in-
clinatior ad sinistrum quam ad dextrum latus." Of the sudden
crushing and lancinating pain he says, " Pectus quasi constrin-
gente, qui sub sterno modo superiore, modo inferiore, in plurimis
orsus est " ; thence radiating to shoulder, arm, elbow, or hand.
In Percival's case 2 the pain was " about the middle of the
sternum, inclining to the left side " ; and the same is noted in
Alexander's case (both in the third volume of the Edinburgh
Medical Commentaries). Heberden says emphatically that it is
not easy to guess why the pain makes itself felt in these several

1 Heberden, Commentaries, edit. 1807, p. 310.
2 Percival, Med. Observations and Inquiries, vol. v. p. 236 (1773).

sec. ii THE PAIN 283

parts of the " os sterni," but such is his conclusiou from " not
fewer than a hundred patients suffering from this disease."
Fothergill,1 whose experience was considerable, is quite definite
about the pain, a constrictive pain seated in the sternum, usually
in the upper part, and passing across the left breast into the arm.
Before Heberden, Morgagni had said of such a case (Ep. 23) :
" She was subject to attacks of violent anguish in the upper
part of the chest on the left side, with numbness of the left
arm " ; and another (Ep. 4), " a certain divine used to point
to his sternum as the seat of his pain, a symptom which proceeded
from a disease in the aorta, which lies deep in the breast under
this bone " (italics mine) ; Parry 2 describes the pain as mid-
sternal, crossing to the left side ; Jurine, as " douleurs sternales"
. . . "a travers la poitrine " ; Wall,3 as a pain in the upper
sternum, crossing one or both pectoral muscles ; Wichmann,4
as " a bar across the upper chest, the pain being as it were
within the chest." So general is this feature that Baumes5
of Montpellier, in 1808, proposed for the disease the name of
" sternalgia." We note that none of these classical physicians
uses the parrot-like and inaccurate word " precordial " ; they
speak definitely of the pain as sternal or substernal. Trousseau,
although in his general remarks on the disease he more than
once speaks carelessly of " precordial " pain, yet in the descrip-
tion of each of his cases severally, reports the pain as " a la base
de la poitrine, derriere le sternum," adding categorically, " Sans
douleur sternale point d'angine de poitrine . . . si le cceur etait
affecte la sensation au debut de paroxysmes etait precordiale "
(italics mine). And the modern writers to whom we look for
precision are no less careful. Broadbent, who did not copy other
people, wrote : "the pain is chiefly behind the sternum, with
radiations " ; it is " vice-like ; a tearing or burning "... a
" gigantic weight " . . . " usually (italics mine) with a sense of

1 Fothergill, edition of his works, 1783, and previously in Med. Observations
and Enquiries, vol. v. (1773).

2 Parry, C. H., An Enquiry into the Symptoms and Causes of Syncope
Anginosa, commonly called Angina Pectoris, Bath, 1799.

3 Wall, of Worcester, letter to Heberden, Med. Trans, vol. iii. p. 19, 1772.

4 Wichmann, Ideen zur Diagnostik, Hanover, 1797, an excellent commentary
on angina.

6 Baumes, Nosologic, tome ii. ; previously Annates de la Soc. Med. de
Montpellier, Oct. and Nov. 1808.

VOL. II T

284 ANGINA PECTOEIS pakt n

impending death." Sir William Osier, whose mind is trained
on these earlier authors, speaks of " agonizing substernal radial
pain," and distinguishes it from the submammary ache of
ordinary heart - stress. In another passage he says, " the
maximum intensity of the pain is substernal ... in some at
the xyphoid." Throughout his Lumleian Lectures he avoids
the loose phrases of " precordial pain," " pain in the region
of the heart," etc. ; and affirms that heart pain has not
the intensity, the paroxysmal periods, nor the accompaniments
of angina pectoris. Sir Lauder Brunton, in his well-known work
on the subject, writes : " The site of the pain is usually over
the sternum ; sometimes at its lower, sometimes at the upper
part " ; . . . " sometimes it is more to the left, or may wander
to the right of the sternum." At the Belfast meeting (1909) he
went so far as to concede to me that perhaps the cases of sternal
pain were of aortic origin, those of pain about the apex of
cardiac origin. Well, my argument can afford to dispense
with this equivocal fraction. Barie, and Gallavardin likewise,
insist again and again on the retrosternal seat of the pain in
contrast with pain " in the cardiac region." Neuburger from
his very large experience emphasises the same character. Dr.
Morison says the pain is sternal or retrosternal, usually about
the middle of the bone. In the Lettsomian Lectures for 1901, Dr.
Mitchell Bruce describes the " sense of oppression " as " behind
the sternum." Dr. Mackenzie observes the same precision. Dr.
Colbeck x says the pain is primarily " retro-sternal." Sir Thomas
Oliver 2 well insists on the sternal site of the pain, though later
he deviates into the " precordial " phrase, without indicating
any distinction between the sternal and the cardiac sites.
Pawinski 3 says " the seat of anginal pain is ' der obere oder
mittlere Abschnitt des Sternums,' " and he too contrasts it with
the " anxietas praecordialis " of ordinary pericarditis and other
heart diseases. In some cases in my notes, and in some
others which I remember, the chief seat of the pain was not
exactly sternal, but a little to the left of the upper part of
the bone, about the second or third interspace ; an obser-

i Colbeck, Lancet, March 31, 1903.

2 Oliver, Sir T., Lancet, Sept. 16, 1905.

3 Pawinski, Deutsche Arch. f. klin. Med. Bd. lviii.

sec. ii THE PAIN 285

vation which has been made by other authors ; Laennec for
instance speaks of the pain as sometimes seated about the left
pectoralis major. The pain in the spurious form, on the other
hand, is about or below the apex ; a spot often marked
by a persistent hyperesthesia. In angina the hyperesthesia,
often definite enough, is present only during or just after a
seizure, and is not predominant in the submammary area.

If now we turn from the site to the degrees of the pain, I
would urge that, if in one extreme the pain is ruthless, such that
the patient feels as if " the life were being squeezed out of him,"
if, as no other pain, it racks the very depths of anguish, and
in its reiterating paroxysms of torture and dismay seems to be
more than flesh and blood can bear,1 and if in the severest cases a
" status anginosus " may bait the sufferer, making him as one of
the older writers says " furibundus," for hours or for days — for
days in one of Heberden's cases — yet in other cases its passage
may be so light and transient (a degree often called by Brera's
name of " stenocardia," 1810) as only too often to escape serious
attention, yet, even in these minor skirmishes, it brings with it
a peculiar malice, a warning innermost touch ; incomprehensible,
vaguely startling. The instancy of the arrest, though but for
the moment, surprises the man. A moment, and it is gone ; but
it comes again, and again leaves upon him this same uncanny
spell ; so that he goes to his physician, "just to be assured that
it is nothing, nothing but a touch of flatulence, to which he is
subject, as his father was before him." These slighter anginous
tensions are by no means rare in cases of high arterial pressure.
Did such far from uncommon forebodings begin and end
just there, their identity with angina might be questioned (vide
Diagnosis, p. 495), but we have only too much evidence of their
common nature, whether as forerunners of typical attacks or as
minor terms in a series of varying intensity, to doubt their
sinister meaning. Allan Burns says, " Pain may not occur in
either arm ; it is frequently absent and not pathognomonic."
As Dr. Mackenzie 2 writes : " It may be but a slight sensation
of constriction across the chest ... so slight as to pass un-

1 Kiel rb fiev £fj, to 8e pLedicrTaraL kclkov,

rb 8' eKweiprivev olvt'ik il; o.pxV^ viov.

2 Mackenzie, Jas., Heart Diseases, 1908, p. 44.

286 ANGINA PECTOEIS part n

noticed." " If," as Sir James Goodhart x has said, and as
Laennec said before us,2 " these larval forms of angina,
too often put off as false angina, were more seriously
reckoned with, we should hear less of the rarity of the
disease " (vide pp. 242-3). He adds these weighty words :
" Angina pectoris is common among us if we are on the look
out for the milder forms of it. . . . In walking up the smallest
incline, the anginal patient will shy . . . stop to look into a
window ... in a few seconds the pain will have vanished
. . . with nearly always an eructation of wind . . . and be
regarded as a simple indigestion. ... It finds out the city man
after breakfast." Thus in his later years it " found out " an
old friend of mine — a bon vivant, with a big heart, high pressure,
and atheromatous arteries, but no renal disease ; when while
wielding his salmon-rod he had to lie down on the bank for a
few minutes before he could go forward. Gradually the oppres-
sion became more frequent, and occasionally put on the full
dress of angina ; but by a careful and tranquil life he kept it
at bay, and after many years of high arterial pressures died of
cardiac defeat. Dr. Graham Steell 3 says : " True anginal pain
need not descend into the arm, but may be confined to the
chest ; it may descend into the arm later." An unmarried man,
set. 34, was in the Addenbrooke's Hospital in December 1911.
He had never had rheumatism in any form, nor indeed any
illness till the present. Although he could give no account
of syphilis, it was easy to read the story in the physical signs —
aortitis, aortic valvulitis, aortic regurgitation. And he had not
forgotten that, some months before, a slight but disagreeable
pain — nothing comparable in degree to typical angina pectoris —
had at times crossed his chest about mid-sternum, making him
stop for a moment. In such instances it is that the mischievous
confusion between " true angina " and " false " may betray us
into grievous error, for some writers to these stealthy forms
of an affliction only too real, only too ominous, give the name
of " false angina." The minor attacks are quite as character-
istically brought on, by effort, by cold, and the like.

1 Goodhart, Sir Jas., Lancet, July 1, 1905.

2 Laennec, Traite a" auscultation, 3rd ed. vol. ill. p. 351.

3 Steell, G., Med. Chron., Nov. 1913.

sec. ii ANGINA MINOE 287

It is of the utmost importance then to detect, and truly to
interpret, this " petit mal " of angina {A. minor) ; in themselves,
indeed, these arrests are ominous, for even if, as is sometimes the
case, no heavier attacks succeed them, they often indicate that
high arterial pressures of long duration are straining a not im-
maculate aorta ; and that, unless they are averted, dilatation
and defeat of the heart may be inevitable, and perhaps not
far off. Women often think little of some oppression of breath-
ing on rising a hill, and, if it be unattended by any menacing
sensation, they will forget to mention it. This was the case
of a lady who consulted me not long ago. By no patience
could I make her systolic pressure less than 180-190 ; and a
few questions elicited a clear story of angina minor. Another
lady who consulted me, in much the same condition and about
the same time, did make especial mention of oppressions not
more painful but in her case attended with an uncanny
sensation. In many cases, perhaps in most, this first muffled
aortic groan is but the prelude to the fiercer pang of stark
angina. It is because its character is thus often overlooked, or
its significance even denied, that one would earnestly plead for
more regard to this minor form, and I would repeat that a
substernal oppression of the gravest significance may yet be
very slight ; and that, even if not the precursor of overt angina,
if not the precursor of death by cardiac inhibition in another
and perhaps not severer seizure, it may nevertheless be a grave
intimation or signal of Hyperpiesia. In an infectious disease it
is no very rare sign of a covert aortitis.

I have been asked by more than one correspondent on this
subject, if excessive tension of the ascending aorta would not
suffice, without any lesion of it, to cause such a painful or " nasty "
sensation. Well, one is thus tempted to think it may ; but,
unless the vessel were already very taut, its outer investment,
which I take to be the chief source of the pain, would be less
strained than the intima and musculo-elastic media, which
usually are more or less in tone.1 As with other such invest-
ments, the pleura for instance, which ordinarily on expansion
give rise to no sensations, but yet when inflamed may be-
come exquisitely painful, so in respect of the aorta I think
1 That a slack aorta may throb painfully we are all aware.

288 ANGINA PECTOEIS part n

to become painful the outer wall must be in an abnormal
state. But a more effective argument is from clinical experi-
ence. If substernal tightness on exertion (angina minor) do
pass off under treatment addressed to the arterial pressures,
if it pass off even for three or four years, we shall yet find it
prone to return ; only too prone to wax into angina major, or
to merge into strained and failing heart. The more one sees
of these minor cases, the smaller the proportion of those
which might seem to be no more than tension of a normal
aorta. And, conversely, while high pressure conditions, as for
instance in the Bright's diseases, are common, the proportion of
these attended with stenocardia is not great. It is true that
in cases of intense and universal vasomotor constriction of a
passing kind, oppression in the upper thorax, transient and
without ill consequences as it may be (e.g. p. 229), is often
distressing. On the other hand, from certain casual remarks not
infrequently made by elderly subjects of vascular degeneration,
I suspect that fleeting anginoid sensations (without angor
animi) occur more often than we realise in the atheromatous,
without any graver issue so far as angina is concerned. For
example :

Male, set. 55, under my observation for nearly twenty years with
aortic regurgitation of still longer standing, on a recent consultation
told me that at times, especially on moving quickly, he felt " a
tingling in the whole left arm," as if he had lain upon it, but more
transitory.

I repeat that in my experience angina minor is not un-
common in women, in whom angina major is comparatively
rare ; often in them it preludes, rather than typical angina,
a strain of the arterial system by high pressures, to which
they as well as men are liable. I think the attacks of angina
minor are brought on by exertion, however slight ; not so often
by ordinary degrees of emotion, nor by obscure influences moving
in sleep. Sir William Osier duly notes its occurrence in both
sexes, " singly or between-whiles," stopping the patient " with
a nasty indescribable sensation." And Dr. Mitchell Bruce
says " we must enquire for occasional traces of anginous
symptoms; yet unless a man is stabbed and strangled almost

sec. ii ANGINA MINOR 289

to death, these lighter assaults, especially in woman, are
not rarely put by under that equivocal and mischievous title
(italics mine) of pseudo-angina." Stadler also (loc. cit.) warns
us against the possible " tragische Verlauf " of symptoms
called offhand " nervous." Sir James Goodhart I have
quoted to the same effect. The evil nature of this furtive
pain is betrayed by the company it keeps. Physicians
possessed by the " precordial " notion are the more easily
deceived, for the angina minor, except in certain epigastric
cases to which I shall advert presently, is likewise almost
always at mid or upper sternum, and frequently unattended
by cardiac symptoms. On any such complaint then let us
exact a close physical and general investigation, including
estimations of blood pressure.1 To make a diagnosis, and to
communicate it in full to the patient are of course two different
things ; but the patient who has experienced a full attack
learns only too well what gratitude may be due to the physician
who had taken timely warning from the previous skirmishes.

A sure proof of the quality and malign nature of these
minor attacks is to be found in their alternation with
unmistakable attacks. For instance :

Male, set. 70-80. During the first four or five years suffered
from angina intense, complete, and typical ; seizures at one period
brought on by gentlest walking even on the level. Then recovery
set in, so that he was able to discharge all the duties of a responsible
position in life. To his friends he seemed to have recovered
fully ; but during the last three or four years on going up hills or
steep stairs he has been liable again to a slight but unpleasant
substernal constriction.

But we must not flatter ourselves that, in respect of life,
angina minor means a petering out of the peril. A contrary
example I find in the notes of a case kindly sent to me by Dr.
Falkener Hill of Manchester.

Male, elderly. Arteriosclerosis noted for three or four years. In
June 1908 had a typical attack of angina pectoris. Under careful

1 Excessive arterial pressures, as the heart begins to labour, often produce
a vague uneasiness or beating in the cardiac area ; but in a patient of my own,
a middle-aged man, long subject to an obscure disorder of the heart, falls of
pressure, to which he is subject, give him " a bruised feeling about the heart."

290 ANGINA PECTOEIS part n

management and tranquillity he never had another typical attack,
but frequently had slight " turns " — " a substernal tightness which
had been present in the typical attack but afterwards was unattended
with any radiation. Yet in one of these, in the presence of friends,
the heart stopped, and death was instantaneous."

In many cases of angina minor careful treatment and
moderation of the arterial pressures, if in excess, may give the
patient a respite of uncertain duration ; and now and then such
an one is more completely cured.

Some years ago my own attention was especially drawn to the
suprasigmoid area by certain clinical observations which seemed
to indicate that this part is peculiarly susceptible to changes of
blood pressures ; as if by its nervous endowments it might have
some regulative function in this respect. I guessed that the in-
vestments of this part of the aorta were furnished with nerve
end-organs, whose function it was to indicate pressure changes ;
so that if these bodies, and their pain columns, were submitted
under disease to a morbid summation of stimuli, the correspond-
ing spinal segment, or — in case of longer or intenser irritation —
spinal segments, would be thrown into an agitation expressed,
in greater and lesser degrees, as pain. Under ordinary circum-
stances these messages pass from point to point in silence ;
the reciprocating system is in continuous touch ; but if in high
aortic pressures the suprasigmoid parts and arch become impaired,
the resentment may take the form of angina minor — a slighter
lesion of the fabric of the vessel ; if there be deeper lesion, then
arterial fluctuations, on whatsoever planes, may throw the associ-
ated nervous centres into wider and wider circles of functional
dispersion and even agonising vibration. Under these circum-
stances of quivering alertness however the surprise of sudden
death is less frequent, for the vagus is sooner tired than the
augmentors. As in light chloroform anaesthesia, it is in the
startle or nip of an incipient seizure that the fully charged
vagus may sever the thread of life, even before the patient is
aware of his peril. Thus oftentimes it is by inference only that
the name of angina may be called upon to explain the event.

Concerning this mechanism, by which the pain is awakened, we
cannot as yet speak precisely. I had suggested that nerve
end-organs, whose sensitiveness in other parts to pressure, and

sec. ii NERVES OF THE AORTA 291

especially to dragging tensions, are well known, would be dis-
covered in the sheath of the ascending aorta. Hitherto how-
ever I had not succeeded in obtaining dissections made with
this purpose ; but in Dogiel's now classical papers 1 we find
that these end apparatus have been found in the connective
tissues of the pericardial, adventitial, and other investments
about the collar of the heart and along the large vessels.
The pain is of the kind which belongs to fibrous tissues.
That of acute pleurisy, if less vital, less searching, yet is similar
in kind. In inflamed tendinous structures, where pacinian
bodies are abundant, the pain is agonising — as in acute gout.
So it is again with drags on the mesentery.

Into the many records of eccentric distributions of the pains,
which do not serve to illuminate my main purpose, I need
not enter at great length. In Gibson's Morison Lectures 2 will be
found the diagrams, to which I have referred, of these unusual
distributions of pain ; as, for instance, round the points of both
scapulae to a small area about the fourth thoracic spine. And
these eccentricities are not merely curious ; on a true perception
of the meaning of an odd radiation may depend the true
interpretation of a particular case. Tender cutaneous areas,
such as delineated in Mackenzie's and Gibson's text-books, if
perhaps capricious, and so of less practical value, have a physio-
logical interest, to which I will return. Normally, the pain
originating under the sternum radiates, as we know, in the areas
which Heberden described, and which since his day have been
abundantly verified. Beyond the breast, the pains are referred
approximately to the large lateral branch (the intercosto-humeral)
of the second thoracic, which extends outwards and backwards
to the integument of the inner and posterior part of the arm
(cutaneous branch of the n. brach. medialis), reaching nearly to
the elbow, and towards the nerve of Wrisberg and other branches
of the cervico-brachial plexus ; such seems to be the content of
the segmental representation. I note the intercosto-humeral
reference especially, because it definitely brings the second
thoracic segment into the anginous centres. The pain in the arm
and hand is usually referred to the ulnar aspect (eighth cervical

1 Dogiel, Arch. f. micr. Anat., 1898, p. 66 ; and again 1903.
2 Published in 1904. See also Hirschf elder, Dis. of Heart, 2nd ed. p. 373.

292 ANGINA PECTOEIS partii

and first thoracic), but not invariably ; sometimes the distribu-
tion is rather median (see my case of the whole left arm,
of the left thumb and index in Bretschneider's case (p.
298), and many others). Pain referred to the outer half
of the upper arm and the radial half of the forearm and
part of thumb, an infrequent distribution in angina, indicates
the fifth and sixth cervical segments. Pain in the trapezius and
sfcernomastoid suggest vagus and spinal accessory centres, and —
thence the second, third, and fourth cervical segments (hyper-
esthesia of head and neck (Mackenzie)). In forcing attacks
the pain may drive into both arms, the upper left breast, and —
according to Mackenzie's shaded area — the neck, throat, larynx
— especially " pomum Adami (laryngeal vagus) " — and jaw :
" pallid, anxious, and speechless" says one observer of his
patient. In one of Fothergill's cases, and many later, the pain
was referred to both arms. John Hunter's attacks (auto-inocu-
lated syphilis) began, as he carefully describes them, with a sense
of tightness in the muscles of the nose, face, and left jaw ;
then pain passed down the arm to the thumb (not on the usual
ulnar side).1 It was retrosternal also, crushing the bone as it
were to the back. He noted that the arteries of the left arm
became tender, even to slight touch. He also had the throat
pain ; during the attack he could not swallow, and could hardly
speak. He was pinched and pale in face. The aorta after
death was of the (syphilitic) kind described by Hodgson (p.
168) : " The ascending aorta was much thickened and dilated,
and tuberculated on its inner coat." In a case by Dr.
Sidney Phillips, already noted (p. 264), the pain drove itself
sharply into the throat. Dr. Hugh Anderson asks if this
not very uncommon direction of the pain may forebode vagus
perils. Or may pain about the pomum Adami be significant
only of high blood pressures ? In some records we read
how, in forcing attacks, and the more as the spinal segments
under accumulation of stresses become unstable, pains may be
distributed over fields still larger or more exorbitant, such as
the hypogastrium, the tongue (Trousseau, Ebstein, and a case

1 In respect of certain of these pains see Dr. Leonard Kidd's essay on
the " Phrenic Nerve " (loc. cit.). The part of the phrenic in these symptoms is
as yet scarcely defined.

sec. ii SENSORY DISTRIBUTIONS 293

of my own), the testicle (Laennec, and the abdominal case
on p. 309) ; the larynx, causing aphonia ; 1 areas of the
scalp (Head, Mackenzie; Mackenzie says that the sterno-
cleido-mastoid muscle and the trapezius, if gently pinched,
may prove tender). In a case of my own (G. Y., p. 519) the
patient complained of bursting pain in the lobes of the ears.
These and such peculiarities may depend upon obscure
furrows of structure, work, or worry in the individual ; but
no doubt in many cases, could we but decipher the signal,
they might tell of variations in the seat of the lesion.
Many or all of these peculiar symptoms, e.g. pain in throat,
neck, lower jaw, were noted by the elder observers. Laennec's
case of testicular pain was a very curious one ; the radiation
was wholly dextral, and sped downwards to the spermatic cord
and testicle, which became tumid, and to the right leg. Further-
more, as in the case of the fourth thoracic spine just quoted, or in
a supposed " gastralgia," pain at ambiguous points may peep up
alone and, like the trick of the lapwing, divert the unwary from
the true line of quest. When however the peculiarity is but an
accentuation of some point of the ordinary area, as in the left
little-finger case cited by Mackenzie, or as in a case of my own
(p. 294) in which walking uphill, dancing, etc., aroused pains in
the centres of the palms of both hands (7th cervical segment ?),
or as in Heberden's " Unknown," in whom the pain started
just above the left elbow, thence passing to the chest ; or
again, as in MacBride's case,2 where in each arm the pain arose
precisely at the insertion of the pronator teres on the radius —
occupying a spot about the size of a crown piece, the rest of
the limb being free — in these and such instances of Potain's
" angine renversee " the ambiguity is not so great.

A male patient, set. 67, sent by Dr. Dockray of Bishop's Stort-
ford, suffering from angina pectoris, became subject, on walking
up any slope, to pain about the junction of the middle and lowest
third of the sternum, but also — on which he laid more stress — to a
simultaneous pain around the points of both elbows. These elbow

1 A condition which may be hard to discriminate from latent aneurysm,
unless by the laryngoscope, an examination of course impossible during angina.
Fothergill also noted a reduction or suspension of the voice.

2 MacBride, Med. Comment, vol. v. ; (and Smith) sixth volume of Med. Obser-
vations and Enquiries.

294 ANGINA PECTOKIS part n

pains were excruciating ; though often mitigated by dropping the
arms, at times they would bring him in an agony almost to his
knees. These parts — the sternum and elbows — were the only seats
of the pain. He had no definite angor animi.

In a man set. 58, a patient of Dr. Fordyce of Cambridge, the
pain was at first subscapular, on both sides, but especially on the
left ; and, although before I saw him it had taken up the typical
positions, substernal and left arm, yet the subscapular pains con
tinued. The case was one of high blood pressure (pressure at our
consultation at least 180 mm.). I found a systolic murmur at the
base of the heart, and a thudding second sound. The pain, which
coursed down the left arm to the elbow and wrist, did not reach the
fingers, but they would (all) turn cold and numb. Neither then nor
later did we find reason to diagnose aneurysm.

A gentleman, engaged in an anxious business, asked me to examine
his heart. He was a plump and fresh-looking man about 45 years of
age. He denied syphilis, and the Wa. test was not then familiarly
known. His arteries appeared to be normal. I examined his
heart with suspicions awakened by his own ; but, finding the size
of the chambers and the qualities of sounds to be normal, I
assumed that he was frightened or hipped. He had no palpitation
nor shortness of breath, but he asserted that there was something
wrong about his heart which he seemed unable to describe. I
reassured him as well as I could, and advised rest and a sea-voyage.
Two or three weeks later he wrote to me (he lived far away) to say
that he felt no better, that he was convinced I was wrong in my
confidence ; and now for the first time spoke of a pain arising in his
left hand on exertion. This was alarming, and I begged him to
call upon me again. On his second visit I heard from him, what
before he had not thought material, that on ascents he had felt a
pain in the centre of both palms, especially of the left ; and latterly
he had begun to associate this pain with the indescribable suspicions
concerning his heart which had appeared to me to be fanciful. No
more signs were to be discovered, but I sent him home with a note
to a medical friend in his neighbourhood, urging immediate treatment
based on the gravest view of the case. And before long the
symptoms, at first so obscure, assumed the unmistakable form of
classical angina ; so that, instead of taking the change and rest
which he had been contemplating, he was invalided at home ; and in
this state he remained for some time, unable to take any exertion
without the imminence of an attack : for ten days indeed he was
unable to leave the house. His chest was afterwards examined by
an expert observer at a watering-place, who told him that, even
now, no organic disease is to be discovered in heart, arteries, or else-
where ; and that, history apart, he would " seem a proper candidate

sec. ii SENSOKY DISTRIBUTIONS 295

for life assurance." On his last visit lie told me he had been able
to take the sea-voyage with great advantage. [Some time later
however angina reappeared in full dress, and he died in an attack.]

Speaking generally then, the distribution of anginal pains is,
more commonly and typically, by the last one or two (7th rare)
cervical and the first one or two thoracic segments, with frequent
association of the third and fourth cervical, rarely of the second.
The distribution to the upper cervical branches is represented
in the vagus and the spinal accessory segments.1 As the state
grows worse, the pains usually occupy more of their normal
province. Fierceness of assault, or storm, as in status anginosus,
may signify intensity of local lesion ; but is at least as significant
of harassed centres. Stimulation is cumulative ; it calls, but
may be resisted, even up to 15 or 20 repetitions ; it is so stemmed
that the gradient of it has to attain a certain steepness before it
overflows the threshold ; then, if I may use the figure, the
garrison is affrighted, defence is shaken, and agitation spreads
from quarter to quarter.

Dr. Morison draws our attention to the remarkable swift-
ness of the vanishing of anginal pain, that is to say, in
the ordinary run of cases, and in the earlier stages ; a
curious feature, which may depend on tides of blood pressure.
But in one definite case of angina of my own (Mrs. K.,
p. 242), the left arm on the contrary became the seat of
pain intense and continuous, apparently not confined to
particular nerve tracks, for ultimately it occupied the whole arm
up to the wrist, and after fatigue or anxiety would become for
many hours, or a day or two, so agonising and persistent as to
drive away sleep. The patient was indeed far more distressed
by the arm pain than by the " stenocardia," which in this case
never attained any great severity, and was evoked only by
walking upwards. While the patient at rest might be suffering
much from the arm, the stenocardia was often absent ; though
the connection of the pains was only too certain. Suspicions,
or hopes, of neuritis led again and again to re-examinations
of the arm, which however, except in superficial and transient
degrees after an attack of pain, was at no points tender to
pressure ; and the aspect and nutrition of the arm and its
1 M-Kendrick, J. S., Glasgow Med. Journ., Dec. 1909.

296 ANGINA PECTOEIS part n

muscles were in no wise altered. In this case angina pectoris
gradually became more and more severe and typical, till death
in a seizure. In a syphilitic case in a comparatively young man
(age about 30 to 35), the angina began not as pain but as dis-
comfort or sense of weakness in the arms ; in later attacks
however pain (in both arms) was brought on at once by ascents ;
but soon it occurred during rest also, and became terrible.
One or two of his worst seizures awoke him after midnight.
Either he had little chest pain, or in the agony of the arms
he forgot it (see case, p. 293). But at times the pain took the
ordinary form, including retrosternal distress, and it was in
one of these more typical attacks that he died. I fancied
that in the exclusively arm variety the vagus might not be
affected, but I have an instance of no such immunity. We
cannot then be too suspicious of pains uniformly recurring on
bodily exertion, however eccentric their seat ; especially if in
elderly or possibly syphilitic persons.

Two more cases of eccentricity I have deferred because they
lead to another side of my argument ; cases in which the pain
was most intense in the belt of the eighth and ninth ribs. In
both the pain had been described, according to custom, as " in
the precordial region " ; but, being sceptical about this phrase
and desiring data more precise, I perceived in each case that
the patient put the points of two ringers far below the heart,
namely, on the eighth and ninth ribs in the anterior axillary
line, and towards the costal arch. Dr. Head x says the pain
may be referred even to the eighth and ninth dorsal nerves.
One of these cases was in an elderly man with aortic atheroma,
but with no evidence of mitral disease ; the other in a man of
45, also with aortic disease, but consequent upon rheumatic
fever. In both the pain was very intense, and more distressing
from its association with cardio - arterial disease. In one
it was attended with the dread peculiar to the typical malady ;
in the other perhaps not, but it is not easy from the hospital
patient to obtain discriminating answers. In neither was
the pain substernal, but in both it radiated up the anterior
axillary line to the shoulder and down the left arm, so that
no more could be said of the mere pain than may be said of

1 Head, H., Brain, vol. xvi.

sec. ii SENSOEY DISTBIBUTIONS 297

any pains sweeping the chords of the brachial plexus, what-
ever their origin. My point is that even in these patients the
pain, although undoubtedly anginous, was not " at the heart "
nor " in the cardiac area " ; it was far below it. The dart of the
pain this way or that may be determined by some local condition,
as in a case of Dr. Mackenzie's, in which anginal pains darted
into the lower jaw, where were two decayed and tender teeth ; *
or the sensory centres fretted by more than one eccentric
provocation may be doubly irritable. Dr. Head sums up the
anatomical lines, tentatively, thus : — Transverse arch, inferior
laryngeal segment ; ascending arch, third and fourth cervical,
and first, second, and third thoracic ; ventricles, second, third,
fourth, and fifth thoracic — corresponding to the 2nd-7th rib,
inner surface of upper arm, and ulnar surface of forearm 2
(I think there may be some merging here of the aortic and
left ventricular areas) ; auricles, fifth, sixth, seventh, eighth
thoracic, to which must be added the vago- spinal strands
(" bulbar autonomic ") which carry afferent fibres. But there is
much baffling overlap of areas. The auricles in their development
are posterior to the ventriculo-aortic parts (more caudal). The
spinal and cerebral paths are unknown. Pain may be referred
from the descending aorta to surfaces below the nipple and to
the upper abdomen. On clinical experience I cannot take the
innervation of the heart and of the aorta to be quite identical.
And there is much in these diagrams as yet hypothetical ; Dr.
Otto May,3 for instance, has published three mitral cases with
" aortic " areas of pain ; and, as Dr. Beddard has remarked,
physiologists in discussing these problems are tempted to argue
in a circle.

Finally, the pain of angina pectoris is generally paroxysmal,
rarely a " steady grind." The reason of this is not obvious.
Even in the " status anginosus " flashes of pain are continually
smiting across the storm. A continuous thoracic pain, however
urgent, if of vascular origin at all, signifies rather some
accident to the heart itself ; such as a parietal rupture, or an

1 Mackenzie, Jas., Heart, vol. ii., May 1911.

2 See also Mackenzie, Jas., Diseases of Heart, 1908, where he explains how
as the upper limbs bud out from the trunk portions of the cervical and
upper dorsal nerves are distributed to these areas of the arms.

3 May, 0., Brit. Med. Journ., Jan. 1, 1910.

298 ANGINA PECTOEIS partii

acute coronary thrombosis. But if, and how, severe pain may
originate in the heart itself is a question to be considered
presently (p. 440).

On the parcesthetic and even paretic affections of the arm in
radiating cases, or possibly in cases without pain, I have nothing,
except a few curious records, to add to what is well known to
students of angina pectoris. In an arteriosclerotic case of
Bretschneider's,1 angina, with spasmodic pains radiating from
the angles of both lower jaws to the points of the shoulders,
and thence down the left upper- and fore-arm to the thumb and
index finger (p. 292), led to an almost complete loss of power in
the whole musculature of this arm ; due probably to exhaustion
of the segmental cells. The reporter correctly explained these
symptoms as arising from the arch of the aorta (" von sklerotisch
erkrankten Aortenbogen "), by way of reflex from the third and
fourth cervical and the first dorsal segment. A patient of
mine, set. 51, who, though a teetotaller, had had many attacks
of gout, and whose father was gouty and " died of atheroma,"
sought advice for well-marked angina minor. His systolic
blood pressures were over 200. The physical signs were those of
dilated aorta. Although there were no pains in them, both
arms (during the seizures) " became useless." Such was the
symptom of " sinistri brachii stupor " in a case of typical
angina in a woman described by Morgagni (p. 283). Heberden
too said that in some cases the arm is benumbed. As with the
pain, the distribution of the parsesthesia is mainly ulnar, the
median area being generally free, or but slightly and partially
included ; though, as in the patient mentioned on p. 338, all
the fingers turned numb and cold. A white arm, " dead fingers,"
gooseskin, and the like are not very uncommon. I have
mentioned (p. 288) my patient with aortic insufficiency
without angina who, in the later time of his life, told me that
in certain positions of the body a sense of numbness would
pass over his left arm — the whole arm and hand ; but, being so
transient, it could not be tested, nor even exactly described.
In a case recorded by Dr. Warton of Redditch,2 after the
attack, even so long as twenty minutes after (compare my

1 Bretschneider, Berl. klin. Wochenschr., 1911, No. 19.
2 Warton, Lancet, April 16, 1898.

sec. ii SENSOKY DISTRIBUTIONS 299

case of not simultaneous sweating, p. 339), the extreme tip
of the middle finger would turn numb and pale, whence
blanching and complete loss of sensation would spread
gradually up the finger, which, unless restored by warmth
and friction, would remain for half an hour dead and cold.
The ring-finger also was affected occasionally. In Charles
Sumner's case the attacks would leave the left arm numb
and almost palsied for hours afterwards.1 It has been alleged
that in angina the left radial may shrink, while the right
remains unaffected, but such records are not beyond question.
That the pupils may alter in diameter, with perhaps some
protrusion of eye -ball and elevation of upper lid, are points
of some interest ; in severe seizures the pupils are usually
dilated, especially, it is said, on the painful side (Gibson) ; but
in fear or pain of any kind a symmetrical dilatation of the
pupils is too frequent to permit us to attribute to it a
particular significance. Dr. Mackenzie says that by chafing
under the nipple variations of diameter of the pupils, and
gooseskin, can be elicited. To some of these signs I may
return when discussing the nature of anginal pain. In the one
case we are observing a direct paresthesia, in the other a vaso-
motor constriction. The vasodilators of the arm pass through
the posterior roots of the sixth and seventh cervical and first
and second thoracic segments.

Not a few cases are on record, in genuine angina pectoris,
of outbreaks of herpes on the painful arm. In the case of a
lady who arrived at my house after an attack, the left arm had
to be gently borne on a pillow by her maid as she passed from
the carriage to the house. Burns says, " In Mr. Hunter the
left arm could not bear to be touched." Two physicians 2
have described a case of angina pectoris in which an eruption
of lichen planus broke out on the inner aspect of the left arm,
along the distribution of the intercosto-humeral nerve ; in one
of them was also a small patch on its intercostal anastomoses,
above and outside the left nipple. The whole of the same

1 Johnson, J. T., of Washington, Boston Med. and Surg. Journ., Oct. 15,
1874.

2 Gasne and Chiray at the meeting of the Societe Medicale des Hopitaux de
Paris, March 31, 1905.

VOL. II U

300 ANGINA PECTOKIS paktii

area was tender to touch and heat. But a doubt arises
whether some of these cases of trophic or paretic affection of the
arm were cases not of mere angina, but of mixed origin ; as of
aneurysm or intrathoracic growth ? We know that herpes of
the arm may arise from aneurysm or new growth, apparently
by irritation in the course of the nerves. In one of my own
cases, and in one among those provided for us in an R.A.M.C.
examination, herpes had thus broken out in the line of radiation ;
and Sir W. Osier had published a case of the kind.1 In a certain
intensely severe case, of my own, of anginal pain in the left arm
the limb more than once became largely cedematous ; and on one
occasion I witnessed this effect. Gibson, Mackenzie, Head, and
others have given a good account of such phenomena ; and of
graver trophic effects, such as atrophy of the arm (Gibson, Eich-
horst), in Eichhorst's case with the reaction of degeneration ; to
these I can add little or nothing. In one of Dr. Windle's cases 2
the left fingers were flexed and rigid. The hand may be white
or cyanotic.

Characteristic " tender points," in my experience, as in that of
Frankel and others, are often wanting, and generally inconstant.
For a short time after the attack the muscles of the area
affected may be tender, all over or at particular spots ; but, as
these tender spots or areas are thus inconstant, and the sensation
fleeting, they have not been fully verified ; unless perhaps for the
left pectoral and brachial areas. Dr. Head thinks that a
hyperesthesia of the upper part of the chest, front and back,
towards the left side and left arm (second-fourth thoracic seg-
ments, and often third-fourth cervical) is often found in aortic
insufficiency, and disappears on mitral regurgitation (see p. 389).
The frequent absences of this reaction Mackenzie explains
by the reasonable assumption that a certain height of excitement
of the corresponding spinal centres is required, when a very slight
additional factor may determine it. These hyper aesthetic areas
on the chest, etc., had been picked out by many of the earlier
writers on angina : e.g. Desportes, Jurine, Laennec.

To " dextral " cases I must make some allusion, if to
little purpose. Wall described dextral radiation. The pre-

1 Lancet, April 9, 1910.
2 Windle, D., Lancet, May 13, 1911.

sec. ii DEXTRAL CASES 301

sumption of Gibson, Morison, Schmoll of San Francisco,1
and others, that these are cases of right-sided heart-disease, is
not yet fortified by conclusive evidence ; the distribution of
the cardiac nerves, vagus, spinal accessories, and right and left
sympathetic, between the parts of the heart, e.g. rightwards or
leftwards respectively, is little known. The septum is of course
a late development. In many cases at any rate dextral radiation
seems to represent only a more violent storm, a more forcible
extension of the primary radiations. For, as I have read often
and seen more than once, in the same case the pain in one
attack may be confined to the left side ; but in the next, if
more severe, or quickly following, it may cross over. On glanc-
ing through my own cases I am surprised to find in how many
dextral radiations occurred, more or less. I find only one in
which they were dextral only, and in this case no necropsy
was obtained. Still, there are not a few records of cases con-
sistently dextral, and dextral only. One by Dr. Morison 2 was
as follows :

Male, set. 29. Malignant endocarditis. Severe attacks of pain
" over the heart," passing up to the right shoulder and down the
right arm, being particularly felt at the tip of the right little finger.
Also frequently acute and constricting at the lower end of the
sternum. There was a double thrill on palpation over the second
and third left rib cartilages, and a harsh double murmur there ; also
a systolic murmur at the apex — not traceable to the left. P.M.
Gross lesions of the pulmonary valve, the base of the pulmonary
artery (italics mine), and the septal wall of the right auricle. Aortic
side fairly free from disease.

Even if a right-sided angina were attributable to some lesion
of the pulmonary artery near its exit, yet it is not easy to see
how the seat of origin of the irritation, if virtually within the
heart itself, could have much influence in determining the range
of the radiations to right or left ; if it be outside the heart and
in the pulmonary artery, then sinistral angina is of aortic origin.
Dr. Morison includes his case of dextral angina among the effects
of dilatation of the right ventricle ; a common event, of which
such pain is no ordinary sign. Dr. Sidney Phillips also, starting

1 Schmoll, Munch, med. Wochenschr., 1907, No. 41, see p. 353 note.
2 Morison, A., Trans. Path. Soc, 1872, and Lancet, Jan. 8, 1910.

302 ANGINA PECTOEIS partii

according to custom from the assumption that strain of the left
ventricle is the cause of sinistral angina, is of opinion that dextral
angina pectoris may result from affection of the right ventricle.
When, as occasionally happens, the right-sided radiation is
primary, and even exclusive, there must be some determining
factor of this distribution.1 Dr. Byrom Bramwell suggests
that pain in the right arm may point to the aorta, in the left
to the heart.

But evidence of another kind, published by Dr. Drummond
of Newcastle, may have more bearing on this problem. In
a very interesting study of aortic aneurysm,2 illustrated by
diagrams, Dr. Drummond found that when this affection is
associated with angina pectoris the radiation is usually to the
left side, butsometimes to the right. He then believed himself able
to formulate certain relations between the distribution of referred
pain and the site of the sac ; the rule seemed to be that a sac
springing from the anterior aspect of the arch was associated
with pain referred to the left arm rather than the right, whereas
the nearer the sac approached the upper and posterior aspect
of the inside of the transverse portion of the arch the greater
the tendency of the pain to pass to the right shoulder and arm.
Sacs originating beyond the subclavian artery do not produce
pain in the arms. " One of the most interesting and constant
observations," he adds, " was the connection between the root of
the innominate and pain at the back of neck and occiput." Dr.
Drummond tells me however that two ambiguities in the
records made his results less trustworthy ; first, that of de-
fective clinical records, and?, secondly, in the case of the larger
sacs, that of determining from post-mortem appearances the
point of the arch from which the sac really sprang. An interest-
ing case, in some corroboration of Drummond's opinion, was
quoted by Dr. H. B. McCaskie in his M.D. thesis.3 In a
patient suffering from angina, the pain radiated down the right
arm. Now on autopsy an aneurysm was found on the ascend-
ing arch ; but there was also a second one, and this arose from

1 Vide Brit. Med. Journ., June 13, 1908.

2 Drummond, D., " Thoracic Aneurysm," Brit. Med. Journ., June 13,
1908.

3 McCaskie, thesis for M.D., Cambridge, March 6, 1909.

sec. ii DEXTKAL CASES 303

the summit of the arch. Dr. Bradbury and Dr. Wright read
notes and exhibited the parts to the Cambridge Medical
Society, on November 3, 1911, of a case of rupture of the
aorta in a man set. 53. The rupture took place on the de-
scending arch ; the severe paroxysm of pain, " like angina
pectoris," which attended it was referred to midsternum. The
whole arch however was very atheromatous. Radiography
may produce evidence for us on this part of the problem. I
see that Neuburger had an autopsy in a dextral case, but he
offers no explanation of the aberrancy. With the customary
prepossession he seems to have confined his attention to the
heart and the coronary arteries. (See also p. 421.)

That left and right angina depend on disease of the left and
right coronary arteries respectively, and their relations to the
cardiac plexuses, is a fanciful notion which has been disproved
by many observations.1 For my part I repeat that severity of
the pain has much to do with this cross over to the right. A
patient of mine, a lady who suffered by ill-hap from syphilitic
angina, told me that when the pain was at its worst it would
pass over to the right arm also.

Some interesting observations upon the courses of aortic
pain were published, also in an M.D. thesis at Cambridge, by
Dr. Willoughby,2 who investigated embryological evidence of
referred pain. Beyond the innominate, the origin of the arch
rises entirely from left-sided vascular arches, which may imply
referred pain on the left side. The first portion of the arch
originates in a fusion of two symmetrical right and left ventral
vessels, so that it would be impossible to say how far pain from
thence should be distributed right and left respectively ;
especially if the seat of the lesion on the circumference were not
precisely ascertained. Dr. Willoughby accepted my attribution 3
of angina pectoris to lesion of the arch of the aorta, and
considered that this view " broadened the horizon of the etiology
of the disease." The distribution of atheroma did not seem to
him to betray any genetic lines of incidence. Embryologically

1 E.g. von Neusser, Clinical Treatises on Disorders of Respiration and Circula-
tion, Part III., Eng. trans., New York, 1909, p. 13.

2 Willoughby, W. M., reported in the Lancet, April 16, 1904.

3 In my Lane and Cavendish Lectures, and earlier and later papers.

304 ANGINA PECTORIS part ii

speaking, he gathered that pain taking its rise from the supra-
sigmoid part of the aorta might be bilateral ; that it would be
referred to the region about the junction of the manubrium with
the body of the sternum, and radiate probably to left, or to both
left and right. The left ventricle, being wholly formed from left-
sided embryological parts, should refer its pain entirely to the left.
On the whole, he thought the predominant bent to left-sided
radiation of anginal pain to bein accordance with the preponderat-
ing left embryonic origin of the seat of the causative lesion.
As regards left -sided radiations, some anatomists describe
the anastomoses of the cardiac nerves, and the corresponding
spinal segments, as closer on the left than on the right side ; if
so, it would be easy to understand how slight individual varia-
tions in this construction might vary the quarters of radiation.

In the earlier attacks of a series, the pain usually ends with
surprising promptitude ; the patient passes from hell into heaven ;
but as controls weaken, and centres by summation of stimuli
are fretted and exhausted, the relief comes more slowly, and is
less complete ; the patient is left tremulous and enfeebled.

It is of more practical importance to turn to a grave and
deceitful class of rarer cases ; namely, the epigastric or abdominal
angina — " precordial " in a more proper sense of this ill-managed
word. It seems that these cases, long recognised by students
of atherosclerosis and angina, are not yet familiarly known
in general practice.1 Yet Heberden did not fail to describe
this distribution of the pain : " alii alterio ex abdomine
orientem, tumque demum pectus corripientem." 2 Von Dusch
recognised this epigastric variety of angina, and stated that the
pain, or peculiar uneasiness, referred to this region, may radiate
backwards to the spine ; as it did in Brunton and Williams'
case (p. 309). Butter,3 while describing the usual seat of
the pain as mid - sternal, says it may arise occasionally at
the pit of the stomach. But Butter is not so accurate a writer
as Heberden or Parry, and seems to mix up with angina

1 See Discussion in the Lancet, May 18 and June 1912, where more than one
eminent speaker referred to abdominal angina as a new clinical discovery. It
is of more frequent occurrence than those speakers then supposed ; and has
long been familiar at any rate to French and German physicians.

2 Heberden, Edin. Med. Comment, vol. ix. p. 307.

3 Butter, On the Disease commonly called Angina Pectoris, London, 1791.

sec. ii EPIGASTEIC ANGINA 305

different kinds of distress, such as " gout of the stomach "
and other cardiogastric perturbations. In a letter to the
Lancet, on one of the dates mentioned, Sir W. Osier attri-
buted to Leared the honour of the first description of " Angina
abdominalis " as a group of cases. To Potain these cases were
well known in the vessel as " angina subdiaphragmatica " ; to
Huchard and Neusser as " angina pseudogastralgica," and later,
under names even more complicated, to Ortner, Hasenfeld,
Pal, and others. K. Muller of Budapest described it as angina
abdominalis, and dwelt on the difficulty of diagnosis. There is
no doubt nevertheless that many kinds of disorder have been
indiscriminately gathered under this last equivocal title.

More than twenty years ago, with Professor Bradbury, I
visited Professor X., a man of sixty years or more, with
degenerate arteries, who, after hastening upstairs with a small
portmanteau in his hand in a foreign hotel, had felt rather
distressed, and began to complain of recurring attacks of
" indigestion." We saw him soon after his return home. He
assured us that if he could but get rid of a " nasty feeling of im-
prisoned flatulence at the pit of the stomach, he would soon be
all right." But as the uneasiness — for, importunate as it was,
it scarcely could be called severe pain — was recalled by walking,
and carried with it a subjective sense of indefinite apprehension,
Professor Bradbury's fears were aroused, and a consultation was
held. In view of all the phenomena, we agreed without hesita-
tion that the case was one of epigastric angina pectoris, and, for
the moment, we hoped in a manageable degree ; but the patient
grew worse, and within a few days died in an attack. Romberg
reports a case of this distribution in which the pain in the same
area was more severe, so severe that the first notable seizure was
momentarily mistaken for perforation of a gastric ulcer. Another
case, in which the epigastric uneasiness was little more than a
vague subjective sense of oppression and distension, was in a
Mr. A., an elderly man with degenerate arteries and enfeebled
heart whom in my Leeds days I often saw with Dr. Clarke of
Doncaster. This discomfort, and indeed the sudden death which
took place later, were not inconsistent of course with mere cardiac
decay ; but our suspicions of epigastric angina were aroused in
part by the general features of the case, but especially by two

306 ANGINA PECTOEIS part n

facts observed by Dr. Clarke, that the attacks were brought on
by exertion, rising to the night-stool, or contact with cold bed-
clothes ; and that they were readily subdued by nitrites. And
in the subsequent course of the case his diagnosis seemed to be
verified. I would remind the reader that the connective tissue
about the pancreas and solar plexus and the adventitia of the
larger blood vessels of the part are rich in Pacinian bodies.1
Enterospasm or any drag upon the mesentery thus endowed
may give rise to agonising pain. We shall agree that disease
of the aorta, and possibly of other large abdominal vessels,
may make itself felt after the fashion of angina ; but paroxysmal
pain alone is no criterion.

Clinical observation suggests that epigastric angina may
come of a thoracic lesion, for some obscure reason referred
now to the breast, now, even in the same patient, to the
abdomen. In Dr. Glasier's case, mentioned on p. 149 of this
book, the patient's first attack, or attacks, were epigastric ;
afterwards they settled wholly in the breast, and remained there.
Dr. Johnson Smith 2 also has related a case in which the attacks
alternated between the chest and the abdomen. In one of the
cases published in Sir W. Osier's Lumleian Lectures a man,
set. 59, had both ordinary (typical) attacks as well as attacks
of the epigastric form. He died in one of the ordinary attacks.
Osier agrees with other authors that the pain in the upper
abdomen may " rise up " ; so that, as one patient put it,
" when it gets beneath the breast-bone, it cuts me short as if
the machinery of life had stopped." Pal's case (recorded in
his Gefdsskrisen) moved in like manner from abdomen to
chest. But long before these Hamilton 3 had published a
case of this metastasis of the pain from abdomen to chest. In
some cases of coronary thrombosis (cf. Morgagni's " Medicus,
set. 62 ") the pain has thus started from below and ascended
from the abdomen to the thorax (p. 311). Of such a case I owe a
report to the kindness of Dr. Campbell Smith of Tunbridge Wells.

An elderly man had been subject occasionally for eight or ten
years to symptoms of doubtful interpretation, whether of dyspeptic

1 Vide p. 421, and also Ceelen, Virchow's Arch., June 11, 1912.

2 Smith, Johnson, Lancet, May 18, 1912.

3 Hamilton, Med. Comment., Edin., vol. ix. p. 307.

sec. ii EPIGASTEIC ANGINA 307

or of cardiac origin. But he had had long intervals (even two years)
of freedom. No gout, no lead, no tobacco, no alcohol ; but a
sedentary life. In 1910 began definite attacks of angina in the epi-
gastrium— not radiating towards the heart or elsewhere. He would
sit up, and take nitroglycerine tablets in large numbers — on some
days as many as eighteen or twenty, usually six or seven, and one
or two inhalations of amyl nitrite. As a rule, no alteration in any
quality of the pulse could be felt by the finger, but sometimes the
pressure seemed to rise. His systolic pressure at rest was usually
150. The urine was quite normal, both as to constituents and the
proportions of its solid contents. In the later stage of his illness,
however, the pulse became " weak and irregular " ; and on one of
these occasions it was that he died suddenly.

Vaquez and Bordet,1 again, describe a case of unquestionable
angina, starting from the epigastrium, and afterwards seating
itself behind the sternum, thus :

Mons. X., set. 55, had suffered for six months from typical angina
pectoris. The crises started at the epigastrium, but then mounted
up " behind the sternum," taking the usual course. Percussion
and auscultation were negative ; but not so the orthodiagram :
this revealed " une alteration tres prononcee du vaisseau " (i.e. of
the thoracic portion of the aorta).

So that epigastric angina does not necessarily signify a sub-
diaphragmatic lesion of the aorta.

The absence of dulness over the aortic region they explained
by the dilatation — to almost double its normal diameter — not
at the " cross," where it nears the surface, but at the ascending
portion of the vessel. The authors are of opinion that in high-
pressure cases the dilatation is chiefly to be found at the " cross."
This is not my experience ; I have often seen it there in many
cases, especially in Hodgson's aortitis, with pressures no more
than ordinary ; as also in cases of aortitis in which the tone of
the vessel was much slackened, as it is liable then to become. In
such cases the vessel may rise and fall, as in Minet's case, p. 309.
Edgren has given a clear description of these epigastric and
abdominal varieties of angina ; William Russell likewise, Stengel,
and other authors ; Neuburger again has met with a few defi-
nite and unmistakably genuine instances ; so that the variety

1 Vaquez et Bordet, " La Radiologic dans les aortites," Paris mid., juillet
1911.

308 ANGINA PECTORIS part n

is really fairly well established and defined. When this pain,
as in many of these cases, is seated at the ensiform cartilage
it falls geographically within the sternal district. Of Breuer's
two cases of " abdominal angina " * the pain in the first was
at the cartilage :

Male, set. 40. Fearful pain at ensiform cartilage, brought on or
aggravated by meals or exertion, especially on ascents, compelling
him to stop "as if an iron fist were crushing his stomach " (Magen).
" At the time is pallid, speechless, and anxious. One of the attacks
began during the night in sleep. He was relieved by half-drachm
doses of diuretin."

Relief by nitrites is often mentioned as a criterion of
diagnosis, but nitrites may relieve a gastro-intestinal colic. The
abdominal crises of tabes however are not relieved by nitrites,
so far as I know. Dr. Somers of Selby, of a published case of
his own, said that in the abdominal attacks the pulse was never
appreciably affected. Dr. Walter Verdon 2 explains these cases
as a cardiospasm of the stomach, a suggestion to which I shall
return. Other physicians have explained them, not as angina,
but as an, ill called,3 " dyspragia intermittens," with morbid irri-
tability of a stomach atrophied by arteriosclerosis, an opinion
more opaque than Dr. Verdon 's. F. R. Miller 4 of Toronto points
out the different effects on different animals of irritations of
stomach or oesophagus. Dogs, cats, and rabbits differ thus. In
rabbits, which cannot vomit, the blood pressure rises ; the con-
trary is seen in cats.

I believe then that epigastric angina is but a somewhat
aberrant mode of ordinary angina, and due, broadly speaking,
to disease of some part of the thoracic aorta ; but it is not easy
to detect the conditions which determine the pain to the
abdomen. Can it be diaphragmatic in origin ? The diaphragm
is innervated by pairs of spinal nerves, besides the phrenic ;
and the muscle was originally a circulatory mechanism, its
respiratory function developing later. Vaquez and Bordet give
good grounds for hope that radioscopy will serve to indicate

1 Breuer, " Zur Ther. u. Pathogn. der Stenokardie etc.," Munch, med.
Wochenschr., 1902 (No. 39 et seq.).

2 Verdon, Walter, Lancet, June 8, 1912. 3 Dyspragia means ill luck.
4 Miller, F. R., Pfliiger's Arch. vol. cxliii., 1912.

sec. ii ABDOMINAL ANGINA 309

the seats of many of these latent aortic lesions, acute and
chronic. (For Diagnosis see p. 500.)

Angina more definitely abdominal may be an event of
disease in the lower portion of the aorta or in other large
vessels there. In a case recorded by Max Buch,1 the pain was
in the upper abdomen ; it was much intensified by exertion,
and accompanied with great tenderness of the abdominal aorta.
After death a cirsoid aneurysm and highly atheromatous
abdominal aorta were revealed.

The following very interesting case was recorded by Minet : 2

Male, set. 27. On the seventh day after defervescence from scarlet
fever the temperature rose to 100-4, with abdominal pains. He
was sleepless and had cold sweats. Pains grew worse, and pulsa-
tion in abdomen was seen and felt in time with the pulse, and
became " enormous." The pains also became agonising and struck
into the testicles. The abdominal aorta was tender to the touch,
enlarged, and curved, with concavity to right. No albumen, nor
other suggestion of renal disease. The symptoms slowly subsided,
and the case ended in complete recovery.

A clearer proof of (syphilitic) disease of the abdominal aorta
was published recently by Nixon and Walker Hall 3 :

Girl, set. 20. Congenital syphilis. In the presence of the
physicians an abdominal aneurysm burst suddenly, causing a horrible
agony of pain, due no doubt to the sudden stretching of the investing
tissues there so rich in sensory end-organs. The whole length of
the aorta was diseased ; the adventitia was abnormally thick and
dense, full of cell-nests, and the vasa vasorum much diseased. Much
small-cell infiltration in the media.

In Breuer's second case (loc. cit.), of syphilitic origin, the
pain was definitely below the xiphoid and epigastrium. In a
man set. 68, Brunton and Williams 4 reported that the pain
struck from the navel to the back, and thence to the chest.
The heart seemed normal, and the blood pressure was normal.

1 Quoted Stengel, Brit. Med. Journ., Oct. 20, 1906. In Stengel's reference
list, Max Buch, Progressive Medicine, Dec. 1905.

2 At a meeting of the Soc. Med. des Hop. de Paris, on July 12, 1912.
Quoted in the Lancet, August 10, 1912.

3 Nixon and Walker Hall, St. Barth. Hosp. Reports, vol. xlvii., 1911.

4 Brunton and Williams, Lancet, April 1912, p. 921.

310 ANGINA PECTOEIS part ii

The attacks were started by effort and relieved by trinitrine.
A necropsy was not obtained.

Max Buch surmised that atheroma of the mesenteric vessels
might give rise to soreness, paroxysmal colic, windy distension,
and oppression ; and of late under this name of Abdominal
Angina many such cases have been described and discussed
(vide essay on Atherosclerosis, p. 445), first perhaps by Schnitzler ;
but the name is often misleading, often the symptoms have not
the definite form of angina, nor yield, or not distinctively, to
nitrites. Perutz 1 however, in discussing these abdominal sym-
ptoms in a case in which atheroma of the thoracic aorta and of
the coronary arteries were also present, attributed them to
sclerosis of the abdominal aorta. When, as in a certain
syphilitic case, there was dyspnea, we may presume that the
mischief had gone beyond the conditions of angina. The
often repeated experiment, originally Bernstein's, of irrita-
tion of the sympathetic in the abdomen, which, unless both
vagi are cut, stops the heart in diastole, may throw some
fight on the mechanism of death, but does not locate the pain.
Moreover the phrenic nerve is finked to the cervical nerves, and
these again to the cardiac. But I find that Haddon's well-
known case of angina,2 in which the phrenic nerve was involved in
an enlarged gland, was complicated with an " atheromatous " and
aneurysmal aorta (syphilis ?). Many authors attribute the pain
in these cases to the sympathetic branches and ganglia,3 but it
is fairly certain that these ganglia or fibres are not conductors
of pain. I suggest that the pain arises by irritation of sensory
nerve-endings in the investments of this large vessel. However,
the obscurity of the origin of such pains, and the ambiguity
of using for them the name angina, makes us uncertain whether
the paroxysms are aroused in the vessels themselves (adventitia)
or in the highly sensitive mesentery pulled upon by windy or
oher commotions. I have argued already (p. 445) that cases of
many origins are confused under the accommodating name of
abdominal angina. However, as Breitmann 4 says, in patho-

1 Perutz, Munch, med. Wochenschr., May 22 and June 5, 1907.

2 Haddon, Edin. Med. Journ., July 1870.

3 See Pal, Wien. med. Presse, quoted Lubarsch's Ergebnisse, 1910.

4 Breitmann, M. J., in a Russian journal, abstracted by the author himself
at sufficient length in Zeniralbl. f. Herz- u. Gef.-krankheiten, Dec. 15, 1913.

sec. ii ABDOMINAL ANGINA 311

genesis some cases of abdominal angina very closely resemble
the thoracic. But, if so, may I ask, Where is the inevitable
heart factor in this variety %

Breitmann agrees that abdominal angina is rare in women,
and that many cases are syphilitic. This form prevails between
the ages of 40 and 50, but a few of his syphilitic occurred set.
20-25. He puts all down to the arterial disease, and does not
see that stretching the investments may cause the pain in
the aortic disease, in the thrombotic, and in other accidents in
the same region which simulate it. Breitmann's list is a
heterogeneous collection, and seems to contain thrombotic
cases (he refers the melama to vasodilatation !), gall-stone, and
other colics ; tabes is deliberately included as " anginoid " !
His diagnoses of leading cases are not by any means always
confirmed by necropsies. Clinical and pathological precision
has yet to contribute to a better analysis of these phenomena.

The pressure pains of aneurysm are not very likely to be con-
fused with these anginous symptoms (see Diagnosis, p. 498). In
Sir William Osier's Lecture on Aneurysm of the Descending Aorta,1
neither in the case histories nor in the summary are anginous pains
mentioned. I have heard it said that aneurysm of the abdominal
aorta may be attended with symptoms of anginiform character ;
still it is noteworthy that in abdominal aneurysm definite reports
of anginous symptoms, or sudden death, are hard to find. The pain
of embolism of the mesenteric arteries has never, I think, been taken
for angina? For these reasons I am disposed to think that " epi-
gastric angina" at any rate springs from lesion of the thoracic
aorta, but, after a manner not unfamiliar in other cases of the
kind, it is by some unknown interference shunted on another line.

Furthermore, in Osier's article on Angina and Aneurysm,2
a patient suffered for six months from attacks of abdominal pain,
attributed to colic or flatulency, but ultimately traced to an
aneurysm of the thoracic aorta. In some other cases the seat
of angina, at first abdominal, has afterwards settled in the usual
sternal position. On the other hand, it is true that in some of these
cases of paroxysmal pain, and death by inhibition, in which the
pain was seated below the epigastrium, atheromatous disease

1 No date or place on my reprint of it.
2 Osier, Medical Chronicle, May 1906.

312 ANGINA PECTOKIS part ii

has been discovered in the abdominal aorta or coeliac axis ; but
atheroma of the abdominal aorta is common enough, and careful
comparisons with possible disease elsewhere are not recorded.
However Barie and Colombe have published two very signifi-
cant cases,1 for in both extensive disease of the abdominal aorta
was disclosed at the necropsy ; in one of them the coeliac axis
was almost occluded. Teissier's test for angina of abdominal
origin of excessive pressure in the dorsalis pedis is in more
than one respect fallacious. In the discussion 2 on Brunton
and Williams' case subsequent speakers seem to have mixed up
many kinds of irregular spasmodic abdominal pains with those of
Sir Lauder's text ; still some were mentioned in which atheroma
of the abdominal aorta and coeliac axis were discovered after
death. But again no careful comparison of states of other
portions of these vessels was recorded. Albu3 says that
in these abdominal cases, if the patient be thin, the thickened
arteries may be palpable ; he remarks on the combination with
angina of the breast, but thinks it is rare. As differential
features from colic, he gives short duration, complete independ-
ence of meals, and arousing of the pain by bodily effort.

Dyspnea. — It is agreed among careful observers that in mere
angina there is no dyspnea. Records to the contrary are,
generally speaking, to be counted as errors or shortcomings in
diagnosis. A desire for air there may be, but the respiratory
movements, if quickened at all, are shallow, weak, and not
urgent. Seneca (Ep. 54), who described his angina as " brevis
autem valde et procellae similis impetus," did indeed use
the word suspirium, but probably meant no more than a sigh.
The voice, if speech be possible, is hollow and distant. In his
article on Angina sine dolore, Dr. W. W. Kerr 4 has not avoided
this ambiguity. Some of his cases are no more than the
ordinary recurrent attacks, often nocturnal, of cardiac dyspnea.
Morgagni 5 acutely commented on this inexplicable absence both
of cardiac disturbance and of dyspnea, as on the sufficiency of

1 B. and 0., B. and M., Soc. Med. des Hop. de Paris, Feb. 1913.

2 Proc. Boy. Soc. Med., April 1912, p. 53.

3 Albu, " Diag. d. abdom. Krampfzustande," Deutsche wed. Wochenschr.,
1912, No. 22.

4 Kerr, W. W., Joum. Amer. Med. Assoc, April and May 1910.

5 De Sedibus, Ep. xxiii. (8), " De palpitatione et dolore cordis."

sec. ii DYSPNEA 313

the ventricular function ; and to this effect quoted and compared
cases from Cowper, Haller, Vieussens, and other authors. Des-
portes says emphatically that neither in pulse nor respiration are
generic characters of angina to be found. If, he says, dyspnea
be present, the case is mixed with cardiac, pulmonary, or renal
disease. Usually it signifies that the heart is succumbing
to high pressures, or with intrinsic disease. Allan Burns says
clearly (p. 140, ed. 1809) : " If there be actual dyspnoea present
you may be certain that the disease is either not Syncope anginosa
or that it is a complicated case — such as effusion into the chest,
ossification of the valves, or asthma." He cites John Hunter's
personal testimony to this effect. For good records of such
" mixed cases," I may refer to the interesting paper by
Dr. Davenport Windle 1 on angina coincident with cardio-
arterial disease, pulsus alternans, and dyspnea chiefly of the
paroxysmal high-pressure kind ; but, as Heberden says of one
of his patients, " adeo ut cordis et pulmonum negotium plane
cessare sibi videretur," and adds, as a general maxim, " nulla
tenentur spirandi difficultate." This to the elder writers, who
did not always discriminate between angina and asthma, was
one of its strange ambiguities ; " quod de nullo alio
asthmate, ut videtur, valet." " Sine quavis tamen dyspnoea,"
declares Willis. " If he breathes," said John Hunter, " it is by
an effort of the will." Parry and Wichmann also speak no
less definitely of the exclusion of dyspnea from the characters
of angina ; and Jurine says, " l'acte respiratoire continue a
s'exercer . . . n'est que tres peu interverti, meme dans les
plus forts acces." In one severe case Jurine records the respira-
tion as, during the attack 26, and in the interval 23. Raige-
Delorme,2 summing up the knowledge of angina as it was a
hundred years ago, says " all observers are agreed that the respira-
tion is not affected ... or it may be a little quickened." Von
Dusch says clearly that the respiration is mechanically free ;
that if the respiration be quickened it is in fear, or there is a com-
plication. He adds that the diagnosis from cardiac dyspnea,
from neurotic panting, and so forth, is not difficult. Watson
writes : " Yet the patient is not out of breath." Flint and

1 Windle, D., Lancet, May 13, 1911.
2 Raige-Delorme, Diet, de med. 22e ed., 1833, vol. iii. p. 142.

314 ANGINA PECTORIS part n

Walshe are no less positive ; Walshe, in differing from Stokes (p.
317), says dyspnea is, if present, incidental; that in pure angina re-
spiratory action is " below par." Broadbent 1 says, " Not ventur-
ing to make the least movement, and scarcely seeming to breathe."
Gallavardin urges the same point. Dr. Morison, describing a
particular case, says " the respiration was restrained during the
agony, but not otherwise disturbed or difficult." Frankel says
clearly that though angina pectoris and cardiac dyspnea may
concur, or in the same patient alternate, yet that these con-
ditions are to be considered severally, though we often fail to do
so (" streng von einander zu unterscheiden, wie es vielfach nicht
geschehen ist "). Sir Thomas Oliver, noting this peculiarity, asks,
" How (in angina pectoris) do we explain the absence of shortness
of breath ? " 2 The usual and plausible answer is that the sufferer
dare not breathe for dread of instant death, and something must
be credited to this deterrent. Josue,3 in respect both of respira-
tion and pulse, states, " The respiration is free and undisturbed ;
auscultation and percussion reveal no modification of the
respiratory mechanism, no fixation of the chest " (see p. 385).
Rosenbach 4 says that not only in pure angina pectoris is there
no dyspnea, but even a voluntary refrain of respiration ; " eine
willkurliche Hemmung der Athmung, in dem Bestreben moglichst
geringe Athmungsexcursionen zu machen " ; as Dr. Morison puts
it, " the breathing during the agony is restrained." A case of
my own well illustrates the distinction between angina and
heart disease in respect of dyspnea.

Male, set. 26. No rheumatic fever ; denies syphilis, but had
been in the army. No very hard labour. For two months — it
began suddenly — attacks of severe and piercing pain at the sternum
— penetrating, as it grew worse, to the back, and down the left
shoulder and arm (in the usual anginous way). During this period of
his illness " no physical signs of cardiac disease and no shortness of
breath were present " (his own physician's letter). But then severe
dyspnea set in suddenly, when on examination a murrnur of aortic
incompetence was distinctly heard, and the left ventricle was dilating.
The case, undoubtedly one of syphilitic suprasigmoid aortitis, pro-

1 Broadbent, W. H., Heart Disease, ed. 1879, p. 298.

2 Oliver, T., Lancet, Sept. 16, 1905.

3 Josue, Arteriosclerose, p. 245.

4 Rosenbach, Path. u. Ther. d. Herzkr., 1899.

sec. ii DYSPNEA 315

ceeded on its usual course from the suprasigmoid area to the valve.
Unfortunately after this, the only consultation, I lost sight of the
patient.

Notwithstanding, such nowadays is our slovenliness in the use
of clinical language, we are ready to give the name Angina pec-
toris offhand to any grave thoracic crisis with dyspnea. The
name " Cardiac asthma " is another instance of such abuse ;
Asthma of course is not a cardiac affection at all, and is not to
be confounded with affairs primarily of the heart or circulation.1
Asthma is an expiratory hindrance. Yet if, even without
pain, the patient fall into an agony of paroxysmal dyspnea, his
physician may clutch at the name of " Angina sine dolore,"
an error of which so great an observer as George Balfour
cannot altogether be acquitted (vide p. 324). So it comes
about that this name is given promiscuously to processes
so various as syncopic heart failure, the paroxysmal dyspnea
of high pressures, nocturnal cardiac orthopnea, and so forth.
A gentleman (set. 75), in apparent health, while walking up a
hill, was pulled up rather suddenly by a gasp and a depressing
ache, of no great intensity, about the heart, and for shortness of
breath found some difficulty in reaching home. Three physicians,
one after another, diagnosed his case as " Angina pectoris " !
The attack was in fact, as the subsequent history proved, not
one of angina at all, but the breakdown of a long-standing Hyper-
piesia ; on further examination we discovered abiding high
arterial pressure (about 200 mm.), a considerably hypertrophied
and dilating heart, and cardiac dyspnea on slight exertion.
He lived two years longer, suffered two slight apoplexies, and
died of defeated heart, with never a symptom of angina. Such
confusion of diagnosis is presumably due, not to ignorance, but
to random language, engendered of lax or sophistical arguments.
Again, a younger man — a physician, aged about 43 — -consulted
me under the diagnosis of " angina pectoris." His blood pres-
sures ranged very high, and the left heart was big and dilating.
There was no symptom nor sign of renal disease. He had been
stopped on rising a hill by " a pain at the heart " ; but a closer
enquiry elicited that what pulled him up was not the ache — for

1 This distinction I have emphasised elsewhere, as in the Brit. Med.
Journ., Oct. 28, 1911.

VOL. II X

316 ANGINA PECTOEIS part n

that he could have proceeded — but an imperious dyspnea. And,
on being asked where the pain was, he laid his flat hand under
the left nipple and towards the anterior axillary line. There
were no radiations, and the ache was not paroxysmal but con-
tinuous. The pain was not the distress ; the distress was
the hard breathing. Unwittingly he also had been for some
years a victim of Hyperpiesia, and the strained heart was
giving way. In the course of the next few months it yielded
more and more ; anasarca appeared, arterial pressures began
to fall, and, " nearing his end with labouring breath," he
too died of cardiac defeat ; but he never had angina pectoris.1
It is because of our respect for our late colleague, Professor
Dieulafoy,2 that I feel compelled to deprecate even in him
descriptions of this kind ; for the example of so great a clinician
leads to the greater misconception. After speaking of the
pain of angina as " partie du coeur," he brings in " dyspnea . . .
agonizing paroxysmal dyspnoea resembling ursemic dyspnoea,"
which, he adds, may so dominate a case as to throw the pain into
the background, or even to replace it, with or without palpitation.
In these words the distinguished Professor masterfully confused
two wholly different maladies ; namely, the high - pressure
dyspnea, so well described by Pal, and angina pectoris. Again,
a physician of well-merited distinction, concerning a case of post-
diphtheritic myocardial disease in which the patient had begun
work too soon, reported that he had an attack in which he became
much agitated, and his breathing rapid and panting ; he com-
plained also of " distress over the lower part of the preecordium
[st'c]," the pulse weakened and quickened, and physical signs of
cardiac dilatation appeared ; yet this set of alien symptoms the
author discussed unreservedly as an attack of angina pectoris !
Again and again by distinguished authors agonising respiratory
spasms of high pressure, of uraemia, or indeed of pulmonary
embolism or acute oedema, are thus spoken of as angina pectoris.
One says, for instance, that " the strain of angina pectoris may
arise on the pulmonary side of the circulation," and cites as
examples " the not infrequent anginal seizures in mitral

1 This high-pressure dyspnea is discussed in the chapter on Arteriosclerosis
(Vol. I. p. 402).

2 Dieulafoy, Path, interne, ed. 1908.

sec. ii DYSPNEA 317

stenosis," which " may be warded off by haemoptysis." By
the context it would appear that here the author is con-
sidering paroxysmal dyspnea (pulmonary embolism ?). In what
sense angina may occasionally depend upon mitral stenosis
will be discussed on p. 443.

Even the great Stokes, in his unhesitating attribution of angina
to failing heart, did not see his way clearly between angina
pectoris and the dyspnea which he supposed to be of similar
nature. The fact was, as he admitted, in his practice he saw
little or nothing of angina pectoris. A like undiscriminating
diagnosis we find in one of von Basch's cases :

Male, set. 54. Angina pectoris extending to the arm, but with
great dyspnoea, sense of palpitation, a hurried irregular heart, and
death. The attack permitted the estimation of arterial pressures
which fell from 160 to 105.

This was a case of angina, no doubt, but of angina com-
plicated with some grave cardiac lesion. Yet this master
of his subject allows himself, without qualification, to call this
mixed case an " angebildeter Fall " of angina pectoris.

Let us remember then that the distress of angina pectoris is
not any paroxysmal thoracic distress, but a peculiar distress ;
distress of cardiac origin, or of high pressures, whatever its
gravity, is of other kinds ; it is the horror, not of a crushed
thorax, not of the bottomless pit, but of the garotte. In com-
pound cases, one and the same patient may unhappily have an
experience of both miseries ; sometimes he may be attacked by
paroxysmal dyspnea, nocturnal dyspnea, or dyspnea on exertion,
at another by angina ; sometimes the two conditions may fall
upon him together, as asthma may appear during bronchitis,
or as cirrhosis of the liver may be associated with delirium
tremens. It is for this reason that I have ventured to insist at
length upon the postulate that dyspnea, be it never so sudden,
so violent, or so suffocative, is no essential symptom of angina
pectoris. It is usually the first betrayal of cardiac inadequacy.

Of one manner of termination of angina, namely, by gradual
heart failure, I have already spoken ; from such phases cardiac
and cardio- pulmonary dyspnea can scarcely be absent, and
usually have made their own independent way. In a simple case

318 ANGINA PECTORIS part n

of angina pectoris, however vehement, the results of physical
examination of the heart are as likely to be negative as positive ;
in cardiac dyspnea, on the contrary, a negative result of examina-
tion of heart and lungs would rarely happen. Paroxysmal " toxic "
dyspnea — bulbar dyspnea, if it be fitly so called — is not an
agony of pain, but a desperate fight for breath. It is true, as
Vulpian, Huchard, Pal and other observers record, that, if now
and then in an anginal attack respiration be not arrested, its rate
may be increased, even considerably ; but, as these authors have
noted, in such cases the respirations are shallow and hasty, with a
more or less restrained thorax, and are not, of themselves, a cause
of distress, nor indeed of much importunity. As Vulpian (Clin.
Med.) remarks, if in angina there be any dyspnea, it is not of the
cardiac form ; it is a retarded and somewhat spasmodic sighing,
like slight asthma. Finally, although in some mixed cases certain
remedial means, such for instance as those which reduce arterial
pressure, may mitigate both the angina and the dyspnea, as by
breaking a vicious circle, yet, broadly speaking, the therapeutical
methods which we bring to bear upon cardiac dyspnea differ
considerably, even essentially, from those in which we have
learned to confide for the relief of pure angina. That Balfour, in
his opinions upon angina pectoris, was not always consistent with
himself, I have ventured to suspect, as I have questioned his
use of the term angina sine dolore (p. 324) ; but the independence
of angina both of asthma and of cardiac dyspnea, he never
failed to perceive.

However, Erasmus Darwin (Zoonomia) thought angina akin
to asthma, and related a case of their coexistence. The
suggestion recalls to me a compound case of angina and asthma
which I saw many years ago with a physician in Ripon :

Mr. T., a man in later middle life, had been attacked by angina
pectoris presenting the usual characters. On listening to the
left side of his chest behind, the respiration was audible ; but
on transferring my ear to the right mid-lung it was inaudible. I
tapped the side anticipating the signs of fluid, but the resonance was
normal. Puzzled for the moment, and then diverted by some agita-
tion of the patient, both I and my colleague were surprised to find
him (to cut the story short) under a seizure not of angina but of
asthma. I think the patient had suffered from asthma in former
years, but not for a long time past. It seemed that in the excite-

sec. ii ANGOR ANIMI 319

ment of the consultation the bulb (?), vexed by attacks of angina,
lapsed on the line not of angina but of asthma. He had suffered
from angina only on walking uphill.

My impression is that the arrest of breathing or the sighing,
seen in most cases, is an inhibition analogous to the inhibition of
the heart, of which I shall offer some illustrations later. Inhibi-
tion of respiration is often seen during a drag on the mesentery
in animals (p. 422). All I will add now is that, as in ordinary
respiration the cardio-inhibitory centre is more active during
expiration and less active during inspiration, in angina we may
suppose conversely that an intenser cardio-inhibitory influence
may reduce the breathing in the direction of expiration. Irrita-
tion of the interior surface of the ventricles, as we know, inhibits
the respiration. Of the three neighbours in the bulb, the re-
spiratory centre seems to be the most susceptible, both from above
and below (Brodie and Russell). Wenkebach 1 says, " During
compression of the vagus the patient holds his breath, generally
(" vielmals ") in the inspiratory position (so that the cardiogram
appears lower), while there is no diminution in the radial wave "
(italics mine). But these factors, bulbar, respiratory, cardiac,
musculo-cutaneous, splanchnic and the rest, are too complex for
easy discrimination.

Angx>r Animi. — The horror — the angor molestus of Morgagni —
which in its extremer degree is almost peculiar to angina pectoris,
is so well known, and so impressive, that I need not dwell upon
its character. To return to Seneca's story of his own case 2 (of
angina), The attack is very short, and like a storm. It usually
ends within one hour. ... To have any other malady is only
to be sick, to have this is to be dying." Well might his physician
call it a meditatio mortis 3 — to die piecemeal. Morgagni, in the
case of an elderly woman (xxiii. 8), describes it, " tanta ad cor
angustia atque anxietate, ut saepius quamprimum moritura
videretur." Extensive aortic atheroma was found at the
necropsy. It is not a reasonable apprehension, nor a fright or

1 Wenkebach, Arch. f. Anat. u. Phys., 1908.

2 See the interesting essay by Pawinski, " Das Leiden Senecas," Zeitschr. f.
klin. Med. Bd. lxviii. Hte. 1 u. 2.

3 Meditatio here does not mean a "contemplation of death," but an exercis-
ing in death ; e.g. " In cursuram meditator me " ; or, as Pliny the Younger uses
the word, an exercising or practice for a campaign.

320 ANGINA PECTOEIS part n

alarm, as at a snake in the grass, but an organic sensation. As
even in moderate cases the pain is menacing, and in severe
cases atrocious, and as it is natural to attribute the dread to
the vehemence of the pain, it seems difficult to realise that the
angor J and the anguish can be separable, and presumably there-
fore may own somewhat different origins. Still these two
symptoms by no means run parallel in intensity ; in one case we
may see flashes of pain, so furious and incessant that, as in the
terrible case described by Dr. Knott (loc. cit.), the sufferer may
well fear indeed to be overwhelmed by them, yet he may not be
possessed by the spectral horror which, in another case, may dog
the mildest series of attacks ; indeed this dread often sets its
seal upon attacks in which the pain might otherwise have
been equivocal. A step farther, and I am a dead man ! In
the successive seizures of the same patient, it is true, the blend
of pain and horror may be fairly uniform ; but a strange in-
describable fear is no uncommon feature of cases which, in respect
of pain, may be no more than angina minor. Indeed, as I have
said, it is often by this touch, rather than by any intolerable pain,
that in minor warnings the patient is appalled.

•Verum ubi vehement! magis est commota metu mens,
Consentire animam totam per membra videmus ;
Sudores itaque ei pallorum existere toto
Corpore, et infringi linguam, vocemque aboriri,
Caligare oculos, sonare aures, succidere artus.

Shall we guess that Lucretius also, like St. Luke, Dante, and
Shakespere, was a physician ? 2

One of my patients under middle age, perhaps 40, not more, a
subject of severe syphilitic angina of four years' duration, told me
he had experienced the sense of impending death in one attack
only — once in many a score — " and on that occasion the pain was

1 Angor primarily had the meaning of suffocation or strangulation ; Cicero
carried the word metaphorically into anguish of mind.

2 We may recall also in this horror these lines from the Dream of Gerontius :

" Down, down for ever I was falling through
The solid framework of created things,
And needs must sink and sink
Into the vast abyss. And, crueller still,
A fearsome, restless fright begins to fill
The mansion of my soul."

sec. ii ANGOE ANIMI 321

not much." Thus by a typical case, as this was, we see that the
angor is by no means an essential feature.

My own experience suggests that in cases of angina in persons
with sound hearts — for instance in the syphilitic, rheumatic,
influenzal, or other kinds of aortitis in young, or comparatively
young persons — the horror is less manifest and often absent ; it
seems rather in older persons, with shaky hearts, that the shadow
of this passion may even obscure the pain. Indeed many of these
sufferers have more dread of the death portent than of the pain,
terrible as this may be. A lady who for seven or eight years
has consulted me occasionally for typical angina, the attacks
being often severe and persistent, has never had any trace of
dread. The attacks are frequent, at times when more exertion is
demanded of her, almost incessant, yet hitherto her life has
been spared ; the closest examination reveals no sign of cardiac
disease, nor usually of any very excessive arterial stress,
though she has occasional periods of high pressures. So far, the
absence of dread has seemed to be a favourable prognostic. Pro-
longed rest for a day or two puts the symptoms into abeyance,
but as she finds inaction very irksome, she breaks through our
restrictions ; now the patient who has once felt himself hanging
over the mouth of the pit will submit to any advice. We shall
see indeed that, as in another patient I shall describe, in some
rare cases the dread alone may fill the bitter cup.

It is remarkable that this peculiar awe, as distinguished from
reasonable apprehension or awareness of the menace of death,
this organic sensation, is rarely met with in heart diseases. Even
Stokes- Adams' disease — if I may rely upon the symptoms of
some exemplary cases of my own — is not, or not usually, attended
with this " Todesgefuhl." One very intelligent patient, who
suffered for a long period from the syncopic and convulsive
phases of this disease, told me that the "going off" was but " a
dreamy sensation, not in itself unpleasant."

The absence of the sense of impending death, intimate symptom
as it is, is then consistent with a diagnosis of angina pectoris ;
this is proved over and over again, both by its inconstancy in
cases of all degrees of severity and, if the diagnosis in such
cases be questioned, by its presence in some attacks of the same
patient, and its absence in others. In this statement Sir William

322 ANGINA PECTOEIS part n

Osier concurs.1 Conversely, Heitz (p. 194) and others note its
occurrence in chronic aortitis, in distinction, as they put it, from
" coronary angina " ! So inconsistent are the coronarians.
That in the several attacks of the same patient the proportion
of the symptom to the pain may be far from constancy
is a point to which I shall return in the interpretation of the
disease. As a symptom then the angor animi is frequent,
characteristic, and dramatic ; but far from universal, and
cannot be accepted, as many would have us accept it, as a
warrant.

That this awe may depend upon a consciousness of forced
inhibition of the heart (vide p. 466) presents itself to the mind,
for it is met with in some cases of interference with the vagi,
such as the pressure of a tumour (Skoda's well-known case),
and in a once well-known example quoted in Miiller's Physiology.
In certain old notes on angina pectoris, notes made when I
was preparing for my final M.B. examination at Cambridge,
I find the following extract from the edition of 1841 (iii.) : —
" The heart's movements were occasionally checked for intervals
of four or six beats, when sensations of fearful anxiety
were felt " (with other symptoms). "... After death an
enlarged bronchial gland was found pressing upon the great
cardiac nerve." To like effect Dr. Mott 2 relates, of a highly
intelligent man afflicted with a cerebral tumour, that suddenly
a sense of fear would possess him, with pallor, momentary arrest,
disturbance or weakness of the heart, perturbed respiration,
trembling and weakness of limbs, a feeling of anxiety, suffocation,
and vague unpleasant sensations in the breast ; a fear which
came and went with the fluctuation of the other organic disturb-
ances. I am disposed therefore to attribute this symptom to
some echo in consciousness of a vagus crisis. Conversely, it would
seem that fear may strike down the vagus path with fatal result.
Fretfulness, anxiety, and forebodings are of course common
symptoms of all kinds of heart affections ; and we are accustomed,
no doubt, to speak of vagus inhibition — as perhaps in certain
intermittences of the heart — as common enough, and unaccom-
panied by no queer sensations. Recent researches however

1 Osier, Sir W., Angina Pectoris, p. 51.
2 Mott, F. W., Brit. Med. Journ., April 4, 1908.

sec. ii ANGINA SINE DOLORE 323

are making it doubtful if irregularities of the heart are to be
referred to the vagus so readily as has been our wont.

Angina sine Dolore. — In his now classical letter to Heberden,
The " Unknown " stated that, amid major attacks, occasionally
he suffered from transient seizures (without pain) in which, as it
seemed, " there was a general suspension of the inner operations
of nature for three or four seconds." On this report, Heberden
remarks that in some 50 cases, which up to that date he had
observed, he did not remember ever to have heard this mode of
angina mentioned. Watson,1 on Quain's authority, says " the
inexpressible sense of dying is sometimes the only symptom
of the disease." In Miss Mamie Dickens' recollections of her
father, it appears that Dickens, for some time before his death,
had been subject to attacks of vague but overpowering dread,
and in one of these attacks he died. Charcot's single attack,
in which he died, may have been of this form.2 What can that
sinister touch be which, until the final stroke, does not even
make the heart falter ? To identify this spectral visitation with
angina does indeed sound like a contradiction in terms, as if one
should say angina sine angina ; and had I not witnessed an
exemplary case of this extremely rare variety of the disease,
I might have continued in some scepticism concerning it. The
title should indeed be used with the utmost discrimination ;
we have to regret that into this accommodating pigeon-hole
are stowed all sorts of obscure catastrophes or sudden death.
For authors to whom any release from the discipline of facts
is welcome, the name is happy enough, for it will fit almost
any painless but startling thoracic distress. Accordingly
it is made to fit events so alien one to another as syncope,
bradycardia, paroxysmal dyspnea, cardiac or toxic, any fatal
stoppage of the heart, acute pulmonary oedema ; or, on the
other hand, the comparatively harmless " vaso-vagal " storms.
On the use of this name Gairdner himself wrote, in consent with
me,that its indefmiteness made its application too often ambiguous
or otiose. I quote the pertinent portion of his letter, dated
June 15, 1894 :

1 Watson's Lectures, vol. ii. p. 285, ed. 1857.
2 See Parkes Weber, Medical Magazine, Nov. 23, 1893.

324 ANGINA PECTOEIS part n

" Angina sine dolore " is perhaps entitled to be called an " enfant
gate," but if so, has not been coddled into notoriety by anything
done for it, or to it, by its unworthy parent, but rather by its having
somehow " caught on " in the shape of reference by outsiders to
whom it has seemed to convey something that was within the range
of their experience. What I believe to be true about it has been
briefly and modestly set forth in a few words in my article in Reynolds.
I have always marvelled a little at this phrase coming up again so
much as it has, when better things have been left in the cold shade of
neglect, showing once more how much lies in a name.

May I add it is one more illustration of the truth that we invent
catchwords at our peril ; they are handy to catch popular im-
pressions of things we have never thought out and, with the new
resource of a name, need not think out. Our brilliant French
colleagues have helped us to too many of these dialectical counters.
To quote examples of the ambiguous use of the name Angina
sine dolore is no very gracious task ; but may I not reason in
this matter with George Balfour, a memory too great to be
touched by my cavilling? When Balfour x writes " termination
suddenly in asystole, death from angina sine dolore," may we
not ask, Why angina ? Cannot a man die suddenly of heart
disease without angina ? And in a following, and surely incon-
sistent, sentence, he writes, " Cardiac asthma is another variety
of angina sine dolore," the very error we have just been
deprecating ; for the distinguished author himself had written
on angina pectoris (p. 315) — " There is nothing pulmonary
in this seizure ; the air goes less freely into the lungs if the
patient has the courage to breathe " ; and he proceeds, " it has
no connection with spasmodic asthma, nor with ordinary cardiac
breathlessness " (italics mine). Let us take again the following
case, published by the friend lamented by so many of us, Dresch-
feld of Manchester, and quoted by later writers as one of angina
sine dolore, yet surely in no sense a case of angina pectoris at
all ? Briefly thus :

Female, set. 49, one night suddenly was seized with severe
dyspnoea, but not with pain. Seven days later a repetition of the
seizure with fatal issue. At the necropsy, left coronary artery
occluded by an atheromatous plate ; the apex of the heart the
seat of fibrotic degeneration. Blood pressures not recorded.

1 Balfour, Geo., Diseases of the Heart, 3rd ed., Sect. " Heart and Aorta."

sec. ii ANGINA SINE DOLOEE 325

All we know then of this case is that the heart was gravely
diseased, that of this disease the patient died suddenly, and that
the eminent symptom was dyspnea. But we have seen that
dyspnea is not a symptom of angina, dolorous or indolorous.
However, it is true that angina sine dolore, if extremely rare,
does occur ; I will now record a genuine case of it, the one
well-marked consistent case which has occurred in my own
experience ; fortunately I witnessed a characteristic attack.

A gentleman of some 70 years of age was on his way from
the North to visit me in Cambridge, when his illness so increased
upon him that he was laid up at an hotel in London, whither
I went to him in haste. I found the patient, a pallid, worn-
looking, but not emaciated man, in his dressing-gown, seated in
an elbow-chair in his bedroom, and surrounded by the aids and
restoratives of the sickroom. The radial artery was large, thick,
and tortuous, and the pulse thrusting ; the heart was large and
labouring, with evidence of atheroma in the aortic area. While
I was examining him he blanched, either with fear or in some
organic vascular tide, and in a hollow voice whispered, "It is
coming, it will kill me." For a few minutes he sat thus stricken
into stillness ; until his countenance began to open, he drew
breath, and moved on his chair. During this interval, some three
minutes perhaps, while his servant, familiar with these attacks,
applied some stimulants, he did not disengage my finger from
his pulse, which had not faltered, nor betrayed any vacillation,
but became transiently a little slower and more laboured
(longer diastole and larger output ?). In these attacks of sudden
dread, terrible as they were, and he had had not a few of them,
there had been no pain whatever, not, I believe, in any one of
them. He was fain to wish for any alternative suffering to
compete as it were with this death-like touch. " A faint cold fear
thrills through his veins, that almost freezes up the heat of life."
In one of these attacks, a few weeks later, he did die, suddenly.

Neuburger (he. cit.) reports that in exceptional cases an
exhausted sensation, or intolerable depression in the region of
the stomach (" Magengegend "), especially in the " epigastric "
cases, and after a full meal, may take the place of the pain.
Mrs. M., a patient sent to me by Dr. Forrest of Terrington,
complained more of the " sense of fearful faintness and of

326 ANGINA PECTOEIS part n

death," than of the characteristic pain. She was subject to
occasional nocturnal attacks, without the pain, which may
have been wholly of this kind. They seemed to begin in a
dream of annihilation.

From my experience, such as it is, and from the records of a
few similar cases, I am of Gairdner's opinion that a category of
Angina sine dolore should be recognised ; but that it must
contain cases only in which such paroxysmal crises, if devoid
of pain, are marked nevertheless with the seal of the death
terror, and indeed chiefly consist in this ; and are not to be
confounded with startling symptoms of cardiac or cardio-
pulmonary disorder. Moreover the crises must be paroxysmal,
and disposed to recurrence. Of course a first attack may be
fatal ; if so, the diagnosis could not be decisive, not even, in
the present state of our knowledge, with a necropsy. Even if
the patient should have time and breath to describe his
sensations, it would rarely be possible at so brief and critical a
moment to discriminate between it and the alarm which may
accompany an ordinary cardiac crisis. But of course in mixed
cases, as with anginal pain so with angina sine dolore, there
may be a complication of cardio-pulmonary, renal, or other
concurrent malady.

Some years ago I saw an Essex squire with Dr. Prince, then
of Buntingford, a very old man, in whose case attacks of angina
sine dolore were now and then intercalated between the ordinary
seizures. Dr. Prince's description was quite characteristic, but
I myself did not witness one of these. Sir John Broadbent has
kindly reminded me of the following passage in his father's
book on The Pulse (p. 178) : " The patient would be seized in
the street with sudden faintness and deadly apprehension. The
attacks ceased with the disappearance of the high tension from
the pulse." In him I suppose the suprasigmoid aorta to have
been in a morbidly sensitive state, and the already excessive
stimulus to the vagus intensified, so that the automatic
regulation of cardiac energy and aortic pressure, which is con-
tinuously at work in all of us, in him became so unbalanced
as to enter into consciousness. Schmoll (loc. cit.) describes a
case of angor animi with slight numbness and paresis of the left
arm, but no pain.

sec. ii ATTITUDE 327

To sum up, I repeat that, dramatic and ghastly as is this metus
deliquii,we must not take it as a criterion, nor declare that without
it there is no angina. Merklen agrees it is not " pathognomonic,"
as he considers "retrosternal constrictive pain to be, especially if
associated with the slightest numbness of the left arm." And as
we have seen, it may accompany vagus irritation under other
conditions. This Sir William Osier x has made quite clear, and
by many cases proved, that it may be absent, as in epilepsy
aura, or convulsion, may be absent. But I do not agree that
the angor animi is called forth by the severity of the pain. We
have seen that anginal dread may occur without pain ; and
although it is true that a bad case is prone to be bad all round,
still I would urge that there is many a case, especially of acute
aortitis in young persons, in which the pain is extreme, and yet
without angor.2 If I may venture to repeat my own notion
on this point, it is that the dread is more frequent in de-
generative cases ; and is often absent in the acuter angina,
such as the syphilitic, the influenzal, or the rheumatic, of
younger persons.

Once more ; we cannot, in cases of sudden death by the
heart, predicate angina as the cause without either some report
of the peculiar pain or of the peculiar organic dread ; not
indeed even if the patient had been a subject of angina.

Immobility, in a wider range than of the respiratory system,
is the ordinary condition of an anginal attack, and the contrast
of this with neurotic agitations has often been pointed out.
Heberden graphically describes how these patients, walking
hastily, or against a cold or contrary wind, or up a hill, " simul
ac pedem figunt et quieti sese dant ; subito plerumque omne
incommodum evanescit." " The pain," said one of them, " com-
pelled me to sit down." Fothergill, and Gruner,3 concur in this
description. Forbes also graphically describes the sudden pause,
the extension of a hand to some support — " or it may be the
patient imperceptibly sinks down on a chair or bank, as if unable
to stand, yet afraid of the movements necessary to seat him."

1 Loc. cit. Ang. Pect. p. 51.

2 See Sir W. Gowers, Brit. Med. Journ., July 21, 1906 ; and Dr. Mildred
Burgess, Lancet, Nov. 12, 1908. But in these passages the authors scarcely
distinguish between an organic passion and a reasonable fear of death.

3 Gruner, Spicilegium ad Anginam Pectoris, Jenae, 1787.

328 ANGINA PECTOEIS part n

And yet in this he saw nothing to separate such a summons from
the mere shudders of vasomotor oscillations !

But rest is no warrant against an attack. Parry,1 and
Gruner — and of course many later writers — describe attacks
arousing the patient even from sleep ; a point of diagnosis,
when it so happens, from spurious anginas. Of one case
of angina, due to an aneurysm just above the heart,
Morgagni wrote, " Noctu pectoris angore molestissimo, cum
suffocationis metu, corripitur." To explain this, as Obrastzow
says, we need not speculate with Romberg and Ortner on
diminished circulation in the heart in sleep, when as the rate
is then slower and diastole longer, less nutrition is needed ; we
may be content with a thrust-up diaphragm or too good a supper.
The slower and shallower nocturnal respiration in sleep which
favours cardiac dyspnea probably has no bearing on angina.

Although for the most part, nearly always, the patient is, as
it were, frozen for the moment into stillness, yet it is not true
that agitation never accompanies attacks of true angina. In
some such stories the diagnosis may have been erroneous, but
Dr. Mackenzie,2 who is not likely to have erred in this respect,
speaks of such a patient " rolling on the floor in an extremity of
agony." In the anginous cases, which I shall describe later,
of acute plug of a coronary artery restlessness is often terrible,
but the pain may be incessant for days. The " Unknown "
said if he did not " indulge " the pain he could walk it off ; and
one of Sir William Osier's patients, by a strong effort of the
will, could walk the pain off ; yet this was possible only in
moderate attacks. Probably in this, as in many other such
instances, as the muscular and cutaneous circulations open out,
the intra-aortic pressures give way, and thus the tension is
moderated. Mr. Sumner it was, I think, who found that he
could shorten the attack by walking the floor, " but it in-
creased the agony at first." Parry quotes the case of a lady of
great force of character, who could compel herself to walk on,
when in five to ten minutes the pain would be dispelled. My
own experience has been that in single and transient attacks,
however severe, stillness has been invariable, but that pacing,

1 Enquiry into symptoms and causes of the Syncope anginosa, C. H. Parry,
M.D., 1799. (In a note the author corrects anginosa, which he says is not strict
Latin, to angens.) 2 Mackenzie, Jas., Heart Diseases, p. 45.

sec. ii THE PULSE 329

rocking, or sometimes agitated movements have accompanied
the more protracted assaults. Jendrassik says he has seen
no more movement than an instinctive desire to get the hands
forward, or upward and forward ; one of his patients begged the
bystanders to hold his arms up. Or we may see a movement,
even a large movement, made to secure the position of least agony,
often a strange posture. In mock angina the agitation is prim-
arily psychic, and often attended with whimpering and choking,
plaints which before angina pectoris are silenced.

Pulse. — The symptom next to be considered, namely the
pulse, requires a close scrutiny. My own experience, which
fortunately has included the witness of many seizures, and in a
fair number of sufferers, is that in the large majority of them
the pulse was unaffected ; and that abnormal characters, if any,
belonged to some independent disorder. I have said that, amid
the agitation of patient and attendants, the heart, assumed to be
the protagonist in the conflict, often seems to be the one impassive
actor. Here again we find how much more definitely the early
observers of angina pectoris wrote concerning its clinical features
than later writers have done. By them this imperturbable atti-
tude of the heart was taught distinctly ; though it is true that
von Leyden, Osier, James Mackenzie, Morison, and other recent
authors give the same clear testimony. Morgagni writes (Ep.
xxiii.) : " Huic pulsus nunquam intermittentes." Heberden
noted that often neither pulse nor heart were disturbed, even at
the height of a paroxysm. His words are : " The pulse is at least
sometimes not disturbed by this pain, consequently the heart
is not affected by it, which I have had the opportunity of knowing
by feeling the pulse during the paroxysm." Parry says there
is never any palpitation ; and the pulse is usually little altered,
so little that one would not suppose the heart to be affected.
He adds that assertions about the pulse are too often mere hear-
say, not of eye-witness. During the attack however, as the face
pales, the artery often constricts. Burns made too much of such
pulse changes as may appear in dilapidated cases, and the name
" Syncope anginosa " probably beset him ; but he adds never-
theless (p. 144) that " the pulse is not so much affected as one
would expect." Jurine * records the pulse of a patient during

1 Jurine, Mem. sur VAngine de poitrine, Paris, 1815.

330 ANGINA TECTOEIS paet n

the attack as 86, and in the interval 82. He had never
had his finger on the pulse in the articulo mortis of angina ;
but otherwise he had never detected either palpitation or
intermittence : often it is " serre " and a little accelerated ; the
face often pale, but not always. " How," he reflects, " if
angina be due to coronary disease, can the heart go on steadily
in this way, and then drop out suddenly ? " Desportes asks
the same question. Van Dusch x says the heart's action
during an attack seems to be little altered, unless the seizure
be fatal ; occasionally, he adds, we find some enfeeblement
of the heart's action, but very rarely palpitation ; though this
he noted in a case of aortic insufficiency in which " the action
of the ' colossal heart ' was very energetic." Balfour bears the
same witness. Latham, of a severe paroxysm of angina in a man
set. 64, reports: " Auscultation found his heart beating with a
perfect rhythm, and neither with excess nor defect of impulse,
and its sounds were natural." Walshe says decisively: " In the
very extremity of pain the pulse may be perfectly regular, and
barely exceed by half a dozen beats per minute the rate
normal to the individual." Eulenburg and Guttmann,2 who
carefully noted this point, found the action of the heart and
pulse, unless for an occasional slight " Irregularitat," to be
normal all through the attacks. They felt assured that the
explanation of the attacks could not lie in alteration of the
heart's action. Frankel writes : " The pulse is either not
changed, or deviates (abweicht) but little from the norm."
Edgren3 reported that during the attacks the " definite ob-
jective changes in the heart's action, pressure- wave, or frequency,
are as a rule not important ; on auscultation the heart seems
quite quiet, and just as in the intervals of pain " (italics
mine). This is his conclusion, " having examined many cases
curiously." In one case, in which death in an attack was sudden,
Edgren had several times {mehrere Male) in previous seizures
found the heart's action quite tranquil (vollkommen ruhig). In
two other cases, which ended in status anginosus and death,

1 Van Dusch, Lehrbuch d. Herzkrhtn., 1868, p. 33.

2 Eulenburg and Guttmann, Die Pathologie d. Sympatheticus, Berlin, 1873.

3 Edgren, Die Arteriosklerose, Leipzig, 1898, note, p. 227. In another
place he says, " Bei den Anfallen . . . konnten keine bemerkenswerthen
Veranderungen des Herzthatigkeit oder des Pulses nachgewiesen werden."

sec. ii THE PULSE 331

the heart, except for a slight occasional irregularity, was, until
the final stage, for the whole time almost unaltered. Von
Leyden x testified emphatically that by auscultation there is
plenty of evidence that during attacks changes in the sounds or
pulsations are rarely observed. Dieulafoy 2 wrote, " During the
attack . . . auscultation reveals no abnormal sound ; the heart
beats are normal or retarded (" ralentis ") ; if the angina is
associated with cardie-aortic lesions they may become irregular ;
but in some cases they are accelerated " (italics mine). In a case
on my notes, a certain patient, who had had a few attacks of
angina, but was able to do a good deal at times, to take long
walks, and go to business, was under medical care for bron-
chitis, and his own doctor was feeling his pulse ; it was steady
and regular. But at an instant he cried out, and then whispered,
" I am losing myself " ; the pulse without a falter had suddenly
stopped in death. Till then the heart had presented no abnormal
signs. Pawinski, in the interesting paper on basic peri-
carditis as a cause of angina pectoris to which I have made
repeated reference, after noting the disturbance and embarrass-
ment of the pulse in more extensive pericarditis, says of the
basal form that, severe as the angina may be, the pulse may
be a little retarded, or normal ; unless, with extension of the
inflammation, dyspnoea set in with other symptoms of heart
affection (italics mine). In another paragraph he says that a
pulse, previously of high tension, as the heart becomes involved
may soften and quicken ; and conversely, that not a few
cases are on record in which the heart, irregular between the
attacks, became during an attack normally rhythmic. Dr.
Mackenzie 3 writes : "In the vast majority of cases I could
detect no change in the heart or arteries, and there never
was the slightest enlargement of the heart coming on during
an attack." We do not realise what these large admissions
signify. In another place he says, it is true, in the small
minority " the pulse may become small, soft, and scarcely per-
ceptible, from weakness of the heart " (or from vagus inhibi-
tion ?). Sir James Goodhart writes that, as a rule, the pulse is

1 Von Leyden, Zeitschr. f. klin. Med., 1884.
2 Dieulafoy, Path, interne, 1908, vol. i. p. 1045.
3 Mackenzie, Jas., Diseases of Heart, p. 47.
VOL. II Y

332 ANGINA PECTORIS part n

wholly unaffected, either in rate, rhythm, or tension ; and this
he states, " having had my finger on it through the spasm many
a time. And yet," he exclaims, "we call it heart disease ! Why,
for the life of me, I cannot imagine. These are not the symptoms
of heart disease. The heart has too much grit in it to tumble
down dead, except under well-known and definite conditions." x
In one case he carefully watched a series of paroxysms
lasting half an hour, and reports, " his pulse never altered a
bit." 2 Of another case he says " the pulse neither altered nor
faltered in any way. From the pulse (in many cases) you can
get no indication of any value of the gravity of the attack through
which the patient is passing." Dr. Verdon (loc. cit.) says that of
62 observations during angina he found in 30 no change of pulse,
radial or jugular ; in others unimportant changes. Moreover he
found all five myocardial qualities intact. Josue 3 reports :
" The pulse is normal, regular, unchanged, though sometimes
it may slow down, or hasten a little (legerement). One finds
indeed on auscultation the same conditions during the attacks
as during the intervals ; there is no change in any particular."
Now let us ponder over such statements as these by skilful
and experienced clinical observers : testimony which could be
collected in greater abundance.

When however the heart's rhythm does alter, the alterations
are broadly and naturally divisible into the early and the late
changes. Early changes, if perceptible, may consist in retarda-
tion and sometimes an unevenness in rhythm, even to inter-
mittence ; the later may be acceleration and arrhythmia.
Although I have spoken of the heart as often or usually
impassive, yet not uncommonly by the sensitive finger there
is to be noted in one or more beats a deliberation, an impression
of delay which may or may not become still more manifest to
touch. Many observers who have declared the rule in ordinary
cases to be that the heart is little, if at all, disturbed, make
this exception of a slight occasional lag. It reminds one of the
momentary self-collection of a horse before he leaps (p. 469) But
this transient hesitation is to be distinguished from any element

1 Goodhart, Jas., Lancet, July 1, 1905.

2 Goodhart, Jas., Clin. Journ., April 4, 1894.

3 Josue, Arteriosclirose, p. 245.

sec. ii THE PULSE 333

of heart block ; if degenerative disease about the root of the
aorta invade also, as well it may, the tract of Gaskell and Kent,
the case is complicated by this lesion; it is no longer a case of mere
angina. Thus in one of Osier's list (Case XXIII.) the rate fell
from 96 to 42 ; in one of Verdon's to 40. It is possible that
a very angry vagus might make such an effect ; but it is in the
cases complicated with dilapidated heart and gradual dissolu-
tion that acceleration or arrhythmia may set in ; albeit it is
during this hesitant phase of comparative stability that the
heart is prone to trip over. Osier quotes a case of Thayer's
in which this phase was very brief ; the pulse stopped almost
at once ; and in others of the few cases where the pulse
happened to be in touch at the moment of sudden death, the
arrest seems to have been nearly or quite instantaneous. On
the approach of death in angina many authors have taken
note of swerves of rhythm or falls of pressure.

If in some cases the arterial pressures are excessive, in the
majority the pressures are normal ; or at any rate not in excess of
the standard for elderly persons (Osier, Morison, Gibson, Allbutt,
and others). In the angina of younger persons — as in influenzal,
rheumatic, or syphilitic aortitis — the arterial tree and the pres-
sures are indifferent, except in so far as pressure may be driven up
temporarily by the attack. Dr. Morison,1 of a case which was
long under his observation, says, " The pulse was not quickened,
but during the pain it occasionally intermitted, as we know experi-
mentally often happens when the vagus is faradised ; after the
attack passed off the pulse was smaller and more rapid than
during the persistence of the pain."

When the mortal issue is deferred till the later stages of illness,
and a period of acceleration and arrhythmia comes about, the
failure of the heart is more gradual and intrinsic ; but the two
modes of death may cross each other, the period of exhaustion
being suddenly and mercifully cut short. Dr. Uhtoff of Brighton
kindly sent me the notes of such a case in a lady, set. 61, subject
to severe attacks of angina. In her last seizure the pulse, which
had been feeble and irregular, was improving under treatment,
becoming steady and even regular, and she was talking quietly
when, his hand still on the pulse, without any preliminary stagger
1 Morison, A., Cardiac Pain, p. 287.

334 ANGINA PECTOEIS part n

or falter the beat suddenly stopped. At the same moment pallor
overspread the face, the gaze fixed ; then came lividity, a con-
vulsive movement, failure of breath, and the end. Under rise
of pressures the pulse may slow down ; but a slowing due to the
vagus signifies, not a rise, but rather a fall of pressure. Again, in
Sir William Osier's treatise on Angina, I may refer to his case of
status anginosus in which, after some fourteen days of agony, the
pulse rose to 115, and began to fail in volume, while the sounds of
heart became enfeebled, and the ingravescent dilatation became
manifest by the usual symptoms and physical signs ; but this
patient also in his last attack died suddenly. The experience of
authors who assert that in ordinary cases of angina the heart is
agitated — as, for instance, when so able a physician as von Basch
speaks of angina pectoris as "that turbulent disorder of the heart"
— must have been peculiar ; or they have confused simple angina
with angina plus heart affection ; or described what in their
opinion ought to have been rather than what was.

Dr. Mackenzie, as I have said in another paragraph (vide
p. 471), has laid emphasis on the pulsus alternans as an
occasional phenomenon of angina. Dr. Davenport Windle
also has published,1 with analyses of the pulse and respira-
tion curves, some interesting cases of angina with pulsus
alternans ; but his cases were so variously complicated with
cardiac and other diseases as to be of little service in this
narrower enquiry. Although the symptom has no direct con-
nection with the angina,2 and although in cases of high pressure
it may be a sign of aortic tension rather than of intrinsic default
of the heart, yet it is so significant of the perilous susceptibility
of a wavering heart to interference, that I shall return to the
subject under the head of Inhibition (p. 472). (See also remarks,
Vol. I. p. 401, in essay on Arteriosclerosis.) I have observed
this form of pulse very plainly in the stage of cardiac hyper-
trophy, in nephritic hearts for instance, when indeed, under the
long persistence of high pressure, the ventricle is beginning to
"give." The pulsus alternans is not of course necessarily, nor
associated often, with angina ; Dr. Mackenzie3 records a case

i Windle, D., Lancet, May 13, 1911.

2 Since this was written Wenkebach has since reviewed this symptom in
his work quoted p. 476 n.

3 Mackenzie, Jas., Brit. Med. Journ., Oct. 20, 1906.

sec. ii BLOOD PEESSUEES IN ANGINA 335

of angina with pulsus alternans in which the maximum systolic
pressures were 190 mm. : now the angina (which recurred from
time to time on exertion) was always promptly relieved by amyl
nitrite, yet this relief was unattended by any alteration of the
pulse ; indeed the alternating rhythm was more marked in the
intervals of the angina, when the pressure had risen to 200. A
certain anginous patient of my own, set. 45, found no relief
from any form of nitrite ; with other signs of weak and dilated
heart he had pulsus alternans ; at a cuff pressure of 140 mm.
only about 50 per cent of the beats came through.

Of volume and tone the changes are inconstant ; sometimes
the radial artery is constricted — " serre " as say Desportes and
Jurine — scarcely however so generally tight as Sir Lauder
Brunton suggests ; in elderly persons, for instance, we meet, even
more frequently, with the large leathery vessel characteristic of
their time of life. Brunton's sphygmogram, published in 1897,
which was said to represent such a constriction during an attack,
has obtained a great vogue, because it led the author to prescribe
nitrites with the success which has become memorable. Yet,
in my opinion, this very success has blinded us to other facts
which suggest that this sphygmogram was a more eloquent testi-
mony to the diligence of the experimenter than to the capacity
of the sphygmograph. The instrument is incapable of analysing
a pulse such as that recorded ; evidently there is no articulation
in the curve, and such superficial form as it has is susceptible of
more than one interpretation. We have a far better testimony
in his remark that under his finger the pulse felt unmistakably
tight. As a basis for hypotheses, such as the vasomotor
determination of angina, it is, as probably Sir Lauder himself
would admit,1 almost worthless ; probably he has relinquished
his maxims — no high pressures, no fear of angina. I have found
the radial in angina now constricted, now dilated ; and cases are
recorded in which the vessel was constricted in one arm, but of
full diameter in the other. Of two such cases of my own one
was clearly a " vaso-vagal " case, and in the other atheroma had

1 The same criticism is no less true of Sansom's series of sphygmograms in
Angina Pectoris (Diog. of Dis. of Heart, 1892, pp. 429-30). The curves in attacks
Fig. 104 1 and 2 are quite undefined, and this is even still more true of Fig. 105
1 and 2 ; the arteries are too contracted to show details ; the second may show
a rise of pressure. No. 1 (aortic insufficiency) might be quite a healthy curve.

336 ANGINA PECTOEIS part n

probably encroached upon the mouth of the subclavian. Von
Ley den says (loc. cit.) the artery in the attack may become smaller
or larger. Sir James Goodhart writes : x " That high tension
is the sole cause, or even the usual cause, of some of the most
typical cases, I am quite certain is not the case. ... I
have had a finger on the radial in angina pectoris from the
beginning to the end . . . and I am certain there has been
no excess of tension of any kind." He adds that Hilton
Fagge was doubtful as to a high tension in all cases ; and
both authors have argued that, if decrepit, the heart must
be incapable of maintaining it. Arterial pressures may rise, and
vessels may constrict, under any painful impressions. However
Sir William Osier2 remarks, of a case in his consulting-room,
that the pulse rose to 90, and became smaller and harder " ;
though he was " surprised the pulse changed so little ; " after-
wards, "as the attack subsided, the pulse became softer and fuller,
and of decidedly lower tension." Sir Richard Douglas Powell
relates a case in which during the attack the pulse was thready,
very small, scarcely perceptible, but very hard (see Sansom p. 341).
In another case he speaks of the pulse as small and thready ; and
iu a third " An attack of pain came on attended with quickened
action of the heart, and diminution in size and increase in tight-
ness of the pulse ; the diminution in size proceeding almost to
extinction, a mere tightened thread being felt under the finger.
Dr. Morison observes that a dwindling of the artery might
signify a syncopic decline rather than an exacerbation of tone ;
in one case (loc. cit.) he reports of the radial : " Its palpability
varied : it was at times large and more easily felt, and again
smaller and less palpable." This fall may happen no doubt,
but, as we have seen by general testimony, it is not the rule.
A medical man of large experience, who consulted me for angina,
found that his blood pressure, which usually ranged from 125-135
(his age was then 67), when an attack came on, " jumped to 150
or more." Here however we have the anxiety of a medical
man observing himself. Dr. Hunter of Glasgow has narrated
a case 3 in which blood pressures were taken during severe

1 Goodhart, Clin. Journ., April 4, 1894.

2 Osier, loc. cit. p. 79.

3 Hunter, W. K., Brit. Med. Journ., Oct. 16, 1909.

sec. ii BLOOD PKESSUEES IN ANGINA 337

attacks. In tranquillity the pressures ranged about 145-150 ;
during a paroxysm pressure would rise even to 240 ; one minute
after a dose of nitrite of amyl it would fall to about 150, and
then rise again to about 190, until the attack had ceased, when
it would have fallen again to 150. The attacks would last from
a quarter of an hour to an hour, with temporary reliefs by the
amyl. At the onset of an attack the patient " felt his heart
(which was large with aortic regurgitation) becoming stronger
and stronger." Dr. Hunter thought that the rise of pressure was
not secondary to the pain, but the initial factor in the attacks.
But these are only systolic pressures ; the amplitude, which
I have measured in the acuter stages of anginal aortitis — syphilitic
or other — may be enlarged ; and Dr. Mackenzie has proved
instrumentally, what my finger had perceived, that in the attack
there need not be, and often is not, any rise of pressure. The
coronary hypothesis implies a fall of pressure. Merklen (loc. cit.),
in some carefully observed cases of angina, found the blood pres-
sure never exceeded 125. Speaking generally, in the syphilitic
cases, and they are many, the arterial pressures are not
increased. Sir Thomas Fraser has remarked : 1 " Sometimes
there were angina pains, with no tenseness of vessels, a
condition I am unable to explain." The explanation surely
is that at the focus of the disease the vessel is so sore
that pressures not preternatural suffice to exasperate it.
Schabert,2 in a series of careful measurements in many kinds of
disease, found in two cases of angina that during the attacks
the systolic blood pressure fell (vagus effect ?). Gibson also
recorded in a case of angina a fall of pressure during the
seizure3 (under vagus influence?). In another curious case4
which seemed to me however to be more — probably a case of
neuritis, or pressure from growth, than of angina ? — he found
the pulse during the attacks of pain to contract, but on
administration of amyl nitrite to expand by bounds. I observed
in a certain high -pressure case that attacks might come on
during remissions of the pressure.

1 Fraser, Sir T., Cardiac Tonics, Edin. Med. Chir. Soc, Feb. 6, 1895.

2 Schabert, Petersb. med. Wochenschr., 1911, No. 4; quoted Deutsche med.
Wochenschr., March 2, 1911.

3 Gibson, G. A., Edinburgh Hospital Reports, 1895, vol. hi. p. 250.

4 Gibson, G. A., Brain, 1905.

338 ANGINA PECTORIS part ii

It seems then that the blood pressure in angina is inconstant ;
it may be excessive, normal, or even low ; the psychical element,
as in the case in which I found the pulse amplitude increased,
must affect the pressure, in some cases considerably. In
accordance with these observations on the heart, is the cognate
testimony that in mere angina the brain remains clear — " even,"
says one physician, " when death is imminent."

Or a change of tone may be but local. Heberden reports
a case of asphyxia of the left forearm and hand, in which
during the attack the extremity would suddenly become
cold. Trousseau also reports a case where extreme pallor
was followed by a pronounced violet and bluish coloration
of the arm and hand, the natural colour being restored as soon
as the pain ceased (vide p. 298). Balfour records of a lady that
her attacks were always preceded by pallor of the face and
fingers ; and Bristowe speaks of the affected limb becoming pale
and cold. It seems then that in angina pectoris the vasomotor
conditions, both general and local, are inconstant. It is probable
that by the disease of the aorta its sensitive endowments, those
which regulate blood pressures, are disordered — exalted or
impaired ; and, during or near an attack, pain, dread, or
distress make all measurements of blood pressures untrust-
worthy. As regards atheroma of the coronary arteries, I may
remark here that their decay is more frequent and extreme in
decrescent than in high-pressure arteriosclerosis ; if of coronary
origin, angina should therefore be a low-pressure disease.

Sweating may be a feature of any conflict, of any agony ; it
is a curious character of angina pectoris, as it is of ursemic or
hyperpietic paroxysmal dyspnoea ; and likewise is variable,
some patients keeping a dry skin. In one of Dr. Morison's x cases
the patient felt cold in the attack, and did not perspire during
or after it. Possibly in some there may be areas of in-
hibited sweat, to be detected by Dr. Purves Stewart's black-
powder test. Osier writes that occasionally sweating is absent ;
I can say that it may be so slight as not to attract attention.
But its occurrence seems to stand in some more intimate relation
to the symptoms than as a function of effort or prolonged distress.
In most cases indeed the effort is one of endurance and fortitude
1 Morison, A., Cardiac Pain, p. 32.

sec. ii SWEAT. FEVEE 339

rather than of muscular conflict ; moreover the sweat may
break out before the torture is applied, even before it is imminent.
Such a case I saw, at the R.A.M.C. examinations in February
1908, in a subject of syphilitic arteriosclerosis and aortitis with
angina pectoris. The attacks were severe and not infrequent ;
the pain travelled in the usual course, according to type, but
stopped precisely at the pisiform bone. Now in this man a
profuse sweat always preceded the attacks by half an hour. Thus
the patient could foresee, not only the return, but also the prob-
able severity of a seizure ; for before the severer seizures " sweat
would break out all over him, and drop from his whole body ;
then the angina went into his breast like a knife." Morgagni, in
one of his cases (" insultus vehementiores, angore molestissimo
cum suffocationis metu "), mentions " sudor copiosissimus "
as remarkable. Dr. Mott, in his recent Lectures, refers the
cold sweat to an excitation of the sympathetic, with contraction
of the involuntary fibres of the sweat glands ; some recent
observations have suggested that the vagus also may have some
influence upon the secretion of sweat. In this connection the
pupils and palpebral fissures should be noted. A critical ery-
thema of the face, neck, and upper chest, with a sensation of
warmth, is said by some, I think by Eulenberg, to mark now
and then the abatement of the attack, especially in women.
Sometimes the colour appears in small red patches, like measles.1

A flow of saliva has often been recorded during an attack, or
after it. Dr. Mackenzie explains this as a cardiac reflex acting
through the vagus on the lingual nerve ; but I shall return
to this symptom presently. The difficulty in swallowing,
observed in some cases, may own the same cause. This
symptom likewise, as other secretory, paresthetic, or vasomotor
conditions, may forerun the attack.

Fever is present in the acuter modes of aortitis, as in the rheu-
matic. Often of course it escapes attention, but, in cases such as
Dr. Windsor's of Mr. B. (p. 157), it obeyed plainly enough the
periods of rheumatic aortitis. Stengel indeed speaks of febrile
periods as well known in aortitis.2 Popoff 3 also says, " Contrary

1 Gilbert and Descamps, Paris med., 1912, vol. xvii. p. 044.

2 Stengel, Brit. Med. Journ., Oct. 20, 1906, p. 1011.

3 Popoff of Moscow, Zeitschr.f. Bin. Med. Bd. Ixxv. He. 5 und 6, 1912.

340 ANGINA PECTOEIS part n

to the usual opinion, aortitis is often attended with fever, though
it may be too slight to attract attention if not watched for."

Gibson included as "by no means rare concomitants of
anginous seizures," vertigo, visual and auditory hallucinations,
and even delusions. Such symptoms we may observe not in-
frequently in aortic insufficiency, or arteriosclerosis, with or
without angina ; but not, I think, or not characteristically, in
angina sole. However by many authors vertigo is mentioned
as an incident of angina. I would add, as occasional prodroma,
yawning and a vague sense of unrest.

It is for reasons such as these that I have placed the vaso-
motor symptoms in the secondary list (pp. 226 and 280), as inci-
dental ; in radical divergence from Nothnagel who, in an article
written, it is true, forty years ago,1 placed them in the first
rank {vide pp. 224 and 236) ; whereby in my opinion he thickened
the fog through which we have had " on each quarter to
descrie the distant foe, Where lodged." Every fox-hunter
knows how a flock of sheep may make his sport or mar
it. By their movements a quarter of a mile off he may
learn that the fox is passing their way ; now the vasomotor
nerves are these sheep. In some cases the stealthiest approach
of angina pectoris may ruffle the watchers, and may startle them
into an agitation under which the enemy may slip away un-
noticed. But in angina this flutter, if it be caused by the enemy,
is not the enemy. I have argued that under the irritation of any
sensory nerve -trunk such vasomotor reactions readily appear,
and the more as the centre becomes unstable ; not only so, but
in angina pectoris an emotion of them, like other, even subjec-
tive, causes, may by vasoconstriction determine the moment of
a paroxysm. Still, this sympathetic disturbance is not of the
essence of the malady, nor, as we have seen in discussing the
pulse, is it a constant. In particular cases, or attacks, it
may be difficult to disentangle a chance vasomotor commotion
as a determinant of a seizure from one ensuing upon the distress
of it ; but the distinction is a real one, and in most cases is to
be made out by the history of the seizure itself : was it instantly
preceded by an annoyance, or a chill ; or was it rather provoked
by some muscular effort ?

1 Nothnagel, Deutsche Arch. /. klin. Med., 1867.

sec. ii VASOMOTOR SYMPTOMS 341

The complexion of the sufferer does not tell us all that
might have been expected. Many anginous patients are of
turgid or weathered complexion, as some are spare and sallow ;
and the testimony is conflicting. Here again nature has no rule.
Heberden speaks of pallor ; Fothergill, a close observer of large
experience, says distinctly that the face at first reddens, then
in an instant turns very pale. Broadbent writes : " The face
may be flushed or pale, or may keep its natural colour."
John Hunter's face in his two attacks became pale and
pinched. Of one of his own cases Sansom (loc. cit.) noted that
in the attacks the radial artery contracted, and the face and
mucous membranes turned pallid ; the vessels then dilated, and
the face and lips flushed. Sir James Goodhart,1 in narrating
a series of attacks, says, " His face flushed decidedly in the
paroxysms." I saw more than once a subject of true and typical
angina, who assured me, and her daughter was not less con-
fident, that with the onset of a seizure her face flushed deeply,
and the arteries of her neck began to throb ; it was that as
the attack passed away she turned pale. Nitrites increased
the face flushing and made her altogether worse, as follows :

Mrs. W., set. 60 ; angina pectoris ; frequent attacks twelve
months, especially after meals or on the least exertion. Previous
health very good. With the onset (says her grown-up daughter)
" her face always flushes, to turn pale when the seizure is over."
When she feels the flushing coming on she is aware also of a throbbing
in the notch above the sternum and in the neck, and the arm turns
numb, without much pain in it ; but the pain at the sternum is such
that " if it didn't stop, her heart must cease to beat." Was it because
of this vascular relaxation that, though the case was one of high
pressure, nitrites made her feel worse and increased the face flush.
The pressure, when she was as tranquil as one could expect,
was about 200. There was a soft systolic murmur at the base.
Perhaps our doses of nitrite were insufficient ; some other areas of
the periphery, e.g. the splanchnic, may still have been constricted.

Sir William Osier writes : " A sudden pallor of the face may
be the first indication, and as a rule vasoconstrictor influences
prevail in the severe paroxysms." In another patient, whose
attack took place in his consulting-room, he reports : " The attack
lasted a minute and a half ; the face, normal at first as to

1 Goodhart, Sir J., Clin. Journ., April 4, 1894.

342 ANGINA PECTOKIS part ii

colour, then flushed deeply." But he adds, " Though not absent
in the organic form of the disease, these vaso-constrictor dis-
turbances are often more pronounced in the hysterical angina."
In another paragraph he says, " The face may be death-like,
ashen, or suffused or deeply congested even from the outset."
In private notes of a certain case, sent to me by Drs. Mackenzie
and Price, the complexion during the attacks turned " grey."
Of another case Mackenzie 1 writes that " at the onset the face
turned pale, and the radial artery became constricted and
small " (see previous paragraphs). This case, like John Hunter's,
of syphilitic aortitis, was made very interesting by the close
observation of its clinical features. As the attacks came on,
and they were almost incessant, the systolic pressures rose from
a common level of about 160 to much greater heights- — to 240,
and, on one occasion at least, to 300. Among other interesting
comments, Mackenzie suggests from his reading and experience
that such fluctuations are especially frequent in aortic regurgita-
tion, a malady in which a very powerful heart and an
abnormal vascular adaptation are well-marked coefficients He
thinks that the abnormal attitude of the vasomotor system
makes it peculiarly liable to these extreme oscillations. My own
recollection of such cases is in accordance with this suggestion.
The author observes, in accordance with what I have said, that
in some other cases of angina, in which he had made the same
pressure observations, these rises of pressure with the pains did
not occur. Gibson supported the general opinion that a deadly
pallor is a frequent initial feature ; but added that in his experi-
ence it had been " quite common to find the surface suffused
by a bright flush."

Cyanosis is sometimes mentioned, but often no doubt in cases
with dyspnea, and complicated with heart or lung disease.
Profuse voidance of urine occurs in some cases after an attack,
and suggests large areas of vasoconstriction other than renal.
But, having already discussed these vasomotor phenomena under
the head of mock angina, here I do but touch on them as
subordinate symptoms of the true.

Dilatation of the stomach, by some process of sympathy or
exhaustion, may be induced by angina pectoris ; it is frequently
1 Mackenzie, Jas., Heart, vol. ii. No. 3, 1911.

sec. ii GASTKIC SYMPTOMS 343

associated with it. Broadbent * and myself made this obser-
vation ; and so before us did Eisner explicitly, but rather in
respect of treatment — under which head I shall return to the
subject — than as a point of pathogeny. It may be a consequence
of vagus irritation, and we have noted that eructation often
signifies relief. If then gastric ectasis is not to be reckoned as a
correlated symptom of angina, the coexistence is by no means
to be overlooked, as the mere oppression of it may provoke the
recurrence of seizures, or even determine the moment of death.
Dr. Verdon, in placing the seat of angina pectoris in the stomach
— a hypothesis to be discussed presently (p. 344) — seems to
me to exaggerate an important, but a secondary, element of this
disease. One case, cited by Broadbent, of a distended stomach
with a suspicion of angina, was a sequel of influenza ; in this
infection genuine angina, is apt to ensue, but the interpretation
is open to question. In one of Sir William Osier's cases — ■
of a patient who died in status anginosus of fourteen days'
duration— the author noted great gastric distension. The im-
minence of angina during digestion, whatever the explanation, is
well known. As regards arterial pressures, these during digestion
fluctuate a good deal. Usually there is an initial rise for a few
minutes, then a fall on the whole for about an hour; then a rise
of some duration. This excitement of angina on a full stomach
can scarcely then be due to blood pressure. Flatulency has been
regarded by all writers on angina pectoris as a general, a
pressing, and perhaps a cardinal factor ; but its significance
is not easy to interpret. Dr. James Mackenzie has pointed out,
with truth no doubt, that patients, attributing the distress to
flatulence, belch and gulp in such a manner as to swallow
air, and thus to produce or increase the very distress they
apprehend. I have noted this point more carefully since,
and think this explanation inconclusive. For instance, I
noted this point in an elderly man whose first attack was
severe and sudden. Setting aside some general arteriosclerosis,
of which he had known nothing, he was well ; nor was he beset
by any dyspeptic symptoms. But, as this attack passed off, he
said spontaneously that he became aware for the first time of
flatulence, which rumbled up in " enormous quantities." Before
1 Broadbent, W. H., Lancet, May 27, 1905.

344 ANGINA PECTOEIS pakt n

it he had not belched or gulped, nor during it. His subsequent
attacks were marked by the same sequence, although on my
warning he took especial care to avoid every chance of wind-
sucking. My own observations and those of others prove again
and again that attacks of angina — of angina major or minor
— often appear without any eructatory efforts, yet the wind
and the pain may be discharged together. In some cases of
angina pectoris swallowing is in abeyance. Now the suspicion
of wind as the enemy is true not of angina only; it is one
common to sufferers from almost all cardiac disorders, who
suspect some correlation or bond between the wind and the
heart's behaviour. Whatever the nexus, whether a vagus
reflex from heart to stomach, or a mechanical butting at
the heart itself, we are not yet in a position to say, everyday
experience tells us that cardio-aortic maladies are mitigated
by rules of diet which guard against generation of wind in the
stomach, and are relieved by cordials which expel it when there.
Dr. Verdon was a bold man when he passed an oesophageal tube
during an attack of angina, an operation which might stimulate
the lethal activity of the vagus ; but the results in the two
cases in which he tried it — one of angina pectoris, the other one
of grave cardiac asystole — were no doubt strikingly successful.
Dr. Verdon's opinion, which in several well-known papers he
has acutely advocated, is that angina has its seat in the stomach,
and consists in an unruly gastric function which he defines at
one time as " intra-gastric pressure" (distension ?), at another
as " gastrismus " or " spasmodic constriction " of the viscus or its
orifice. The author has examined the tender areas of skin and
muscle, studied the intricate nervous connections of the stomach,
and formed the opinion that referred pain in the eighth and
ninth intercostal area signifies " hypertonus of the gastric
muscle " (not " intragastric " pressure or distension ?). He re-
minds us of the several component strands of the vagus, of its
distribution to the gastric muscle, of its radical association with
the medullary portions of the spinal accessory, of the spinal
connections on the cervical chain, of the association with the deep
root of the musculospiral, and — at the seventh segment — with
the ulnar deep root. Also he makes an interesting note on the
salivation of some cases, which he traces through the chorda

sec. ii PHYSICAL SIGNS 345

tympani to the vagus. He illustrates his theme by the well-
known complaints in angina of flatulence, loaded stomach, and
so forth ; associated gastric phenomena which, we shall agree,
are found, not in angina only, but in almost all diseases
and disorders of the heart ? The close sympathy between
these two viscera — partly nervous partly mechanical — and the
great importance in therapeutics of realising these associations,
Dr. Verdon has ably vindicated ; but it is another and as yet
an unverified postulate to assume that angina is not a cardio-
vascular lesion aggravated by gastric reciprocity, but itself an
outcome of no more than storms in the cup of the stomach.
" Cardiospasm " is an old story ; one of my earliest consulta-
tions was in a case of this kind, one which Mr. P. Teale helped
to relieve by bougie. The attacks were relieved, but we did
not put the malady to flight. Yet of all the many such cases
of cardiospasm in my recollection not one suffered from angina
pectoris. However I am glad to welcome Dr. Verdon as at any
rate a disciple of my hypothesis of death in angina by vagus
inhibition.

On the -physical signs of the conditions congruous with angina
pectoris I have little to say which is not common knowledge.
Angina is prevalent among elderly and degenerated persons,
and is apt therefore to be associated with signs of decadence ;
but the current opinion that the disease is always, and by its
own nature, associated with widespread senile cardioarterial
degeneration, is far from correct. The disease, as for instance
we have seen in infectious aortitis such as the syphilitic or
influenzal, is frequent in patients wholly free from either heart
disease or arteriosclerosis. We have seen that the late Dr.
Sansom, who for some years had shared the current preposses-
sions on this point, found himself obliged to revise his opinions ;
he frankly admitted to me that many cases had come before
him in which neither hypertrophy of the heart nor thickening
of the accessible vessels was to be detected. Sir James Goodhart
(loc. cit.), after watching a series of paroxysms in a certain case,
reports: "The heart was to all means of examination perfectly
healthy, and upon a second examination I made this note : ' I
am perfectly certain that if he went to an insurance office
and said nothing, he would be passed as perfectly sound.' "

346 ANGINA PECTOKIS part n

Disorder of rhythm, if haply concurrent with angina, is no
character of it; in an anginous patient "gallop rhythm" may
of course be casually present ; but it is said that this character
is never heard during an attack, that then it always ceases.

In the high-pressure cases the heart may be enlarged without
other signs of disease. In uncomplicated angina, neither during
the attacks nor between them is there any rule of dilatation or
other static cardiac disorder. Is not the throbbing about the
arch of the aorta, up into the throat, felt by many persons
under excitement, as for example before rising to speak in
public, sometimes enough to suggest not only a transient
aortic dilatation, but even the sort of discomfort we are wont
to associate with slight degrees of " stenocardia ? " It seems
certain that the arch may undergo considerable changes of dia-
meter from vasomotor causes, as may the abdominal portion ;
and that these may be manifest as physical signs. Chafing
or a cold sponge might reduce such an area of dulness.
A very important physical sign, pointed out first by Peter, and
often to be noted in angina, is the area of the aortic dulness
already mentioned in the Section on Aortitis (see p. 198). We
have seen that this area extends to the right of the manu-
brium, on the second space and third cartilage, forming
more or less of the outline compared by Potain to the peak
of a fireman's helmet. In normal persons submanubrial
dulness is rare. And such dilatations may now be recorded
by radiography. In two cases of my own we had this veri-
fication. The vessel may also be palpable in the episternal
notch, and tender to pressure (see Mrs. X., p. 427) ; and the
right subclavian may be elevated. Yet how punctilious we must
be in taking comparisons at many points is illustrated once
more in an important paper by Wenkebach,1 where he argues
that signs of dilated aorta may be simulated by a forcing
up of the thoracic viscera by a high diaphragm. In such cases
the heart may be bothered ; but this bother is not angina
pectoris. The dilatation of the aorta is most frequent and
largest in certain syphilitic cases ; in some of them so wide and
the percussion note so flat as to suggest aneurysm or growth ;
but in some acute infections in young persons, as in rheumatic
1 Wenkebach, Nzderl. Tijd v. Gen., 1907 (translated).

sec. ii PHYSICAL SIGNS 347

aortitis, angina or no angina (p. 150), it is plain enough, if
sought for. In some cases the aortic distension may be due, in
part at any rate, to a paresis of the vessel, analogous to the
paretic distension of an inflamed bowel ; an interpretation which
on recovery is often justified by the restoration of the aorta to its
normal dimensions. Moreover during the same illness, as may be
seen by radiograms, it may vary from one period to another. We
have seen that aortitis is more frequent in acute rheumatism
than is supposed, and in most cases is to be detected by physical
signs only. Although not of the " muscular type," the aorta
contains much muscle, and probably in health enlarges and
contracts a good deal. Of Abram's reflex {vide p. 198) I have
no practical skill, but I presume this method might assist
us to distinguish static from dynamic expansions of the
vessel.

When, as in chronic cases, the condition of the patient per-
mits, before pronouncing that no signs of disease are present,
the patient should be directed to perform some simple arm move-
ments, as in dumb-bell fashion when, with an atheromatous aorta
or valve, a systolic murmur, if not already present, may be
elicited. On reference to my own cases I find that in the
majority of them a systolic murmur was audible at the
base. In syphilitic cases even a slight alteration of the first sound
at the base must be regarded with grave suspicion, for a little
muffling of this sound often — perhaps always — precedes a
murmur. The suprasigmoid disease is then creeping upon the valve
(p. 175), and the next event may be a murmur of regurgitation,
when the case, if curable as angina, may as heart disease have
become incurable. In such circumstances no vigilance can be
excessive ; no treatment too prompt. Dr. F. Jackson x discusses
cases of his own in which disease just above the aortic valve,
without perhaps invading it or the orifice, is marked by absent or
very feeble sounds, even although the left ventricle be somewhat
hypertrophied. " Such persons," he adds, " are liable to angina
pectoris." In practice we are all familiar with the weakening of
the first sound, and of the impulse (emphysema and fat chest
wall excluded), which may signify a loss of vigour of the left
ventricle, as in degeneration of the myocardium, or in anaemic or
1 Jackson, F., New York Med. Journ., April 28, 1894.
VOL. II Z

348 ANGINA PECTORIS part n

convalescent persons, or, as Baumler says, in nodular fibrosis of
the myocardium * (see p. 20). But so far from these signs being
characteristic of angina pectoris, they are frequently absent.

Dr. James Mackenzie cites a case of angina (in a man
set. 42) in which signs of dilatation of the arch thus advanced to
slight incompetence of the valve, and slight hypertrophy of the
heart. The systolic blood pressures stood about 150, until, as his
state grew worse and his sufferings more continuous, the pressure
fell to 95. He died in a run of attacks sinking into heart
failure. I have seen only too many such cases, especially in the
syphilitic ; but, with Mr. Balding of Royston, I saw two or three
times a London merchant, aged 59, who six months before
had begun to feel on exerting himself a tightness under the
manubrium sterni ; this grew worse, and a pain began to radiate
into both shoulders, then down to both elbows, then to both
wrists. If anything, the right side was the worse. Such was
the dread of the attacks that he would take cab or bus to go
but fifty yards from his office. The systolic blood pressure, under
the ordinary circumstances of consultation, was not more than
140 ; and the accessible arteries were straight and soft. In
this case syphilis was improbable, and on careful scrutiny
no specific stigma was discovered. There were no symptoms
of renal disease. Now his heart, as regards apparent size,
position, and sounds, was normal, with one exception, which
was this ; there was a very distinct, almost musical, systolic
aortic murmur ; but the aortic second sound was not abnormal
in quality. Our diagnosis was angina pectoris with subacute
atheroma. As regards diastole, we did not forget how elusive
an aortic regurgitant murmur may be ; exceedingly soft and
distant, especially so perhaps when first established, and then
audible, or distinct, only perhaps in a small area to the left of the
sternum. It is unnecessary then any longer to insist on close
appreciations — of the quality of both first and second — of any
undue stress, or alteration of it, whether of muffling, of reinforce-
ment, or in what acousticians call " clang." The peculiar quality
of the second aortic sound often present in these cases, and first
observed by Gueneau de Mussy, I have described on another
page (200).

1 Baumler, Deutsche Arch. f. klin. Med., 1911.

sec. ii PHYSICAL SIGNS 349

The right subclavian may be palpable, as demonstrated first
by Faure * ; the radial pulses may be unequal.

I have said that in young persons an aorta dilated under
acute inflammation, so as to yield obvious physical signs, may
nevertheless pull itself together and recover, even ad integrum,
or practically so ; that in them the physical signs may diminish
and even disappear ; but in later life to the coats of a vessel
which, as Professor MacWilliam, Herringham and Wills, and
others have demonstrated, had been losing with time and wear its
vitality and capacity of growth, such repair and restoration are
less possible. On this point the reader may be referred to certain
reflections of Jiirgensen, in Nothnagel's System, on aortic in-
sufficiency. In children however elasticity is not the factor
chiefly concerned, for in them the arch of the aorta is relatively
less rich in elastic fibres. Indeed there is some evidence that
on the hither side of middle life the aorta may in case of need
develop no little compensatory hypertrophy of a genuine kind.
I have one case on my notes in which the pupils were said to
contract during the attacks. Permanently contracted pupils
in angina, or the light stop, might, of course, suggest other terms
of a syphilitic series, such as aneurysm, tabes, etc.

1 Faure, Arch. gen. de mid., 1874.

CHAPTER VI

HYPOTHESES OF ANGINA

After this summary consideration of the symptoms and signs,
somewhat brief but sufficient perhaps for present purposes, we
may proceed to discuss the interpretation of angina pectoris. This
argument, which in some degree must take the form of controversy,
falls into two parts ; the criticism of those hypotheses which,
whether for their own value or for the eminence of their advocates,
still occupy the field, and an attempt on my own responsibility to
substitute for them another hypothesis which, if it is to command
attention, must explain more of the facts. Concerning the
current conjectures, " theories " as some sanguine advocates
call them, perhaps each disputant would be ready to admit that,
his own excepted, they make an incoherent and motley collec-
tion. If, not united against a common enemy, they fell out
among themselves, they would end in a mutual destruction —
" Ceci tuerait cela." The heart cramp and the heart dilatation
champions would come to a stalemate ; and then the neurotic,
the vasomotor, and the " pseudo " people, entering in and dis-
solving away the disease altogether, would make peace, on paper.
This incoherence was strikingly evident at a discussion on
angina pectoris at a meeting of the Harveian Society in
1909, when once more I offered my own hypothesis.1 Some
speakers were clinging still to the orthodox view of coronary
atheroma with thrombosis ; others descried a ventricular
distension, others a reluctance after the manner of an obstruc-
tive colic, others again a cramp of the heart ; some invoked a
spasm of the coronary arteries, or of the diaphragm, or of peri-
pheral vascular areas ; some, like Merklen, played two cards at

1 Vide Brit. Med. Joum., Dec. 11, 1909.
350

sec. ii HYPOTHESES OF ANGINA 351

once, thus — angina is awakened " soit par la distension ; soit
par l'ischemie des elements musculaires et des fibres nerveuses
contenues dans leurs mailles " ; others were vague, or wisely-
reticent. By a sagacious and discreet speaker the conclusion
was fittingly summed up in these words : " Angina pectoris
is a painful affection of the heart as a whole, depending upon
disorganisation of some anatomical character, or a disorder
of physiological function of one or more factors in cardiac
action ; and associated in some cases with a fear of impending
death." That is to say. angina pectoris is anything you please
• — a very popular sentiment. But really, as Montaigne remarked
on another matter, is there not more ado in interpreting the
interpretations than in interpreting the things themselves 1
The late Professor Huchard is said to have collected and
arranged no less than eighty hypotheses or, may we say,
guesses, on this subject ; I shall not follow his example. I
must content myself with a smaller selection of the more
prevalent conjectures, but these I will try to submit to a closer
appreciation. I will consider the following opinions :

(i.) That angina pectoris consists in distension of an enfeebled

ventricle (Parry, Stokes, Traube) ;
(ii.) That it consists in a cramp, or spasm, of the heart,

analogous to cramp of a voluntary muscle (MacBride,

Baumes, Latham) ;
(iii.) That it is an " intermittent claudication " ;
(iv.) That it consists in a myocardial ischsemia, generally due

to an affection of the coronary arteries (atheroma,

functional constriction, thrombosis, etc.), this ischmnia

being the direct cause of the pain ;
(v.) That it is " neural " in origin ; a neuritis, a neurosis,

a neuralgia, a vasomotor storm, local or general ;
(vi.) That it is not itself at all, but a poor relation ; something

else of the same name flitting wistfully from one

" entity " to another.
It is not, I trust, disrespectful to animadvert upon such a
display of incongruous opinions as this ; to reconcile such con-
tradictions would demand a more than Hegelian insight. If the
curability of a disease be inversely as the multitude of its
remedies, so may our understanding of it be inversely as the

352 ANGINA PECTORIS part n

number of opinions about its nature. It will be pleaded,
of course, that no one holds two of the incompatibles at once.
Well, perhaps not in the same breath ; but the hard-pressed
disputant flies for refuge now to one, now to another ; yet to
bolster up one hypothesis by another does not prove either, still
less both. To quote examples would be invidious, and perhaps
not very useful. Can we indeed avoid an apprehension that the
vogue of such a competition of promiscuous guesses betokens
not a defective knowledge only, but also on this subject an
undisciplined state of medical ideas ? That so heterogeneous a
mob of conjectures should engage our attention, that one of the
ablest physicians and teachers of the day should in a standard
treatise vacillate between such vague speculations as partial
spasms of the myocardium ; a cramp of the heart comparable
with renal, hepatic, or intestinal colic ; a stretching of the
ventricle, and " claudication," seems to argue a defective sense
of proportion, of comparative values. And yet, notwithstand-
ing, I am about to press into the ragged regiment a recruit
of my own.

The older writers, Bonnet (Sepulchretum), Morgagni,
Heberden, discovered in their necropsies on angina morbid states
so many and so various that naturally they were perplexed.
For any or all of these states were more frequent without angina
than with it. But from Jenner's time attention was riveted
on the coronary arteries. It is true, no doubt, that an assumption
of the invariable association of coronary disease with angina, as
first suggested by Jenner and Parry, is compatible with the
attribution of the several attacks to some intermediate factor,
such as a ventricular stress, or a cramp. For this reason I will
begin my scrutiny of the pathology of the disease by examining
the implication of these arteries in the process.

In the later eighteenth and early nineteenth century there
was much scepticism concerning the dependence of angina upon
coronary disease, but of late years the coronary hypothesis has
been urged with an almost blind advocacy. Our fathers took
note both of coronary disease without angina, and of angina
with coronaries intact.

Coronary Disease. — It is freely admitted of course that

sec. ii THE CORONARY ARTERIES 353

coronary disease may, and indeed for the most part does, pursue
its silent way without anginous or other storms ; and that,
while angina is most frequent in later middle life, coronary
disease extends, as years extend, into decrepitude. It is to
be regretted therefore that modern authors should rehearse
the really tiresome burden of " coronary angina," " angine
coronarienne," " die der richtigen Koronarsklerose entsprechende
Angina," and so forth ; as if the two conceptions, that of coronary
disease and of angina, were indissoluble, or at any rate twin ; or
as if on coronary disease depended the mutation, the functional
swerve, the " unhallowed string which vilely jars." " True
angina," says one of the more eminent, " always presents lesion
of the coronary arteries ; this is its anatomical substratum."
Neuburger 1 thinks he clinches the argument by the necropsies
of thirty-eight cases of mortal angina in every one of which
he found some degree of disease in the coronary arteries ; it
appears that all these cases were in old people, yet of the
ordinary incidence of coronary disease in elderly people he offers
no estimate. Von Romberg, even in his last edition (p. 43),
still confidently assumes " the origin (' Entstehung ') of angina to
lie in coronary sclerosis " ; and conversely that this pathological
change is the cause of angina. So Krause likewise, in his new
Lehrbuch, attributes " angina vera " to disease of the coronary
arteries mainly, if occasionally to myocardial degeneration not
so caused. Schmoll,2 with an assurance no less ready, formu-
lates the maxim that angina pectoris is in proportion to the
cardiac disease due to coronary atheroma, and bids us rest our
prognosis upon the degree of this lesion. Balfour, on the
contrary, pondered over the strange inconsistency that such
conditions as these are usually unattended with angina. Un-
fortunately in cases of angina necropsies are difficult to obtain,
at any rate in private practice ; the death is usually sudden,
the occasion fleeting, the household distracted, and the diagnosis
sure enough to warrant a certificate.

Now against the assumption that angina depends upon
coronary disease a cautious writer would recognise no little

1 Neuburger, Deutsche med. Wochenschr., Juni 13, 1901.

2 Schmoll, " Uber mot. -sensor, u. vasomot. Symptomien in Koronar-
sklerose," Munch, med. Wochenschr., 1907, No. 41.

354 ANGINA PECTOEIS part ii

evidence, direct or indirect ; not only from the older authors, such
as Desportes,1 Jurine, and others, whose pathological equipment
might be regarded as rough, but also from modern pathologists.
Fothergill 2 noted disease of the coronary arteries in angina —
they were diseased in the typical case of a man, aged 65, whose
body John Hunter dissected for him — but Fothergill does not
seem to have attached any special significance to this coincidence ;
he suspected rather that the cause was obesity about and within
the thorax. Gibson says indeed that, although Jenner was
the first to correlate coronary disease with angina, Fothergill
was the first to publish the coincidence.3 Then the ossified
coronaries were supposed to offer a mechanical hindrance to the
heart's motion ; but soon, by Parry and others, it was seen
that in this case the nutrition of the myocardium would suffer,
and blood gather in the cavity. Parry and Matthew Baillie took
the coronary hint from Jenner ; and Peter Joseph Frank 4 half
agreed with them ; but they noted exceptions to the rule, and
thought the mechanism of the pain to be not, as Heberden
supposed, a spasm of the heart's muscle, but an oppression of it
by this congestion of blood in the chamber. Desportes shrewdly
demurred that, having examined many bodies of persons over 50
years of age, he found coronary atheroma " at least as common "
in the women as in the men, yet that in women angina was rare.
How far coronary atheroma may be the cause of angina or not is
an open question ; but when it is asserted that Jenner demonstrated,
or declared, that angina depended upon their decay we exceed
historical testimony. In his Letter, it will be found that Jenner,
with true scientific caution, did not attribute the angina to the
coronary changes ; he stated simply that after death in angina
disease of these vessels would be found ; another and a different
proposition. To point out the significance of coronary disease
in angina was true service, but for his successors to force his
meaning, and to declare coronary atheroma to be the immediate
cause of the attacks, is to pass, where he did not, ex errore per
veritatem in errorem. Jenner was speaking of course from the

1 Desportes, Traite de Vangine de poitrine, Paris, 1811, an excellent book.

2 hoc. cit. p. 72.

3 In the Med. Obs. Soc. Phys., London, 1776, vols, ccxxxiii. and cclii.

4 Frank, Peter J., Praxeos med. praecepta, Lips., 1824.

sec. ii THE CORONARY ARTERIES 355

evidence of mortal cases only; if angina kills people, then coronary
atheroma will be found, a true point, to be taken presently.
Everard Home reinforced Jenner's emphasis upon the coronary
disease noted by Heberden and others in cases of (mortal) angina,
by attributing the pain to the pressure of vessels thus hardened
upon the ramifications of the cardiac nerves, a possibility hinted
at again by Dr. Morison in discussing a section (p. 404)
taken by him from the heart substance in a certain case of
angina, in which a small intramyocardial aneurysm was seated
pressingly near a nervous ganglion and fibres.1 But, as we shall
see later, these myocardial ganglia are pretty surely motor, not
sensory structures.

Now Cohnheim says : " Often no trace of disease is to be found
in the coronary arteries of these subjects of angina." Indeed in
one of Heberden's cases the coronary arteries were unaffected,
the only lesion discovered being atheromatous patches in the
aorta. In John Hunter's heart the coronary arteries, though
" ossified " — " they cut with difficulty, and gaped open when
severed " (Home) — seem to have been pervious ; and Jores has
pointed out that ordinarily in sclerosis of the trunks of these
vessels the intramyocardial twigs are unaffected. Dr. Morison,
when publishing 2 a case of angina in which atheromatous
changes in the coronary arteries were in a comparatively early
stage, and the orifices normally patent, ventures so far as
to hint at some dissatisfaction with " this ready coronary
explanation." Before turning to my own evidence, which may
be biassed, let me cite further that of others. Frankel says
(in the fourth edition of Eulenburg): "Angina arises also in other
heart diseases ; for instance in certain valvular affections, and
under conditions where the coronary arteries are intact through-
out (' sich als durchaus intakt erwiesen ')." This is the testimony
of an opponent ; for, in the dilemma, this scrupulous observer
is driven to assume that cramp of these vessels which we shall
see to be a mere guess, and a guess contrary or, at any rate, alien

1 Morison, A., Cardiac Pain, 1902.

2 Morison, he. cit. {Cardiac Pain). This careful writer adds that there was
nothing in the aorta to account for the angina ; but he did not bring the in-
vestigation he gives to other structures to bear upon this one. Minute sections
were made of the myocardium, but no sections of the aorta ; here a glance of
the naked eye, and probably at the inside only, is too often sufficient.

356 ANGINA PECTOKIS pakt n

to what we know of their nervous endowments. Hirsch x freely
admits that most cases of coronary sclerosis take the course of
chronic heart insufficiency without any symptoms of angina,
and in these cases he finds amyl nitrite to do more harm than
good. Thorel, in his review of " Angina Pectoris " in Lubarsch
for 1907, says the interpretation of the disease as a myocardial
ischaemia is far from proved ; for life is often prolonged with
both of these vessels closed, yet without angina. There is, he
adds, some factor of this disease as yet unperceived (" ein un-
erklarHches Etwas "). As to the fibroid nodules resulting from
coronary disease, we may find, he says, even with these
masses in abundance, that conductivity is quite unimpaired.
Dr. Samuel West 2 reports a case in which one coronary was
completely obliterated, and the orifice of the other so minute
that no blood could have traversed them to the heart, yet
without angina. Conversely, in many cases of angina pectoris
the myocardium has proved to be perfectly normal, even without
interstitial fibrosis, as in cases examined by Gennari.3 Balfour,
as I have said, frequently returns to these difficulties : for
instance he writes : 4 " Coronary sclerosis is too often present
when there has never been any angina to permit the occurrence
being looked upon as anything more than accidental. . . .
These arteries, being unsupported, are very liable to stretch and
twist." Again he reflects : " Like arteriosclerosis, fatty degenera-
tion of the myocardium is too often found when there has been
no antecedent angina ... to allow us to regard the association
as more than a concomitant." He then drifts into speculations
on imperfect metabolism, cardiac reserves and so forth.

To cover the many exceptions, and to get over these difficulties,
a spasm of the coronaries has been postulated, an argumentative
resource first supplied, I think, by the ingenuity of Neusser.
Thus one influential author speaks to us of " spasm of the coronary
arteries causing high vascular tension within the myocardium," a
process I have tried to picture to my mind in vain. He is more
intelligible when he adds that the temporary ischsemia thus

1 In Penzoldt and Sterzing, new ed., vol. iii. p. 372.

2 West, S., Lancet, Oct. 16, 1909.

3 Gennari, Arch, four les sci. med., dec. 1905, and p. 17 of this volume.

4 E.g. Balfour, Senile Heart, p. 127.

sec. ii THE COEONAEY AETEEIES 357

produced provokes a spasm of the heart muscle. Yet, on the other
hand, Wooldridge and others have shown that a transient myo-
cardial anaemia is no very grave matter. In a recent authori-
tative work it is said positively that " nitroglycerine is used to
dilate the coronary vessels in angina pectoris." Sheer guess
work ! Ortner talks, as if they lay visible before his eyes, of
forcing blood into the constricted coronaries by means of digitalis
or theobromine ; and of combinations of vasodilator drugs with
digitalis in order so to open out these vessels that digitalis may
pump blood in. It takes some presence of mind to realise that
these convenient "facts" stated so calmly and so confidently,
are at best opinions, and hitherto sheer fancy ! How can a
spring up three stairs, an effort at stool, or to walk against the
wind, constrict the coronary arteries ? It should dilate
them ; pretty surely it does. And more plodding observers
might suppose that myocardial anaemia or " ischaemia " would
betray itself by a fall in blood-pressure, a severe fall if
produced by a prolonged or extensive coronary closure. Now
although, as many authors agree x (vide p. 335), the frequency
of high arterial pressures in angina, recorded by Brunton
and later by Pal, has been exaggerated, yet it is also agreed
that persistently high pressures are consistent with the disease ;
and sometimes run very high. Indeed, the opinion pre-
vails, however inconsistently, that the relief by nitrites, and
empirically this relief is obvious, depends upon an abatement
of these arterial pressures. In cases of broken compensation,
said Broadbent, perhaps a little too positively, angina pectoris
is unknown. Again, how is it, if the coronary arteries are
endowed with these vermicular activities, that they do not more
often put them in practice ? Why, if this be their way, are
not casual whiffs of angina a common experience ? Vasocon-
strictions, extensive and partial, are otherwise common enough ;
but if the coronaries were prone to participate in them the heart
would be at a double disadvantage ; with rising peripheral resist-
ance its reserve might be cut off : fortunately, as we know,
peripheral vaso-constriction ordinarily means coronary dilatation.
Yet even von Basch surmised that angina pectoris may be
caused by cramp of the coronary arteries ; Huchard perpetually
1 Mackenzie Jas., Heart, vol. ii., 1911.

358 ANGINA PECTOEIS pakt n

invoked it and its alleged consequence of " increased intra-
cardiac pressure " (!) ; and no less a man than Balfour dallied
with the notion. The explanation is so handy it cannot but be
true ! We are now assured, by Ortner for instance (loc. cit.), that
in the trembling balance of life, spasm may be as well or better
postulated of diseased than of normal arteries, a contention which
may have some grains of truth in it. He betakes himself to the
cramp hypothesis because " we see not rarely very severe
angina pectoris with coronary changes minimal or absent, and
their orifices clear " (italic mine) ; and he finds no proportion
between the degrees of angina and of coronary lesion. Yet
coronary it has to be, somehow ! That the life of the healthiest
of us should be at the mercy of a squall in so narrow a belt of
arterial irrigation, whether in the heart or in the bulb, is dis-
quieting enough, but what is this to a hypothesis ! The truth
is, spasm of the coronaries is a nosologist's conceit to explain
puzzles of his own making.

How far in sclerosed arteries the capacity for spasm may be
presumed to survive, or indeed how far in disease it may be
even in morbid excess, and, if so, how this may be mechanically
explicable, I have discussed elsewhere (Arteriosclerosis, p. 162) ;
suffice it, in respect of the coronaries, to say that in the
first instance it must be proved that in any conditions these
vessels are dominated by vasomotor governance.1 Hey mans
and Demoor,2 in their comprehensive research into the
innervation of the myocardium, Professor Brodie and Miss
Cullis,3 and other observers have, it is true, detected both
vaso-constrictor and vaso-dilator activities in these vessels ; but
Professor Schafer, in the course of a large experience with
adrenalin, concludes that they have very little contractile power ;
and, generally speaking, physiologists are of the opinion that
although such agents as adrenalin affect their muscular coat
directly, usually indeed to dilatation,4 yet it is but slightly, and
their tides are determined by the oxygen tension — and of
course by the blood pressure. Meyer is of opinion 5 that although

1 See Langley, Journ. of Physiol, vol. xxxii., 1905.

2 Heymans and Demoor, Arch, de biol., Gand and Leipzig, 1893-95, vol.
xiii. p. 619 (25 plates, etc.).

3 Brodie and Cullis, Journ. of Physiol, vol. xliii., 1911. 4See Vol. I. p. 230.
B Meyer, F., Berl. Bin. Wochenschr. vol. 1., 1913, p. 920.

sec. ii THE CORONARY ARTERIES 359

after injection of adrenalin the coronaries expand, under more
heart work and higher pressure, yet a dilating effect due to
the adrenalin is also apparent. It is not easy to see how Meyer
can discern this difference, and he seems to me to neglect the
increase of the nutritional and oxidising activity. LangendorfT
had proved already 1 that, when by adrenalin |an extensive vaso-
motor constriction is set up, these vessels expand to support
the heart in the increase of its work ; their feeble innervation
could not, and ought not, to withstand a systemic rise of
pressures, or whence would come the heart's needed increase
of energy ? Mr. Barcroft has demonstrated that coronary
flow, if modified at all, is not regulated by vasomotor govern-
ance ; that their diameter follows the amount of C02 given out
by the cardiac muscle, or the correlative metabolism. As he
illustrates by carefully constructed charts, we see that if the
heart be deprived of oxygen by fractions — e.g. 02 being as
1*0, 0*6 . . . 0-2, 0-1 per unit time, the curve of coronary
flow does not droop in parallel with the oxygen time, it is main-
tained a little longer ; and then falls towards it by a more rapid
gradient.2 Dr. Cow,3 employing Meyer's method, found, in
accordance with other observers, that although adrenalin con-
stricted the arteries of many areas, it did not constrict the
intravisceral branches of the coronary, pulmonary, and cerebral
arteries ; indeed the coronary and cerebral were dilated rather.
Moreover, pursuing the researches of Barcroft, and of Dixon, he
found that COL,, as correlative of cardiac metabolism, dilated
the coronary (as also the carotid, gastric, etc.) arteries. The
gas was bubbled through the Ringer's solution ; as the gas
was turned on and off the coronary arteries responded accord-
ingly. The effect was direct on their vascular coat, not on
nerve-endings. Dr. Argyll Campbell testifies to the same effect.4
Dr. Laidlaw 5 says the influence of the heart-beat on the coronary
flow is profound; but I should hardly say "profound," the pressure
and the myocardial oxidation are dominant. An increased rate

1 Langendorff, Zentralbl. f. Physiol, 1907, No. 7.

2 See also Morawitz u. Zahn, Zentralbl. f. Physiol, vol. xxvi.

3 Cow, Proc. Roy. Soc, Feb. 20, 1911 ; and Journ. Physiol, vol. xlii., 1911.
* Campbell, Argyll, Quart. Journ. of Exp. Physiol, vol. iv. Nos. 1 and 2.

See also Laidlaw, Journal of Physiology, vol. xl., 1910, p. 487.
5 Laidlaw, Biochem. Journ. vol. vi. No. 1.

360 ANGINA PECTOEIS part n

of beat causes a quicker coronary outflow without dilatation of
the coronary vessels (italics mine). As I have said, if the coronaries
took part in extensive vaso-constriction the heart would not
be left wholly free to liberate energy to meet the rise of arterial
pressures. These arteries have developed superficially in order
that they may be thus passive to the blood-flow ; were this free
play impeded by constrictions the coefficient— more heart work,
more blood, would be inconstant. Aschoff 1 infers that because
the coronaries are rich in muscle therefore they are the more
subject to nervous influences ; but this by no means necessarily
follows : the strong muscular tone may as well be to protect
these vessels against the dilating stresses of sudden increases of
demand. The prevalence of atheroma in the coronary arteries
suggests notwithstanding, that, under the frequent calls upon
output, these vessels do suffer under lateral stresses, against which
vigorous automatic tone tends to protect them. Huchard, in his
airy way, said that the coronaries, being near the heart, are there-
fore under the highest pressures. Not so ; although their mouths
are bell-shaped, yet the angle of their bifurcation is sharp, their
size is small for the work they do, and especially small for their
intricate peripheral bed. The velocity is relatively high, but the
friction is high also. Still, as Roy pointed out (Phil. Tr., 1892), an
increase of pressure in these vessels multiplies the cardiac energy
enormously. Coronary supply has however little effect, if any, on
the rate of the pulse. Let us hope then that our coronaries are
incapable of such perilous cantrips, and postpone consideration of
spasm of these vessels, whether in health or disease, whether in
real angina or sham, until we have proof. Whatever the motor
energy of these vessels, it is towards dilatation (sympathetic) ;
for constriction (autonomic) it is very slight.

It is natural to assume that if the coronary arteries are diseased
the myocardium must suffer. Complete obliteration of the
coronary trunks during life certainly often happens, yet, strange
as it may seem, if a very chronic process, as it usually is, the heart
may in spite of it stick to work long enough. Sir William Osier
has said:2 "A man may get on very comfortably with . . . practi-

1 Aschoff in a discussion reported in Deutsche med. Wochenschr., Feb. 20,
1913. Morawitz u. Zahn in the same discussion laid emphasis chiefly on the
blood pressures.

2 Osier, Sir W., " Lumleian Lectures," Lancet, March 26, 1910.

sec. ii THE CORONARY ARTERIES 361

cally a fourth of the whole (coronary) system " (if, that is, the
reduction be very gradually established). Steven 1 also observed :
" The amount of deprivation of nourishment which can be borne
by the heart, if it be slowly induced, is wonderful." Dr. West
{Path. Trans. 1884) has said the same thing; and W. H. Dickenson
testified (also in Path. Trans.) that " closure of the coronary
arteries does not prevent even considerable hypertrophy of the
heart." I have discussed a part of this problem already in the
chapter on Cardiosclerosis (p. 21), and pointed out that " a man
may get on " with the whole system occluded, so far at any
rate as the orifices and main trunks are concerned.

The effect of coronary disease upon the myocardium was
discussed by Morgagni, in a well-known chapter of his great work,
and by Cruveilhier.2 Virchow and his school returned to the
subject, and Huber 3 showed, as the French school has shown,
that the resulting fibroid changes, unless periarteritic, were not
inflammatory, but " dystrophic sclerosis " (p. 23). Cohnheim 4
said that callus and fibrosis (p. 21) (" sometimes a host of callous
bodies scattered through both ventricles ") do not betray them-
selves by any symptom whatever ; and that the same was
true of more diffused " myocardial indurations." It seems
that, so long as there is no heart block, contractility is
but little affected. Although, as I have said, decay of the
myocardium is not a uniform nor a universal result of
coronary obstruction, every physician must of course regard
the state of these vessels as important in so far as the
nutrition of the cardiac muscle may suffer in consequence. Yet
Frankel and many others admit, what Kanthack and I
demonstrated, the frequent immunity of the cardiac muscle
from degeneration, even in obliteration of the coronaries,5 or
at any rate of their orifices — as Frankel says, the muscle is
often normal (" intakt befunden ") — and this is explained, prob-
ably with truth, by supposing some considerable tracts of these
channels to remain, and to receive blood from other sources.

1 Steven, L., Lancet, 1897.

2 Cruveilhier, Traite d'anat. pathologique.

3 Huber, Virchow 's Archiv, Bd. lxxxix.

4 Cohnheim, Syd. Soc, ed. 1889.

6 I learnt afterwards that we were not the first to arrive by this way at the
same conclusion.

362 ANGINA PECTOKIS pakt ii

Kanthack and I concluded that, other things equal, the factor
of safety is the rate of occlusion ; if very slow an alternative
nutrition may be established even when the orifices of the
coronaries are so overgrown that they cannot be detected.1 Dr.
A. Morison 2 has also testified to this remarkable independence
of the myocardium of the coronary main trunks or mouths ; in
a carefully observed case, in which the coronary arteries were
almost completely blocked, he found the muscular tissue of the
heart if in part fibroid yet " on the whole well preserved."
He makes the general statement that a sound myocardium
may concur with extreme coronary occlusion ; and on the other
hand that much degeneration of the cardiac muscle may go
forward while the coronary arteries are open.

Cabot 3 rightly emphasises the importance of comparing
clinical and pathological reports independently of each other ; and
in respect of angina and coronary disease he compared such reports
independently. He concluded that in " patients with well-
marked angina pectoris and clear evidence of a general arterio-
sclerosis," in whom accordingly coronary obliteration or narrowing
and consequent " fibrous myocarditis " were confidently assumed,
he had often been convinced on the plain testimony of post-
mortem examination that the pathological part of the diagnosis
had been wrong. More refined methods of injection have
proved that the coronaries are not " end-arteries " ; their smaller
branches anastomose freely everywhere in the structures to which
they are distributed ; not only so, but cross connections between
arterial and venous branches have been demonstrated. Dr.
West, Dr. Aldren Wright, Orth, and others (see Spalteholz, p.
23) verified Haller's 4 observation of the freedom of coronary
anastomosis ; and injections of red lead and gelatine made
these communications plain in the X-ray pictures shown at the
discussion at the Congress for Inner Medicine held at Wies-
baden in April 1907.5 They were verified also by Janin and
Merkel's beautiful stereoscopic skiagrams showing anastomoses
between branches of no inconsiderable size. Some of these

1 Vide chapter on Cardiosclerosis, p. 23 of this volume.

2 Morison, A., " Treatment," Oct. 28, 1897.

3 Cabot, Massach. Gen. Hosp., Oct. 1911.

4 Haller, Elem. Phys. Corp. Hum., Lausanne, ed. 1757, p. 137.

5 And again at the International Congress of 1913.

sec. ii THE CORONARY ARTERIES 363

indeed, as Professor Spalteholz has shown to me, are visible to
the naked eye. Moreover, Hirsch described some skilful experi-
ments upon dogs and monkeys by which he proved that ligation
of large coronary branches, e.g. the descending branch of the left
coronary, at various levels, if they impaired, did not seem to
abolish the functional capacity of the heart in these animals,
experiments which seem to contradict clinical experience in man ;
but in man muscle and vessel, and the whole complex of function,
may be in more delicate balance ; and animals under experiment
are not exciting themselves. I have quoted the recent obser-
vation of Jores that in many cases of atheroma of the coronary
arteries, if not in all, their intramuscular twigs are not affected ;
a statement largely true of the vessels within some other
viscera also, such as the liver.

Marchiafava 1 has divided coronary disease and its effects into
five varieties, namely : (1) Simple sclerosis without grave
alteration of the myocardium ; (2) Sclerosis with acute or
chronic lesions of the myocardium ; (3) Stenosis of orifices,
without vascular sclerosis or myocardial changes ; (4) Old
obliteration of one large coronary branch without myocardial
disease ; (5) Obliteration of one large coronary branch with
infarct or myomalacia, and with or without rupture of the
heart. He discusses the cardiac consequences which I have
indicated summarily ; my purpose at present is only to show
that as coronary disease, even closure of both orifices, if
initiated so slowly that alternative channels, or alternative
sources for the old channels, can take up the supply, need not,
and often does not, bring general myocardial degeneration in its
train. Dr. Cowan,2 in a summary of such cases, points out that
if one coronary be blocked, the other may hypertrophy to supply
its place ; an observation, by the way, which affords additional
evidence of their confluence. But the effects of block seem better
marked in the left than in the right coronary. Pratt suggested
that the heart was nourished by the veins of Thebesius, but they
open on the right ventricle where the blood is blue. Redwitz,
of the Pathological Institute of Munich,3 likewise compared

1 Marchiafava, Eiv. critica di clinica med., April 13, 1904.

2 Cowan, John, Trans. Glasgow Path, and Clin. Soc, 1902.

3 Redwitz, von, " Erkr. d. Koronararterien u. chron. Aortitis," Virchow's
Arch. f. path. Anat., 1909, Bd. cxcxvii.

VOL. II 2 A

364 ANGINA PECTOKIS part ii

cases in which the coronary arteries were obliterated with
those in which they were permeable, or even normal, but
blocked at their orifices by aortic disease ; in this case they
contained blood nevertheless, and the myocardium kept fairly
good. He thinks the callous lumps are not direct conse-
quences of coronary atheroma, but are a consequence with
it of some common cause, as yet unrecognised (p. 21). Yet,
with the looseness with which our clinical labels are distributed,
the author proceeds to enumerate among other consequences
of coronary disease, " cardiac asthma, or angina pectoris from
pulmonary oedema " ! It would be difficult to get more blunders
into eight words. Broadbent 1 admitted that angina might occur
before coronary disease had brought about any recognisable
changes, before even microscopical blur of the muscular striae. He
persisted nevertheless, on slender grounds as it seems to me, that
in angina " the condition of the heart walls must be the dominant
factor," and elsewhere he speaks of it as an indispensable factor :
now the dominant factor in the mortality of angina it is. Even
Nothnagel admitted latterly that with the angina itself the myo-
cardium has little to do. In all cases then, if used as facts for
argument, the myocardial condition must be precisely defined.

The following cases, out of forty collected by Dr. Aldren
Wright,2 may serve to illustrate the comparative independence
of coronary disease and apparent myocardial degeneration. Of
twenty of these, 300 specimens were cut and stained.

I. Male, set. 56. Angina pectoris. Left coronary closed ; right
artery pinhole. Cardiac muscle of good colour and firm. Micr. no
fatty or other change.

II. Old man, died in attack of angina. Eight coronary artery
admits bristle ; left coronary artery, " much narrowed." Micr.
" Slight fatty degeneration," which " needed some search " to de-
tect it.

III. Male, set. 42. (Angina pectoris, probably syphilitic.) Died
suddenly. Left coronary artery and right coronary artery barely
admitted probe. " Myocardium quite healthy."

In three other of Dr. Wright's cases, in which with angina the
coronary orifices were occluded, or nearly so, of the myocardium

1 Broadbent, W. H., Lancet, May 27, 1905.

2 Wright, Aldren, M.D. thesis (Cambridge), 1902. "Occlusion of the
Coronary Arteries and its Effect upon the Heart."

sec. ii THE COBONAEY AETEEIES 365

" Hypertrophied and slightly fatty," " Slightly fatty," and
" Appeared normal but for a little fibrosis here and there "
were reported respectively. Of course in many of his instances
of coronary occlusion the myocardium was found decayed, but
in no correspondence with a history of anginous symptoms.
In some of the more normal hearts he noted that the fine vascu-
lar network was particularly numerous and open. In the large
majority of his cases of coronary disease Wright, like West,1
found no history of angina.

I will add, by way of broadening my testimony, a few more
cases by other observers.

IV. Notes of a case sent to me by the kindness of Dr. Bennion
of St. Mary Cray. Male, set. 43. Angina pectoris case entered during
his time at St. Bartholomew's. At death, heart 13 oz. ; left coronary
artery " much narrowed " ; right coronary artery, " a slit." Micr.
" Cardiac muscle normal." " Aorta atheromatous and calcareous ;
large atheromatous ulcers in places." Dr. Bennion states : " The
autopsy was careful, suspicious, and complete, yet the musculature
of the heart was proved not to have suffered."

V. Male, set. 45. Angina for three years, died in attack.2 Heart
large and heavy ; left coronary artery closed by atheroma, vessel
collapsed. Eight coronary artery much narrowed at orifice but
pervious, and otherwise retaining its full dimensions. Coats of both
free from atheroma. The atheroma had encroached from disease
of the root of the aorta, where it formed a soft cushion under the
lining membrane. Myocardium " slightly fatty, but not more than
most hearts are found to be."

VI. Male, aet. 42. Soft cushion-like atheroma at the root of the
aorta, under the lining membrane, encroaching on the mouths of the
coronary artery, so that neither would admit the probe without
some pressure. Heart 13| oz., colour and texture natural. Micr.
" trifling diffuse fatty dotting, but not such as to indicate any mor-
bid change."

VII. Practically the same report. Myocardium normal. Coro-
nary arteries : right coronary closed ; left narrowed to about size
of probe. [In referring to these three records, I was much interested
to see that the authors pointed out that coronary disease was less
characteristic of angina than atheroma of the beginning of the aorta,

1 West, S., Path. Trans., 1884.

2 Cases V.- VII. are taken from W. H. Dickenson and Dudfield, Path. Trans.
vol. xvii., 1865, "Angina with Coronary Disease but without Cardiac
Degeneration."

366 ANGINA PECTOEIS part ii

and about the valve ; and that they disagreed with the cardiac
spasm hypothesis. Cases V. and VI. were probably syphilitic. —
C. A.]

VIII. A like case (probably syphilitic) recorded by Balfour (loc.
cit. p. 324).

IX. A like case, described by Bartholmes, in an Erlangen thesis
of 1901,1 as follows: A powerful man, set. 35, ill six months. In
heavy labour as an ironfounder. Moderate in alcohol and tobacco.
" No syphilis." Angina pectoris of great severity, culminating in
status anginosus and death. " Aortitis of ascending aorta."
Coronary arteries extremely narrow throughout, so much so that in
their uniform narrowness the author considered them to be unique.
Of the cardiac muscle minute histological examination was made,
with negative result. " All the fibres were normal " — to all tests —
and interstitially the only intrusion of fat was in very slight degree
about the apex.

X. Male, set. 24, "died of angina pectoris with a practically healthy
heart." A ring of thickening occupied the whole circumference of
the aorta at and beyond the sinuses of Valsalva. The intima was
swollen to twice or thrice its normal thickness, with a clear trans-
lucent deposit. (Obviously syphilitic. — C. A.) The openings of the
coronary arteries in the midst of this area were so contracted that
a probe could scarcely enter. The cardiac muscle, however, was of
a good colour and consistence and microscopically its structure was
normal (italics mine).

XI.-XII. One of Porter's cases.2 Male, set. 56. Angina Pectoris.
Left coronary orifice occluded, right a pin-hole. Myocardium good
colour and firm. No fatty or other degeneration. — Another case
is cited of an old man who died in an attack. Eight c.a. admitted
a bristle ; the left was narrow. Only on close search was a rather
fatty state discerned. (See also Mackenzie's case, p. 434.)

Dr. Aldren Wright found that aortic disease had encroached
upon the coronary orifices in 28 out of 40 cases.

Dr. Poynton 3 mentions a case of syphiloma of the heart,
attended with nearly complete obstruction of the coronary
arteries, in which the myocardium was quite normal. Dr.
Mitchell Bruce, in a review of this aspect of the argument,
says : 4 " My observations confirm Sir Clifford Allbutt's state-
ment, that in syphilis of the aorta the heart below the aortic

1 Extract in Virch. Jahresb., 1902.

2 Porter, Amer. Journ. Exp. Med., 1898.

3 Poynton, British Medical Journal, March 1900, p. 635.

* Mitchell Bruce, " Lumleian Lectures," Lancet, July 8, 1911.

sec. ii THE COEONAEY AETEEIES 367

valve, save for some endocardial opacities, is healthy." Dr.
Morison says decisively that open coronary arteries occur with
myocardial fibrosis, and closed coronary arteries occur without it.
Frankel has rather reluctantly testified to the same effect, and
clings to a supervenient spasm of these vessels. But, as Neusser1
perceived, are we to suppose that with increasing rigidity these
vessels become more and more ready to contract ? However,
we must admit that the muscle, normal as in structure it may
appear, must be more or less short of food, and so far em-
barrassed in function. The fair-seeming muscle, as in Dr.
Anderson's elderly cat (p. 475), is doubtless impaired.

Suprasigmoid aortitis is so prone to involve the mouths of
these arteries that crucial cases of angina, with coronary orifices
intact, are the less easy to discover. However, we see there is
much evidence that coronary stenosis is not necessarily followed
by visible myocardial degeneration, and in alleging coronary
obstruction as the cause of angina we must strictly enquire
whether these orifices were absolutely blocked or narrowed only.2
In many case reports of angina we observe that a partial coronary
occlusion satisfies the reporter, and not unreasonably ; but this
admission cuts both ways. If through minuter orifices the myo-
cardial nutrition can still under hydrostatic pressure be kept up,
why the angina ? Because the cardiac reserve is less ? Then
what of the multitude of cases of obvious myocardial degenera-
tion without angina ?

When witnesses so trustworthy admit that angina may
occur before coronary disease has brought about any visible
changes in the myocardium, when not even a microscopic
confusion of the striae can be detected, and yet in the same
breath protest that " in angina the state of the heart walls must
be the dominant factor," do not we overhear an echo of Vesalius's
final submission to the dogma of desudation of the blood through
the pores of the ventricular septum ? And when, on the other
hand, in the fourth edition of Eulenburg Frankel concedes that
in some cases of angina the coronary arteries are proved after
death to have been sound — durchaus intakt — and yet clings to

1 Neusser, E., Symptomatologie u. Diagn., H. 2, 'Angina P.', Wien, 1904.

2 Atheroma, as contrasted with occlusion by encroaching aortic disease,
in the coronary arteries most frequently begins in the anterior vessel, about
one inch from its orifice.

368 ANGINA PECTOEIS part n

the coronary hypothesis, are we not listening again, not to the
man who " treasures his exceptions," but to one whose judg-
ment is subjugated to an orthodox dogma ?

Let us now enquire if a block of one of the coronary arteries,
or a rupture of one of them, with bleeding into the myocardium,
causes pain. It is true that a sudden thrombosis is often
attended by intense pain so like angina that we cannot refuse
it the name. It is fierce, and in site substernal, though gener-
ally more continuous. To this event we shall return. But that
mere reduction of the blood-supply does or can produce severe
pain, a maxim attributed to Allan Burns,1 and more or less
favoured by Charcot 2 and by Potain,3 seems to be taken for
granted ; though our common experience of coronary atheroma
and of the various anaemias indicates much to the contrary. If
for " can " we were to read may, this opinion might pass, but
in a state so attenuated as not to be worth having. That a
gradual privation of direct arterial blood, by silting up of the
coronary or any other arteries, or stopping their mouths, is a
painless process, is displayed to us every day. Yet physicians
seem satisfied with the explanation, as were two eminent foreign
physicians with whom recently I was in conversation. I re-
minded them that, as I have twice observed, haemorrhage into
the pericardium from a ruptured coronary was quite painless.
It is the return of blood into anaemiated parts which may cause
intense pain, not the anaemia. Why in some cases, even of
sudden coronary thrombosis, there is pain, and not in others, is
a problem which I shall attack presently (p. 450) ; rate and
quantity seem to be the determinants. In some of these
cases, as Sternberg 4 in a very interesting paper has shown
{vide p. 461), the pain is associated with a patch of pericarditis,
apparently produced in the same or a similar way as the patch
of pleurisy over a pulmonary embolism. ' (a

Josue, in discussing cardiac aneurysm from the point
of view of my hypothesis of angina, at which he had in-

1 Burns, Allan, 06s. on Dis. of the Heart. Ed. 1809 (not in the libraries of
Camb. Univ. or of Roy. soc. Med.). Kindly lent to me by Sir W. Osier.

2 Charcot, Gaz. mid,, de Paris, 1859, p. 283.

3 Potain, Diet, des sci. mid., Paris, 1866, ser. i. tome iv. p. 347.

4 Sternberg, " Pericarditis epistenocardiaca," Wiener med. Wochenschr., 1910,
No. 1.

sec. ii THE CORONARY ARTERIES 369

dependency arrived and has recently expressed almost in my
words, says that in cardiac aneurysm pain is far from obligatory,
and from most cases has been absent. With Paillard 1 he closely
examined a certain case, in which the right coronary branch
and all the collateral branches to the aneurysmal part had been
blocked ; but the patient had never suffered from any angini-
form symptoms ; and his systolic pressure was 180. Except
about the aneurysmal area, where of course it had undergone the
usual necrotic changes, the myocardium was normal, and indeed
hypertrophied, because of a pericardial synechia, and also, as it
was supposed, of adrenal hypertrophy (see Vol. I. p. 225). There
was some atheroma of the aorta here and there, though this
vessel generally was fairly supple. The kidneys were normal.

Von Romberg, with some confidence, but without producing
much evidence beyond treacherous analogies, repeats the sugges-
tion of Virchow, that the cause of angina may lie in embolisms of
the coronary arteries, or of their branches, and compares the pain
with that of sudden embolism of an artery of a limb. Death in
senile angina may occasionally be due to a block in a coronary
artery or branch, but it is difficult to suppose that for every
attack there is a new embolus ; and in embolism of a limb two
pains are to be observed, the pain of the striking plug, due to
lateral tension above it, which may be very sudden and severe,
and the later continuous pain of acute obliterative arteritis ; a
disease not very comparable in any direction with the symptoms
or the histology of angina. Moreover, what we know about
thrombosis or embolism of the cardiac arteries, whether experi-
mental or pathological, is not consistent with the sum of our
experience of the conditions of angina, for of these blocks an
immediate and considerable fall of blood pressure is, and must
be, a character ; yet during attacks of angina pressures are
not infrequently high, and a fall of pressure, even by heart
failure, usually abates it. Kauffmann, in the sixth edition of his
Lehrbuch (i. 37), after commenting on angina as a symptom of
coronary embolism, quotes a case in a man set. 35. The
symptoms were sudden agonising dyspnea, fall of blood
pressure, and pulmonary oedema. Death in seven hours.
There was a fresh plug in the left coronary artery ; no other

1 Bull, et mem. de la Soc. Med. des Hdpitaux de Paris, 29 Janvier 1909.

370 ANGINA PECTOEIS part n

cardiac disease. I shall describe angina as a result of such an
accident, but this case, so far as the history goes, was not one
of angina ; there was no pain, and dyspnea and asystole are
not angina. As regards embolism in particular, this in the
coronary vessels is probably a very rare event. Experimental
embolism, even the finest, has been shown over and over again,
recently again by Wassiliewski 1 with lycopodium seed, to cause a
transient fall of pressure and of cardiac energy, a dilatation of the
cavities, a diminution of the systolic wave, and a retardation
of the beats ; with a larger embolus these symptoms are not
transient, but advance with the structural demolition. Such,
whether by block or spasm, must be the instant effect of a sudden
check to the coronary circulation. But is this what we see
in angina pectoris ? Surely not !

Von Basch's cases, if indeed all of them were angina, or an-
ginous, are rather vague. As to the nature of some of them he
himself was in doubt ; others, if angina at all, were complicated
with heart disease.

Many years ago von Leyden also,2 after a careful survey of his
materials, reiterated that angina pectoris was not only, as we
all admit, often absent in disease of the coronaries, and also in
fibrous degeneration of the cardiac muscle, but absent likewise
in some cases of acute thrombosis, or infarct, of either of them,
and in various combinations of such conditions.

Ligation has contributed its part to our knowledge of this
subject. On tying a fairly large branch of a coronary artery, the
systemic pressure falls at once, and the output also ; then the
pressure rises on the venous side ; then beats drop out, and so on.
Erichsen 3 clearly demonstrated this series of events in dogs and
rabbits ; and twenty years later Panum, in a better-known paper,4
added little to Erichsen's demonstration. VonBasch and his pupils
tied coronary arteries and twigs of them, and found likewise that
the arterial pressure fell, the pulse became irregular, and pressure
rose in the left auricle and lungs with oedema and death. To tie
only one large branch sufficed to cause arrhythmia and death.

1 Wassiliewski, Zeitschr. /. ezp. Path. u. Ther. Bd. ix. H. 1.

2 V. Leyden, " Sklerose d. Kranzarterien," Zeitschr. f. Jclin. Med., 1884.

3 Erichsen, London Med. Gaz., 1842.
* Panum, Virchow's Arch. Bd. xxiii.

sec. ii THE CORONARY ARTEEIES 371

Porter's 1 researches on these lines are well known, and his results
supported those of von Basch. He found that the time of the
heart's arrest was, caeteris paribus, proportional to the size of
the branch occluded. If either main vessel was occluded both
ventricles stopped together. These experiments show of course
the effects of sudden, not of gradual, occlusion. The very careful
series of experiments on dogs and monkeys by Hirsch and
Spalteholz 2 showed that by careful ligation of the descending
branch of the left coronary, the initial arrhythmia (at the
moment of ligation) might be transient, and the animals could
be kept alive, though with evidence of greatly reduced cardiac
potential, for three or four weeks, till killed for autopsy. Throm-
boses and callus were then found, especially towards the apex.
To the careful injections by which they verified the fact that
coronary anastomoses were free and abundant, being very evident
in the papillary muscles, I have already referred. Dr. Parkes
Weber found that when one coronary had been closed at a certain
spot for a sufficient time, the channel beyond the block being
patent, an injection into it soon flowed out at the other vessel.
He showed also, as Professor Spalteholz had kindly demon-
strated to me, that the interventricular branch of the left
vessel on reaching the apex could be seen to anastomose with
a twig of the right vessel. In conversation with Professor
Spalteholz on the lymph channels he told me that the blood
and lymph channels in the heart are so abundant and inosculate
so freely, that during life the myocardium may be compared
with a sponge. On such facts Sir William Osier may well
comment : " These experiments, proving arrhythmia and
arrest in diastole, do not throw much light upon the etiology of
angina pectoris." He adds that even in cases of sudden death
due to blocking of one of the coronaries, or of a large branch such
as the anterior, the seizure is usually painless ; the converse of
an ordinary attack of angina in which pain is eminent and
blood pressure, usually at any rate, maintained. Dr. Rolleston
has published evidence to the same effect.3 Huchard admitted

1 Porter, Amer. Journ. Exp. Med., 1898.

2 Hirsch u. Spalteholz, Deutsche med. Wochenschr., 1907, No. 20; with
beautiful plates. See, to same effect, Porter and others.

3 Rolleston, H. D., Brit. Med. Journ., Nov. 1896.

372 ANGINA PECTORIS part n

that angina is not characteristic of, and rarely occurs in,
cardiac aneurysm of coronary origin.1 However, as we shall
see in Sternberg's cases, angina may arise in this condition if
pericarditis intervene ; or even without it (p. 462). Huchard
explains the absence of angina by the deadness of the portion
of myocardium concerned ; but a period, however brief, of
acute ischaemia, with secondary congestion, must precede the
necrosis.

In respect of this part of the argument : if it be contended
that while in chronic cases coronary ischsemia may be too slow
to set up angina pectoris, but that a sudden blanching might
have a different and more intense effect from a slow ansemia
of the myocardium, let us then consider the effects of a sudden
ligation of a large coronary branch in an animal. We find
that in 60 to 90 seconds diastole is extended, and pressures are
falling ; in 30 to 60 more seconds the carotid pressure runs
down by 50 per cent, the heart loses its rhythm, and in a
quarter of an hour ceases to beat. And so in man also a
sudden plugging of a large coronary branch presents a like
series of events. But are these symptoms, with the dyspnea
which accompanies them, characteristic of angina pectoris ?
Certainly not. During an ordinary attack of angina the
aortic pressure rarely falls ; the heart does not charac-
teristically lose its rhythm ; it does not dilate ; there is no
dyspnea. Nay rather, have we not seen on the contrary that
vasodilatation, or mitral regurgitation, factors of falling aortic
tension, so far from calling forth or aggravating these alleged
anginal effects of a failing coronary supply, generally counteract
them. If by others it be urged that, granting such more or less
rapid occlusions as are possible in experiment may produce
symptoms unlike to, or even somewhat exclusive of, the pheno-
mena of angina, yet we cannot be sure that a more gradual experi-
mental occlusion might not produce different phenomena, it may
still be demurred, not only that the symptoms of experimental
occlusion are unlike angina pectoris, but that they dissemble any
such kinship with remarkable uniformity. Even in a gradual
occlusion we find on the whole a gradual reduction of blood

1 E.g. see carefully analysed cases by Josue, Bull, et mem. de la Soc. Med.
des H6p. de Paris ; Seance, 29 Janvier 1909.

sec. ii THE COEONAEY AETEEIES 373

pressures, cardiac dilatation, and an ingravescent tendency to
syncope ; but none of these acute and violent epiphenomena —
variations surely not of quantity only but of kind.

Notwithstanding, I have admitted that in some of these cases of
coronary thrombosis an intense anginiform pain may set in ; these
cases I am to consider later (p. 450) ; but here I must dwell a little
longer upon the preliminary postulate — that in angina pectoris
the coronary arteries are always diseased, or, at any rate, per-
tinently affected ; a postulate which Merklen audaciously calls
" Huchard's law." In weighing our data in this matter,
we He under the difficulty that defects of these vessels are
conspicuous in the mortal cases, while in those which end in
recovery— and they are not a few — there is no necropsy. Still, so
far as I am aware, there is not a case of angina pectoris on record,
on responsible authority, in which disease of the coronaries was
the sole lesion ; none, that is, in which, for instance, the state of
the suprasigmoid aorta also had been histologically examined,
within and without, and declared normal. Barie 1 admits that
cases of angina without coronary disease are not very rare. Yet
Dieulafoy, after recognising angina as arising from acute aortitis,
in his section on this disease, when, in his chapter on Angina
Pectoris he finds himself under the spell of the coronary conven-
tion, cannot but drop into the old chant — coronary disease,
ischaemia of the heart, angina pectoris, death. Even Merklen
(loc. cit.) had to admit that in angina the coronary arteries are
not always diseased, when, losing his customary bearings, he
strayed into vague conjectures.

Statistics taken upon records in the gross, on account of the
imperfection of the data and the laxity of terminology, are so fal-
lacious that we can place no great reliance upon them. I have
made no such collection, and trusted no such inferences. Still,
the computations of others need not be ignored ; they have at
least an auxiliary value. Dr. Graham Steell 2 concludes : " The
disease (angina) may be met with apart from any lesion of the
coronaries." Osier (Lumleian Lects. loc. cit.) in 17 cases — cases
probably well verified — reported coronary disease in 13 only. Dr.
Verdon, in a private letter, very kindly referred me to longer

1 Maladies du cceur, 1912, p. 960.
2 Steell, G., Index of Treatment, 6th ed., 1911, p. 67.

374 ANGINA PECTOEIS part n

series ; 1 on a summary of 283 cases collected by himself, he
found that of fatal cases of angina the coronary arteries were
healthy in 43 per cent. Tacchi in 70 cases found coronary
disease in 38 only ; Sir John Forbes in only 16 of 45 ; Lusani
in 21 of 36. Laennec's experience was curiously negative. " I
have opened," he says,2 " several (plusieurs) subjects of . . .
angina pectoris, but in none have I found (chez aucun je n'ai
trouve) the coronary arteries ossified." (The word " ossifies "
in the writers of the period included atheroma.) When we
consider that angina pectoris is in large part a disease of advanced
life, and of subjects of cardio-arterial disease, this low proportion
does not remove our doubts of the validity of calculations on
reports taken in the gross. Morgan,3 in surveying the literature
of angina, says that whereas coronary disease is found in many
cases, yet " true " angina may occur in patients who are entirely
free from disease of the heart. Such cases are more or less
reluctantly admitted, even by orthodox champions, to be
authentic.

Other cases are mentioned incidentally in this essay ; e.g.
Heberden's (Comm. 296-7) case of sudden death in angina,
of which he reports : "A very skilful anatomist could discover
no fault in the heart, in the valves, in the arteries or neighbouring
veins, excepting some rudiments of ossification in the aorta."
Desportes likewise described a case of rheumatic aortitis and
angina pectoris, in a man aged 25, in which the coronary
arteries and their orifices were perfectly normal. By way then
of concrete illustration only, I will cite here a few more examples
of angina pectoris (mortal) without coronary disease.

Case I. — Baccelli's Clinic:4 male, set. 50; active and healthy, but
a drunkard. Pulse 80, rather tense (no pressure record). No heart
nor anginal symptoms till sudden attack of typical character, very
severe. Pulse 100-120, tense (" teso "). Morphia injected, but the
operation scarcely finished when the patient turned up his eyes and
drew some deep breaths ; the pulse failed, and the heart ceased to

1 Verdon, W., Brit. Med. Journ., March 18, 1911. See also Whittaker,
Twentieth Century Pract. Med. vol. iv. pp. 439-441.

2 Laennec, Traite d 'auscultation mid., 1831, vol. iii. p. 351.

3 Morgan, Journ. of Amer. Med. Assoc, July 1897.

4 Baccelli, Rep. Oalli. ; Gaz. d. osped., Feb. 2, 1908.

sec. ii THE COKONAKY AETEEIES 375

beat ; another gasp and life passed. P.M. heart " completely-
normal — valves, etc. Coronaries elastic and pervious (elastici,
pervie)." No embolism. " Other viscera normal." (No mention
of the aorta, nor note as to syphilis.)

Case II. (Merklen.1) — Male, set. 22. First seen in 1876 for aortic
disease (very big ventricle). Potain's diagnosis was syphilis. (Note
the early age. — C. A.) After a quiescent period, seen again at set. 33 :
pleuritic and pericardial symptoms had appeared (syphilis about
mediastinum?). "Plusieurs crises angineuses" and death. P.M.
Aortic valvular disease, as above ; and also a very limited fresh
lesion of the aorta forming a zone above the valve, and stopping close
to it. There was only one coronary artery, but this was normal
throughout : many sections of its course were made.

Case III. (Jecce.2) — Male, set. 30: in hospital for angina pectoris;
usual symptoms ; died in an attack. Aortic murmur, direct and
regurgitant. Syphilis ; infection nine years before. (Never
rheumatism.) Aortic cusps thickened ; two adherent, causing
stenosis. Coronary arteries both healthy. Aorta " atheromatous."
(For atheroma read syphilitic aortitis. — C. A.)

Case IV. — One of Dr. Lindsay Stevens' cases recently published
in the Glasgow Hospital Reports (no date on my offprint). Male,
set. 44 ; no doubt a true case of angina (many of the cases in his
interesting lists could not properly be so called, and others were
complicated with cardiac symptoms, such as dyspnea, etc.). After
death there was " atheroma " of the arch of the aorta [probably
at set. 44 an infectious aortitis ?], but the coronary arteries were
healthy. The dilated and hypertrophied cardiac muscle had under-
gone fibroid degeneration.

Cases V., VI. — Our lamented colleague Professor Dieulafoy, in the
fifteenth edition of his text-book, in describing multiple aneurysm of
the aorta in two fatal cases of angina pectoris, concludes : " They
succumbed, although there was no coronaritis ; a proof that
obliteration of the coronaries is by no means the sole cause of angina
pectoris " (author's italics).

Case VII. — Dr. Mackenzie has very carefully described a severe
case.3 Male, set. 35, in which however after death " wonderfully
little change was found in these vessels." The right coronary, if
somewhat small, was " apparently normal " ; the left, " patent
and large " — " perhaps slightly thickened, but not markedly so."
Aortic regurgitation and enormous heart. " Aorta somewhat
thickened by patches of commencing ' atheroma ' " (syphilitic
aortitis ?). There was some fibroid deterioration of the myocardium.

1 Merklen, Troubles fonctionnelles du cozur, 1908, p. 162.
2 Jecce, La Rif. med., April 2, 1897.
3 Mackenzie, Jas., Heart, vol. ii., 1911.

376 ANGINA PECTOEIS paet n

Case VIII. — In the chapter on Aortitis (p. 158), and again in
this essay (p. 275), I have quoted Dr. Poynton's case of angina in
rheumatic fever, diagnosed by Cheadle as " true angina " ; in this
case the coronaries, including their finest ramifications, were
healthy.1 "Acute aortitis only was found to account for it "
(italics mine). (See also pp. 435 and 447.)

Case IX. — Dr. Poynton quotes another case to the same effect
(see p. 275), and comments that " although one would naturally
guess, when sudden death with or without angina had occurred,
that the lesion was so distributed as to have closed the coronary
orifices, yet that in the two cases here recorded I do not think that
such an explanation is tenable."

Cases X., XI. — Dr. Raw 2 describes two cases of angina with
disease of the aorta, but " the coronary arteries in both these were
patent, and there was very little evidence of (general) arterial de-
generation."

Case XII. — Reported by Andrew Clark 3 (from the London
Hospital). Angina pectoris, chest and left arm; aggravated by effort.
Blood pressure high ; radials thick. P.M. aortic valve competent,
but " somewhat " diseased. Hypertrophied left ventricle. First part
of aorta much diseased, but beyond arch healthy. " No disease of
the coronary arteries, and nothing found wrong in the heart to account
for the symptoms during life " (italics mine). " Syphilitic gummata "
found in the liver. No other sign of syphilis. (No doubt a
syphilitic aorta. — C. A.)

Case XIII. (related by Ortner.4) — The history was of attacks of
angina in which pericarditis (vide p. 454) had also been diagnosed. But
at the necropsy was found not the serofibrinous kind of pericarditis
expected, but an advanced sclerotic process involving the ascending
aorta and the arch, with many " atheromatous ulcers, one of which
had penetrated through the whole thickness of the wall " (italics mine).
There was thus a " periaortitis at the root of the aorta, which had
extended to the neighbouring pericardium." Now the only coronary
affection was advanced change (hochgradige Yeranderung) about
the orifice (Ausgang) of the left vessel only (to which of course Ortner
attributes the angina). In no other wise were these arteries affected ;
nor was there any consecutive softening (keine Myomalakie) of the
myocardium. No great harm then was done to the heart by the
partial blocking of one of the orifices. The case was probably
one of syphilis.5

1 Poynton, Lancet, May 20, 1899. 2 Raw, N., Lancet, Aug. 21, 1909.

3 Clark, A., Lancet, Aug. 31, 1878. 4 Loc. cit. p. 13.

5 See also for additional instances, Morel-Lavallee, " L'Angor pectoris non-
coronarienne," Rev. de med., 10 Oct., 1899.

sec. ii THE COEONAEY AETEEIES 377

Case XIV. — A similar case, most carefully described by Eist and
Krantz.1 Did this case stand alone, it would be conclusive against
the obligate association of angina with coronary disease (see p. 195).

Case XV. — Dr. Hirschf elder most kindly sent me the second edition
of his important work on " Heart Diseases," but after these pages
were in print. I had just time however to quote from him a case
at the Johns Hopkins Hospital, five years of suffering from angina
pectoris. An aortic cusp was ruptured ; the coronary arteries were
soft, and their walls everywhere normal. The aorta is not mentioned.

To proceed more succinctly : Hoffmann of Dusseldorf 2 says
he has " often observed, . . . after years of the severest attacks
of angina pectoris," that the necropsy did not show the slightest
change (nicht die geringsten Veranderungen) in the coronary
arteries. Of five of Latham's necropsies of angina, three pre-
sented coronary atheroma, two " fatty degeneration of the
myocardium " only ; of these two Arnold's was one. (Arnold's
heart possessed but one coronary artery, which was not diseased.)
In a case of syphilitic angina (periaortitis and aortitis), published
by Dr. Morison,3 the coronary arteries, though in an abnormal
position and somewhat small, were not diseased. My Oxford
brother 4 quotes with emphasis, one after another, three cases
of typical angina (syphilitic aortitis ?), in each of which
the coronary arteries and their orifices were unaffected. He
does not draw the conclusion that coronary disease is not
essential to angina pectoris, yet is not this conclusion — to use
Vaughan's word — inexcussible ? Hirschfelder's case 5 from the
Johns Hopkins Hospital I have quoted already ; Von Leyden
indeed, in the conclusion of his essay (loc. cit. p. 559), admits
that angina may occur without any coronary disease, and
especially cites cases of syphilis, and some other infections, to
this effect. (See also case p. 458.)

Dr. Stengel,6 in the course of an interesting paper on the
nervous symptoms of arteriosclerosis (see essay on Arterio-
sclerosis) writes : "In sclerosis of the arch of the aorta painful

1 Rist and Krantz, Bull, et mem. de la Soc. Med. des Hop. de Paris, 28 juin,
1906, p. 653.

2 Hoffmann, Diag. u. Therap. d. Herzens u. Gefasse, 1911, p. 334.

3 Morison, A., Lancet, Feb. 3, 1912.

4 Osier, Sir W., Lumleian Led., p. 839-840.

6 Hirscbielder, Diseases of Heart, etc., 2nd edition, p. 376.
6 Stengel, Amer. Journ. Med. Sci., Feb. 1908.

378 ANGINA PECTOKIS part n

paroxysms occur on slight exertion, which may have the character
of angina pectoris, even though the coronary vessels are not involved "
(italics mine). Cohnheim1 says, as to the " causal relationship of
angina with coronary disease, . . . often there is no trace of
disease to be found in the coronary arteries of such subjects, and
what is still more common, very high degrees of coronary sclerosis
are met with in persons who have never had an attack of angina."
It is true he tried to whittle down the distinction rather fancifully;
e.g. that aortic pain is more " diffuse," and is in closer relation
to effort than in angina from disease of the coronary vessels ;
but he shifts the onus probandi upon the coronarians.

Again, if it be agreed that " abdominal angina " may arise
from disease of this portion of the aorta (vide p. 309), what
need is there to drag in the coronary vessels ? As regards
fibrosis of the heart (considered in section on Cardio-
sclerosis (p. 21), alleged to depend on coronary disease, and
often associated with it, we know that the presence of these
nodules and diffuse fibrous hyperplasia does not produce angina ;
nor indeed any definite derangement of the circulation, unless
perchance a heart block. That in gradual sterile thrombosis of
coronary branches, of not more than middle magnitudes, no im-
portant symptoms of heart failure (after the initial symptoms)
ensue, although callus and fibrosis may be found after death,
was Kanthack's conclusion ; and it is strongly supported
by Krehl,2 who had often found extensive change of the kind
without record of impairment of cardiac function during life,
and by many later pathologists. Yet surely in no condition
would the alleged " partial myocardial cramps," or " fractional
systoles," be more likely to occur. Anginous symptoms on
plugging of a main branch, or ramus descendens and circum-
flexus, with acute myomalakia, will be considered presently.

Such is the testimony of no very favourable witnesses to the
not infrequent absence of coronary disease, even in mortal cases
of angina ; surely then in the cases which by recovery elude our
proofs, we who from indirect evidence infer coronary integrity
are not without justification. Although for years I have insisted
on this happy issue of many cases, I have been till lately alone

1 Cohnheim, Syd. Soc. ed. 1889, vol. i. p. 37.
2 Krehl, Lehrb. spec. Path., 1902.

sec. ii THE CORONARY ARTERIES 379

in recording cases of recovery. Perilous as the malady is,
death is not of its essence. I shall declare that defect of the
coronary arteries, together with other causes of myocardial
decay, does indeed take a large share, not in the generation of
angina pectoris, but in the mortal issue of it.

I repeat that I am no longer alone in recording cases of
recovery ; Sir William Osier has reported such cases. But, our
critics retort, "then they were not angina pectoris" ; all cases which
do not fit their formula are to be discarded. If the patient died,
the case was angina ; if he did not, identical as the symptoms
might have been, well, it was not angina. In other words, I am to
have all the points I demand, or I won't play. Of such a con-
tested case, Dr. Samuel West says (see p. 271) that " it had the
same characters as angina pectoris" ; in other words, a physician
of his ability and experience could see no clinical difference. How
can we then insist that the disease was not itself, but something
else in the same form ? Is this, in Professor Bateson's words, " to
treasure our exceptions " ? A more effective reply would be that,
recovery or no recovery, the coronary arteries are always diseased,
but not always so far as to forbid resumption of function, at
any rate for a time, with remission of the symptoms. And in
some elderly persons, in whom angina appears, disappears, and
reappears, such may indeed be the explanation. Dr. Morison has
written, and rather surprised me when he wrote * : " I am not
aware of any record of the recovery of any case of coronary
angina, though slow in development and compatible with a long
life " ; for even if by " coronary angina " Dr. Morison means
cases of senile angina in which coronary disease may be pre-
sumed, even from my own small circle of experience I can adduce
four or five such cases at least. And this explanation will
not by any means cover those cases, not infrequent in younger
persons, in which angina arises with great severity, and dis-
appears— as, indeed, in them it usually does disappear — without
ultimately any trace of harm, so far as the angina was concerned.
Here let us remember again Broadbent's gibe on those who seek
for recoveries in the post-mortem room.

That disease of the coronary arteries does not of itself set up
angina, is an axiom founded upon universal experience. These
1 Morison, A., Lancet, 1902.

VOL. II 2 B

380 ANGINA PECTORIS paktii

vessels are atheromatous in at least three-quarters of the bodies
which are found after death to be atheromatous at all 1 ; indeed
few elderly persons die without as much coronary disease as
would content a coronarian disputant, yet angina is one of the
rarer diseases. Potain argued that in many of these cases the
coronaries though calcified might be pervious ; and if so there
would be no angina. Well, this is one good step forward. It
is true that even in tortuous and knotty vessels the epithelial
mosaic, which preserves them more or less from thrombosis, is
very persistent, except in syphilis, in which infection, as I
showed, and Dr. Aldren Wright verified, thrombosis occurs
much sooner. Then what is the factor x — Thorel's " uner-
klarliches Etwas " ?

What is the alleged mechanism, whether in the coronary
area or not, by which this flare occasionally breaks out ? The
chief conjectures are four, two of them mutually contradictory ;
namely, first, that the occasional factor is a cramp of the
cardiac muscle ; secondly, that this muscle is painfully stretched ;
thirdly, that the left ventricle wrestles against aortic pressure ;
the fourth is the pretty fancy of intermittent claudication
of the heart, which of late years has obtained many votes,
and even the suffrages of Sir William Osier and Dr. Parkes
Weber.

When we come to reflect, so far as our knowledge goes,
upon the main facts of this part of the subject we may find
it difficult to be serious in a discussion in which the part
of coronary disease in the causation of angina pectoris is incul-
cated with almost theological impatience while its champions
are content to attach the disease to coronary causes by finks
so slender, and to interpret it by arguments that are, more
than one of them, mutually destructive. As Dr. Knott has
remarked, " It requires no very profound knowledge of logic to
see that a chain of which three essential links are subject to
instantaneous evaporation, has ceased to function as a bond of
union between fact and theory." But it would appear as if
soundness on the coronary question may liberate the disciple
to say what he pleases about other parts of the problem.

1 See a large collection made in the Hospital at Ivry by Auscher and Pilliet,
Soc. Anat., Paris, October 2, 1891.

sec. ii THE CORONARY HYPOTHESIS 381

As with the advocate — it was not Taffy who stole the shin
of beef ; or, if it was, then in the alternative nobody saw
him do it ; or, if some one did, then the beef did not belong to
the plaintiff : so of angina we are told — that it is due to coronary
disease, because this defect causes cardiac cramp ; or, if cardiac
cramp cannot be, then in the alternative, cardiac dilatation ;
or, if cardiac dilatation is inadequate, then cardiac claudication ;
or, if in angina the heart does not " claudicate," then the case
was not angina pectoris at all ! By these sophistications we have
seen one well-known teacher driven to the amazing assertion
that " the intensity of the anginous symptoms corresponds with
the intensity of the heart disease " ; while another says
magisterially, " There is a general consensus of opinion that
those heart affections are most characterised by pain which at
autopsy present most evidence of cardiac degeneration." Could
the tyranny of notions over experience go farther than this ?
More open-minded physicians have found themselves compelled
to admit that angina the most intense is, like aneurysm, com-
patible with a heart substantially sound, or even in normal
condition ; while, conversely, the stealthy way of cardiac
degeneration is but rarely enlivened by interludes so dramatic.
Von Romberg, a devoted adherent of the coronary cause, says,
in the new edition of his work, " a close observation of cases
without heart weakness will prove to us that a reduction of heart
energy cannot be unconditionally attributed to the conception
(Bilde) of angina pectoris." It is strange that he does not
see that, if so, the bottom has fallen out of the cardiac idea of
angina. And these objections cannot be made of none effect
by wilfully pretending that if the causes are not such as we have
postulated then angina is not angina. Heberden said plainly that
the cause is not cardiac, because he had noted pulsum naturalem
ut 'plurimum ; and are we now, on the rebuff of the necropsy,
to protest that, although every term of the morbid series may
be present in typical form, yet unless and until it is agreed to
attribute to the coronary arteries the chief place in the causation
we will plead an alibi or an alias, the name of angina shall be
withheld at pleasure ? Call no man anginous till he is dead ; and
not even then unless he has played the game ! Thus it is that,
with the modern development of neurology, the " soft options "

382 ANGINA PECTOEIS part n

of neurosis, neuralgia, and so forth, return to favour ; and
therewith a wandering after any view which in the haze seems
vaguely attractive. Now let us take the four guesses in turn.

Cramp of the Heart. — The hypothesis that angina pectoris
consists in a cramp of the heart has been, not unnaturally, a
prevalent speculation ; for by no extravagant metaphor the anginal
grip may be called a cramp. Heberden. although he regarded
the heart as outside the argument, thought there was a " cramp
somewhere " ; and among other reasons dwelt on the nocturnal
attacks, and on the free intervals, as in epilepsy and asthma.
We have seen that Erasmus Darwin 1 and later physicians
postulated a spasm of the diaphragm (or gout of this muscle), and
of other thoracic muscles, a notion recalled by James Mackenzie.
M'Bride, Baumes, von Dusch, Latham 2 and Walshe vulgarised
this conjecture of a spasm of the heart, due in Baumes' opinion
to foul blood. But upon cramp of the heart as a whole I need
not spend much time. In my earliest papers I insisted that,
certain poisons apart, the heart does not pass into a prolonged
state of contraction, a statement which rests upon clear
physiological doctrine ; and now on clinical grounds Dr.
Mackenzie confirms the opinion. Immediately on contraction
the function of contractility falls into abeyance. Automatism,
which in skeletal muscle is artificial, in the myocardium is a
natural state. Calcium, which is necessary to the myocardium,
to voluntary muscle is inhibitory. The chemical and electrical
conditions are not identical. Cramp, or clonus, is not the
abnormal but the normal action of this unique muscle ; an
action not balanced by antagonists, nor delivered by parcels.
Besides, under our very eyes during the anginal seizure the
heart does not stand still in systole ; in most cases it continues
normally to expand and contract. As Wassiliewski remarks
(loc. cit.), spasm of the heart in angina is impossible if the
cause be any kind of coronary closure, for this event is
attended not with constriction but with dilatation of the
heart. Von Dusch, too clear-sighted to ignore all this, explains
that by " cramp " he meant something else, namely, " kurze
rasch sich folgende Contractionen," but he does not explain how

1 Darwin, Erasmus, Zoonomia, vol. iv.
2 I think in his paper in Med. Trans, vol. iv. p. 278.

sec. ii CKAMP OF THE HEAET 383

with a normal rhythm and output this can be. But it has
been urged, as by M' Bride for instance, that after death the
ventricle is found tightly contracted. Now it is on the diastolic
phase, and on the later part of it, that the vagus tells. Well,
for my part, poisons, such as certain glucosides, or sodium salts
(Gaskell) excepted, I disbelieve in " deaths in systole " ; in systole
the egg is on end. Post-mortem systole is usually rigor mortis.
We can no longer suppose that the form of the ventricles after
death, a form usually accidental, throws any light upon the con-
dition of the heart during life. Balfour says definitely (loc. cit.
p. 316) that in death from angina the left ventricle may be
either contracted and empty, or flabby and full of blood ; I
can testify that the ventricles may be relaxed and full of clot.
Mackenzie remarks that in angina by a summation of stimuli
the heart becomes painful, but what may be the attitude of
its muscle during the attacks he does not tell us. However
the alleged " cramp " of the heart, or its parts, he admits to
be unthinkable. Sir James Goodhart points out the difficulty,
which should be obvious, of supposing such a cramp to
have no effect upon the pulse. Dr. Morison * supposes a
" crushing in its tonic grip the sensory nerve endings of the
organ." What and where ? In his histological introduction
he gives no description within the muscle of afferent end organs
(see p. 411). And what about the crushing of any such end
organs in ordinary systole, or in the systoles of renal and other
vehement hearts 1

Yet while heart cramp is thus driven from pillar to post, its
supporters still cling to fragments of it, and declare for " localised
(partial ?) cramps," as first suggested by Kronecker. By " local-
ised" cramp is meant, as I am informed, a contraction in a segment
or segments of the myocardium prolonged beyond the cyclic
systole. It is not easy to picture a cubic inch of the ventricular
wall, woven as it is, being held in persistent contraction, while
the portions on all sides of it, as the pulses tell us, are pursu-
ing their rhythmical periods and discharging their functions
adequately ; nor again to explain how such a fragment, if
abutting upon oscillating parts, could persist in spasm without
upsetting the balance of the whole. We might try to fancy a
1 Morison, A., Cardiac Pain, p. 277.

384 ANGINA PEOTOEIS part n

sector of the muscle, in form like those natural divisions of an
orange which children call "pigs," as held in a discordant tension;
but when we come to think of the fibres of the muscle, not thus
departmental but crossing each other's lines of force in many
planes, we realise that this fancy must be unsubstantial.
And fractional systolic efforts of the kind supposed should
be visible in the electro -cardiogram. The cardiac muscle,
whose fibres are not insulated by sarcolemma, does not, after
the manner of voluntary muscle, sustain a contraction by alter-
nations of fractional contractions, but by one consentaneous
and maximal effort of all its integrated fibres ; an effort which
must be followed by a like universal relaxation. Of course if by
coronary embolism a parcel of the myocardium softens, a partial
diastole necessarily ensues ; and generally speaking, the effect of
malnutrition is a blocking or delay of the contractions. Were we
loosely to compare fibrillation of the auricle with " partial
spasm," fibrillation does signify suspense of the function of the
whole chamber. As Dr. Rolleston x has said, the only conceivable
seat of partial spasm is in the musculi papillares ; but, were there
no other objections, it would be sufficient for the dismissal of
this alternative to remember the maxim that, in respect of the
parts of the heart, angina is associated with the aortic ; with
the mitral part very rarely. Well then, replies one able and
pertinacious disputant, " the heart muscle, if not capable of
spasm, may be capable of an abnormal contraction akin to
spasm " — a dilemma worthy of Duns Scotus, a distinction which
may be left to die of its own attenuation.

Dr. James Mackenzie attributes the " gripping sensation of
angina," to " spasm of the intercostal muscles,'" and so decisively
that he " would even limit the name to cases in which, besides
the pain, there is a sense of contraction in the chest ... as if the
breastbone would break." 2 In one of his published cases Dr.
Mackenzie graphically describes an experience only too common
in angina pectoris, that " he (the patient) dare not move for
fear of the awful pain ... a terror such that sweat poured off
him " ; but this stillness he does not attribute to the dread or
agony, but, on Erasmus Darwin's hypothesis, to the cause of

1 Rolleston, H. D., Med. Soc. of London, Feb. 24, 1902.
2 Mackenzie, J., Dis. of Heart, p. 38.

sec. ii CEAMP OF THE HEART 385

the agony, a spasm of the muscles of the chest,1 to which however
Darwin added spasm of the diaphragm. A similar explanation
was advanced by Baumes, who, however, attributed a part of the
fixation of the chest to ossification of the ribs. Now Wichmann
observed the thoracic muscles carefully, and concluded that,
although there is a sense of constriction, the thoracic muscles
are not contracted — the respiration is overawed, but not locked
up. Jurine says that a deep sigh may be drawn, and this I have
seen more than once, even sighings. The respiration in angina
is often abated or in abeyance, it is true, but, in my opinion,
by vagus or other inhibition. Dr. Morison, in a large opera-
tion for synechia,,4 observed that post-sternal angina persisted
notwithstanding the division of the 5th and 6th intercostal
nerves, and removal of the intercostal muscles. Now the vice-
like pain of angina— major and minor — although of all degrees,
from " stenocardia " to unutterable agony, is in kind, in
seat, and in menace, peculiar ; it varies only in the number of
the turns of the screw. The intercostal muscles, when in action,
do not crush the breast-bone inwards ; they expand the chest.
Moreover, if in cramp, they would, as in all muscular cramps,
give pain in proportion to their volume. Cramp of the foot
is vexatious, of the leg it is distress, of the thigh it is the rack.
The intercostal muscles are short and thin ; they are many it is
true, but even if unanimous have nothing like the volume to
set up a pang so poignant as that of angina. A frequent area of
anginous pain is that of the left pectoral muscles, but it is
not by any constraint of theirs that the patient may be deterred
from gripping the arm of his chair, nursing his left arm across
his chest, or taking the medicine cup in his hand ; he is trans-
fixed by the writing on the wall. He could move an he dare.
In muscular cramp we may howl or rage ; angina pectoris
is beyond all raging. By the bed of a strong man in an attack
of the major angina the very chamber is silent with awe. In
this agony — the uttermost torture, so we are told, in the rack of
disease — the wit of the physician only is still vigilant ; and in
this strait can he see no more than the plucking of a few chords

1 Dr. Mackenzie has suggested that the pain of pleurisy is, in like manner,
due to intercostal spasm. Likewise in the older authors we find anginous
symptoms attributed to ossification with rigidity of the ribs.

2 Morison, A., Lancet, Jan. 8, 1910, p. 99.

386 ANGINA PECTOEIS part ii

of fiddle-string muscles at the patient's ribs ! The anguish
is of far grimmer, far deeper significance. Even of attacks
of trigeminal neuralgia no man has died. Some variable
reflex fixation of those muscles there may be ; in diseases of
the thoracic viscera, as WolfE-Eisner has demonstrated in
phthisis,1 the muscles of the walls are in spasm, and may
be felt thus rigid ; but angina is no consequence of this.
Besides, the notion bears not at all on the pain of angina
minor, which, as Dr. Mackenzie himself says, " may be
but a slight sensation," yet the pain is in nature identical.
In the angina of acute aortitis (as in Dr. Christian Simpson's
case (p. 274) and others of status anginosus) I have had time
and to spare for observation of the walls of the chest, and
am in a position to assert that, in this acute form of the
disease, no such locking of the intercostal muscles is to be
discovered. Moreover the pang is usually substernal about
the manubrial joint, away from the intercostals ; and the grip is
described as inward, not as a stitch but as crushing by a
heavy bar, or a vice-like compression of the breast towards the
spine. Furthermore in many anginous patients the lungs are
emphysematous, and the ribs rigid already. As I have said, the
older writers, such as Wall, with some consent emphasise ossifica-
tion of the ribs as a feature, if not a factor, of the disease.

Distension of the Left Ventricle. — Now let us pass on to
the notion of ventricular dilatation — brusque distensions. Of
this hypothesis the supporters are Potain, West, Merklen,
Teissier, and many others. It seems odd in one breath
to assert that angina pectoris is a state of high pressures, to
be combated by nitrites, and yet that the ventricle is dilating ;
in this case, as Dr. Colbeck has argued, pressures should be
falling. Of the distension alternative I cannot select a more
weighty exponent than Dr. Samuel West, who with rather
surprising readiness 2 remarks that " sudden dilatation of the
heart produces angina pectoris, as our daily experience tells
us." My " daily experience," and I venture to think the
general experience, is that the heart is liable to be far more
dilated, and more suddenly dilated, whether on the right

1 See Pottinger, Deutsche med. Wochenschr., April 21, 1910.
2 West, Samuel, Brit. Med. Journ., June 23, 1906.

sec. ii ALLEGED CAEDIAC DISTENSION 387

side or on the left, in disorders and stresses other than
angina, and this without any considerable pain ; while con-
versely in angina dilatation of the heart, whether we look to
the cardiac physical signs or to the secondary evidence of other
organs, is no considerable feature. We often meet with extreme
dilatation, as for instance in infective myocarditis, with no
pain, although the sign of pain would be a useful signal ; there
is no approach to a parallel between cardiac dilatation and
cardiac pain. And when we do find dilatation and pain together
the pain is not characteristically anginal (pp. 430 and 441).
Indeed, as we shall see presently, Dr. West, although he did em-
phasise dilatation, does not now exactly postulate, as the main
factor, dilatation only. All the evidence on the effects of nitrites,
of rest, of mitral regurgitation, and the like, goes to prove not that
the heart is failing in tone, or contractive power, but, relatively
to the angina, is doing not too little but too much. Even
Huchard, not seeing how it told against his coronary hypo-
thesis, admitted, beyond the facts : " L'angine de poitrine ne
peut plus se produire chez un malade en etat d' hypotension
arterielle." I have already quoted (p. 331) Dr. Mackenzie,
and many other authors, to the effect that during an attack
no alteration of the heart's dimensions is to be detected.
Merklen (loc. cit.) says bluntly that dilatation, as an explana-
tion of anginal pain, will not do ; " elle est, somme toute, chose
banale." Moreover cardiac dilatation is apt to set up dyspnea,
which is not a feature of angina. That, as Balfour, Broadbent,1
and Musser (loc. cit. p. 389) pointed out, and as others, such as Sir
Richard Powell,2 Sir Thomas Oliver,3 and Dr. J. S. M'Kendrick,4
have verified, angina pectoris is relieved by mitral regurgitation,
and, as Dr. Mackenzie 5 stated of " a number of cases," " ceases
with the onset of auricular fibrillation," does not look as if dilata-
tion of the heart were the cause of the pain. Nay rather, signs
of yielding heart with its consequences, when the coronary blood
pressures must be at their worst, are not infrequently signs of
departing angina ; and the action of the nitrites is not to

1 Broadbent, W. H., Lancet, May 27, 1905.

2 Powell, Sir R. D. See Report of Harveian Soc. Discussion, loc. cit.

3 Oliver, Sir T., Lancet, Sept. 1905.

4 M'Kendrick, J. S., Glasgow Med. Journ., Nov. and Dec. 1909.
6 Mackenzie, James, Brit. Med. Journ., Oct. 31, 1911, p. 971.

388 ANGINA PECTOEIS part n

withstand dilatation. By what mechanism does syncope or
mitral regurgitation fill the coronary arteries, the emptiness of
which is on current hypotheses a primary condition of the
angina ? It is generally agreed that the onset of angina may be
accompanied not by falling but by rising pressures, whether
primary or secondary ; that indeed, though during enormous
rises of arterial pressures intracardiac diastolic pressure may be
constant,1 the attacks are, almost as a rule, determined by
momentary rises of intra-aortic pressures. We shall see presently
indeed, that it is not intracardiac but intra-aortic tension
which excites anginal attacks. One of the most sudden and
severe modes of dilatation of the left ventricle which can
happen is that ensuing upon a rupture of .an aortic cusp ; now,
although the distress of this rupture is severe, unless there be
such other lesion as to give rise to angina, the characters of
this accident are not those of angina ; the distress is different,
more persistent and attended with dyspnea. As Ortner, in his
elaborate report on Herzschmerz,2 sums up this matter, " the
pain of dilatation, if any, is a much smaller affair, causing an
aching, . or possibly a stitch, in the submammary area, and
superficial cutaneous tenderness." For these and many other
reasons mere distension, which Parry, supposing that it tended
to " exhaustion of the heart's irritability," seems first to have
assumed, which Fothergill and Stokes seem to have meant by
the phrase " weak and fatty heart," which Traube interpreted
as a dragging upon the nervous fibrils in the wall of the tauter
ventricle, and which more than twenty-five years ago von
Leyden 3 and other physicians, abroad and at home, still held
to be the condition of angina, but which Vierordt, at the
Wiesbaden Congress of 1891 demolished, has been dropped ;
although every now and then it is introduced furtively when the
disputant is in straits. But, as Dr. Nathan Raw remarks,4
no one has ventured to say that angina is relieved by the " re-
establishment of compensation " ; though Curschmann contrari-
wise made the curious remark, that with an extremer degree

1 Hill and Barnard, Anat., 1879.

2 Ortner, Jahreskurse f. drztl. Fortbildung, Feb. 1911.

3 Von Leyden, Zeitschr. f. klin. Med. Bd. vii., 1884 (angina as a periodical
asystole).

4 Raw, N., Lancet, Aug. 21, 1909.

sec. ii ALLEGED CAKDIAC DISTENSION 389

of the coronary disease and corresponding enfeeblement and
degeneration of the myocardium, he had seen angina diminish
and pass away ; and Ortner is inclined to agree with him.1

Fiessenger,2 who cannot get rid of the coronary artery decay
and consequent ventricular "fatigue," admits that he is perplexed
and cannot understand his own interpretation, " because the
myocardium is insensitive, and ordinarily myocardial failure is
painless." So he guesses around the cardiac plexus, etc. His
classification of anginas is artificial, not based on the deeper
affinities.

Let us now go a step farther and refer to a paragraph in
the late Professor Musser's well-known article 3 in which he not
only denied that dilatation was the cause of angina, but argued,
on the contrary, that by cardiac dilatation or mitral regurgita-
tion angina pectoris is relieved (see Head, p. 300). Musser cited
the following three cases. The first was one of angina with high
blood pressure, loud second aortic sound, and so forth ; the
state became worse, and dilatation ensued, whereupon the angina
was not exasperated but ceased. The second case illustrated the
same sequence of events ; on " rapid dilatation the angina
ceased." And so it was with the third case ; but in this
instance when by restorative methods the hypertrophy of the
heart was re-established, then the angina reappeared. Balfour's
leading case was even more striking. He happened to be
listening at the heart of a patient when an attack of angina
set in, and he found it possible to continue the observations
throughout the attack. The pain was the ordinary crushing
of the sternum to the back, and radiation into the left arm.
The radial pulse was tense. Gradually a mitral regurgitant
murmur made itself heard, when the pulmonary second sound
became accentuated and booming, the pulse small and feeble,
and as " cardiac asthma " set in the angina ceased (itals. mine).
It cannot be urged in these and such cases that it was a fall of
intraventricular tension on the left side, transferring the stretch
from the left to the right ventricle, which alleviated the angina.
Intraventricular pressure is a very complex subject ; it is suffi-

1 Ortner. See Fortschr. d. d. Klinik, ed. Klemperer, Bd. i., 1910, p. 338.

2 Fiessenger, Acad. d. Med., Paris, Oct. 1, 1912; well reported in Lancet
and Brit. Med. Journ. for Nov. 9, 1912.

3 Musser, Amer. Journ. Med. Sci., Sept. 1897.

390 ANGINA PECTORIS part n

cient here to point out that it was at the moment when, relative
or positive, the pressure seems to have been excessive for that
ventricle, at the moment when it was so stretched as to give way,
when the hydrostatic pressure of the column of blood in the left
auricle began to tell on every square unit of the yielding intra-
ventricular surface, that the angina did not come on, but went
off ! Indeed the maxim of Musser and Broadbent that dilata-
tion of the ventricle mitigates angina suffices almost alone to
extinguish the notion that the pain is due to distension of the
muscular tissues or drag upon the enclosed nerves.

Systolic Effort. — But now we have before us an amended
pleading ; and we are indebted again to Dr. West and Sir Lauder
Brunton for the alternative proposition, that the pain of angina
is caused not by the distension but by a recoil or counter- effort
of the heart against a rising intraventricular or intra-aortic
pressure ; " contracting against resistance." 1 In other words,
the amended plea is that the pain is due, not to passive
stretching, but to effort of the muscle ; but yet, in the opinions
quoted, is generated in no investments or attachments, but in the
muscle itself. This change of the point of view is so important
that I must quote Sir Lauder Brunton and Dr. West textually.
Dr. West 2 drew a parallel between the contraction of the heart
upon its contents, and that of the bladder, intestine, or other
hollow organ upon its contents, when the issue is obstructed ;
it is " a spasmodic contraction to get rid of its contents " ; and
accordingly he called angina " cardiac colic." In similar terms
Sir Lauder Brunton said, " angina is the pain of a tight ventricle
in its ineffectual attempts to empty itself against the excessive
blood pressure in the aorta " ; he too compares it to colic, as
when the colon is urging against obstruction ; or to pain in the
bladder, as when the expulsion of the urine is hindered ; or again
to the effort of the uterus at the beginning of labour. Massay's
article 3 is but a version of Brunton's ; he brings in likewise the
bladder analogy, and so on. Gibson said that this notion in
angina of " strife to surmount an obstacle " was first suggested
by Cahen,4 but the same view of the matter was also expounded

1 See Belfast Discussion, 1909, Lancet, Aug. 7, 1909.

2 West, S., Brit. Med. Journ., June 23, 1906.

3 Massay, Paris mid., 1912, vol. xxxii.
* Cahen, Arch. gen. de med., 1863.

sec. ii CAKDIAC EFFOET 391

in an able paper, published about the same time, by Eichwald * ;
until recently however it had found few adherents. All these
authors have regarded the pain as due, not directly to the
tensile stress on a passive ventricle, which hypothesis they
implicitly demolish, but to a contrary effort — an effort they
would compare with colicky contractions of the uterus upon a
clot. The rather vague opinion of Bamberger, that angina is
due to " over-action of the heart," may in substance be the
same. Now let us consider this crampy dilatation ; this stretched
contraction or contracting stretch, analogous to the pain of a
hollow muscular organ, such as the urinary bladder when
distended by a content which at the same time it is striving in-
effectually to expel— an illustration which, like Mr. Pickwick's
dark lantern, bewilders without enlightening us. In the case of
the distended bladder, the pain is probably not in the muscular
coat, but is set up by the drag upon the parts about its neck and
the prostate ; the fine nerve-twigs passing to the fibres of
visceral muscle are regarded by physiologists as motor. So again
the pain of colic is due, not to the contraction in the muscle
itself, but to its abnormal pull upon the mesentery, a sub-
cutaneous structure (p. 421), largely provided with Pacinian
corpuscles. It is to such a tension at the neck of the aorta that
I attribute angina pectoris; but, however this may be, the bladder,
in the case supposed, is striving with a content which is not
expelled ; the heart on the contrary in the attack of angina,
even during the worst of the paroxysm, is continuing stead-
fastly to deliver its tale of blood, per beat and per minute,
with a tranquillity and effect which under any hypothesis are
rather astonishing. And this it does often against high
pressures. But both in health and disease the heart is con-
tinually called upon for such efforts — in disease of other kinds it
may do it perennially, yet in such frequent cases we hear little
of angina major or minor ; anginoid pain is no characteristic
symptom of aortic stenosis, nor of chronic renal disease, nor of
hyperpiesia, even under the extremest aortic pressures. More-
over in these conditions we find the left ventricle hypertrophied
accordingly, and, in the analogous cases, the muscular coat of

1 Eichwald, " Uber das Wesen der Stenocardie," Wurzburger med. Zeitschr.,
1863, S. 249.

392 ANGINA PECTOEIS part n

the bladder or stomach ; but of angina such a hypertrophy is no
ordinary feature. To conceive of the pain of angina as due
to muscular recoil, or a wrestle against abnormal resistance,
is surely to creep back very near to the notion of cramp,
and to attribute to the striated cardiac muscle the mode of
activity of the unstriped muscle of the intestine, the bladder,
and the womb, and to forget that this labouring of the heart
is not, as in the cases given as analogies, ineffectual, but
effectual : it is discharging its contents equably as in health.

Again ; we are not told what the excessive resistance is.
Certainly the intra-aortic pressure is by no means constantly
raised, and to regard normal aortic pressures as relatively
excessive, is to shift our ground and to return to cardiac
incapacity. Shall we not hesitate then to compare the maximal
rhythmical discharge of their contents by the ventricles, even
if it be against a high aortic resistance, with the slow cumu-
lative progressions of unstriped muscle against an undischarged
content ? We know that every contraction of the heart is a
maximal contraction, whatever the residual blood ; but in cases
of angina we have no evidence that residual blood is larger than
in other and far more frequent states of high pressure without
angina.

If it be replied that in coronary disease the heart is sensitive
in a way that it is not when the coronary circulation is un-
impeded, we have to enquire how defective nutrition makes for a
" tighter " or strenuously " recoiling " ventricle ? Besides, the
suddenness of the seizures is not suggestive of an accumulating
resistance against the heart's expulsive efforts : surely the climax
should be accompanied or even preceded by some sign of cardiac
embarrassment, such as palpitation, or arrhythmia, or some
physical signs of stress. And if squeeze of its intrinsic nerve-
ganglia by a wrestling myocardium were the cause of angina,
should there not be some parallel between angina and hyper-
trophy ? Once more, were angina due to any particular attitude
of the unhealthy or healthy ventricular muscle, if, for instance,
on each laborious heave the intraventricular pressure were
forcing outwards any softened parcel of its mass, the pain
should surely coincide more or less with the cardiac beat.

Merklen, after quoting with approval Sir Lauder Brunton's

sec. ii EEDUCED CONTRACTILITY 393

comparison of the heart in angina with the bladder striving
against an obstacle, and likewise seeming to forget that a
bladder which cannot empty itself is not comparable with a
heart which can and does empty itself, admits nevertheless that
he is puzzled. He also is wistful for the " unerklarliches Etwas" ;
and meanwhile falls back upon the old notions of Charcot,
Potain, and Frankel, that the pain is due to the cardiac ischaemia ;
that it is the cry of the nerves in the heart for blood. Broadbent,
like Dr. Mackenzie, saw that these explanations, spasmodic or
quasi-spasmodic, must fail, and that " the ideas of those who
have employed the term have been very vague." In his direct
fashion Mackenzie concludes (Diseases of Heart, p. 304) : " I
admit I have no definite idea of the state of the heart during
the paroxysms." Thus baffled as we are, is it then wise to
resent the proposal on my part of a new hypothesis as an
eccentricity — in the bantering words of a friend of mine, one
far greater than myself, a " childish eccentricity " ? Nay,
surely, if there be a field open for a fresh eye and a new
hypothesis, it is here.

Reduction of Contractility. — Dr. James Mackenzie * has offered
us partial conjectures rather than a complete hypothesis on the
causation of angina pectoris. He supposes that in angina the
heart's nutrition by long strife has been much impaired, and its
fibre degenerated ; but he finds notwithstanding that in angina
four of the properties of cardiac muscle may be, and usually are,
intact, while that of contractility he assumes to be reduced ;
and for the determination of this single defect he relies upon the
pulsus alternans. But, if the finger be an adequate witness, the
pulsus alternans is not constantly nor even generally present in
uncomplicated angina. However, Dr. Mackenzie denies the
sufficiency of the finger for this observation. Still, how is this
opinion reconcilable with what he admits — the mitigation of
angina by enfeebled systole or mitral regurgitation, and its return
on a rise of pressure ? 2 And when he adds that exhaustion and
shortness of breath on exertion are further evidences of this
defective contractility, he is still travelling outside the argument ;

1 Mackenzie, Jas., Brit. Med. Journ., Oct. 7, 1905.

2 On the disappearance of angina with hyposystole see also Curschmann,
in the discussion on this disease at the Kongr. innere Med. of 1891.

394 ANGINA PECTOKIS part n

for neither of these cardiac symptoms is characteristic of angina.
Nor do I know why Dr. Mackenzie assumes that in angina
pectoris the heart has " been long exposed to excessive strain,"
and is more or less worn out ; this assumption is not justified in
pathology ; in most cases of angina in middle or young life — as
in the many syphilitic cases — the myocardium is quite healthy ;
and we have seen that even in elderly subjects the heart
may still be good enough. Nor is it easy to accept his
statement 1 that angina " is never the outcome of an acute
affection ; that it is invariably led up to by a long period
of gradual exhaustion." Surely that it appears like a bolt
from the blue in many a man apparently healthy and vigorous,
and not only in acute cases such as the influenzal and the
syphilitic than which none are more typical, is a matter of
daily experience, an experience graphically described by
Osier. That in many such cases stealthy degenerative
changes have long been silently at work is true, but these
are not necessarily of the kind of exhaustion ; the myocardium
may be far from exhaustion, or even from impairment.
Pallor, faintness, and " collapse," with dilated pupils, may
be frequent features of angina, as they are of biliary, renal,
or intestinal pain ; but the ordinary interpretation of these
phenomena in angina is that the pallor is due to vasoconstric-
tion, and that syncopic conditions act rather in the way of
relief than of aggravation. Collapse, as Capps's and Lewis's
experiments indicate (p. 478), is one of the exceptional effects of
intrathoracic irritation. But to concentrate our attention upon
defect of contractility ; Dr. Mackenzie says, " with confidence,"
that angina " can occur when excitability, conductivity, rhythm,
tonicity, are unimpaired," and when he proposes — as some-
thing must be wrong — to throw upon the opponent the proof that
contractility is maintained, the reply is that, so far as we yet
know, maintenance of contractility may be as compatible with
angina pectoris as the maintenance of the other four qualities,
or any of them ; and until the high or relatively high arterial
pressures, which frequently occur in angina, are found to be
characteristic of impaired contractility, our anticipations will
follow other lines. Take, for example, from the author's own
1 Mackenzie, Jas., Diseases of Heart, p. 44.

sec. ii EEDUCED CONTRACTILITY 395

careful record, the instance 1 in which during the attack the
blood pressures rose from between 118 and 138 to 240-300 ; and as
the pain subsided the pressures fell. " In another observation
a rise to 160 presaged an attack." I agree that this rise was
probably due to a large vasoconstriction, but what about the
contractile power of a heart able thus to master, or cope
with, increases of resistance so large. As Dr. Colbeck has
remarked, the quality of tonicity, being a later development
than that of contractility, probably would succumb before it.

One element of angina indeed there is, which may give rise to
degrees of loss of contractility ; namely, the cardio-inhibitory.
Gaskell and His both described contractile reduction as a
result of vagus stimulation ; and it is possible that diminished
conductivity may simulate, and practically amount to, defect of
contractility. However, Rosenberg,2 in summing up this part
of the argument, confesses that " no hypothesis will serve
which depends on reduced efficiency of the heart's muscle
(' Verminderung der Leistung des Herzmuskels ') ; this con-
dition in later stages may appear with dyspnea (' Lufthunger ')."

When in his book on heart disease Mackenzie says (pp. 40
and 42) " the phenomena of angina pectoris are not the outcome
of the gross lesions found, but are evidence of exhaustion of the
heart's contractility " — though without any reduction of tone,
he adds (p. 54), although " this exhaustion is the essential
cause of angina ... it is not dangerous," " and the phenomena
disappear with the restoration of the nerve force." Then
what is the danger element — the gross cardiac lesions? But
often enough there are no such lesions, or not in sufficient degree
of themselves to cause or menace death. And, as to the pain, we
know of no severe pain from contractile exhaustion of this
muscle. The arrest of the heart, in a week, in a year, or in a
decade of years, may be due, as the attacks themselves may be
due, to a " summation of stimuli " ; indubitably the pains do
depend upon an exalted state of the sensory paths ; but the
stop is not the angina, nor can it be an essential part of it, for
plenty of people pass through the tribulation of angina and
come safe out of it, not a few indeed safe and sound, while

1 Mackenzie, Jas., Heart, vol. ii., 1911.
2 Loc. tit. p. 310.

VOL. II 2 C

396 ANGINA PECTOEIS part n

others after suffering for many years — twelve, fifteen, or twenty
— die in the end of associated or intercurrent disease. Of the
gravest maladies angina pectoris is one of the more curable.

Dr. Colbeck, in the article 1 to which I have referred, an article
which contains an able criticism of the hypotheses of angina
pectoris, illustrates many of these confusions of thought ; he
points out that not a few writers, by talking in the same breath
of painful distension or dilatation of the heart and of cramp, blow
hot and cold. His own opinion seems to be that angina pectoris
depends primarily on coronary disease ; but that the mechanism of
it lies, not, as Mackenzie suggests, in a general defect of ventricular
contractility, but in partial losses, in the inequality of contrac-
tile efforts in a muscular mass of which some parts are im-
paired ; so that the unevenness of the pull hurts the weak places.
This opinion approaches, or is identical with, that of some German
authors. Von Romberg, after admitting that we cannot predicate
dilatation of the whole chamber as the cause of the pain, men-
tions the conjecture that larger or smaller portions of the wall
may be twitched thus unevenly. Yet, as in the partial cramp
hypothesis, it is difficult to comprehend, whether on experimental
or anatomical evidence, such differential rates of motion, or that
the ventricle can act thus fractionally ; or, in case of local buck-
ling, that portions of the wall could be driven outwards time
after time, without giving place to aneurysm or to some pouch-
ing visible at the necropsy. If, as Dr. Colbeck suggests, the
degenerate patches are carried along in uniform motion with
the rest, the discord may be painful, or may not. But after all,
as Dr. Knott forcibly observes,2 " these cardiac notions cannot
account for the central forms of midsternal pain, which I have
observed to be the most severe, as was the experience of Heberden
himself " ; though it is true no doubt that, cardiac and aortic
innervation being similar in plan, in cardiac distress there may
be, besides the " precordial " weary ache, also some ache in the
shoulder and left arm, but, so far as experience yet tells us, with
little intensity ; rarely such as to cause much complaint. The
truth is, quibble about it as we may, cardiac disease is not charac-
teristically painful.

1 Colbeck, Lancet, March 31, 1903.
a Knott, Airier. Med., Oct. 27, 1904.

sec. ii CLAUDICATION 39V

Claudication. — Now let us turn to that which is just now
the most popular of the current explanations of angina pectoris ;
namely, to Potain's notion of " intermittent claudication " of
the heart ; a notion I have pondered with no little perplexity.
I have read carefully what Potain, Pal, Sir William Osier,
Dr. Parkes Weber, Obrastzow of Kiew, and other supporters of
this hypothesis have said about it, also their tributes of priority
to certain of our predecessors, such as Sir B. Brodie and Allan
Burns ; but so far I have failed to get to close quarters with
their meaning, or to reckon the debt which we owe to any of them.
On the phenomena of this claudication in horses, as described to
us by Charcot, and on its interpreting value in explaining tran-
sitory aphasias, and other intermittent failures of function, in
this area or in that, we have all been fully instructed ; but, as
I have said on sundry previous occasions, I fail to see their
relevance, either by kinship or analogy, to angina pectoris. It
is true that in the reports of senile cases angina pectoris often
happens to be associated with diseased coronary arteries, but
so are all other diseases in old people ; even in angina the
evidence of this proportion is founded upon the partial figures
of the mortal cases. We have seen that no inconsiderable
number of cases of angina — perhaps most of those ending in
recovery — have been independent of coronary disease ; and
even in mortal cases I have quoted no indecisive post-mortem
evidence to this effect (p. 374). Still, for the moment let us
confine ourselves to the ordinary mortal case. Now these,
x«-we all agree, are generally attended with coronary disease,
because the coronary disease is apt to determine, not indeed the
angina, but sooner or later the lethal effect of one of its strokes.
In these cases, as in the horse cases, we have, no doubt, a
special incident of arterial disease, a sudden failure of a muscular
organ supplied by diseased vessels. But with this coincidence
surely the parallel ends. Arteriosclerosis of vessels distributed
to muscular organs is common, yet intermittent claudication is
something of a curiosity ; however this may be one of those
exceptions or eccentricities which now and then throw happy
side-lights on more familiar processes. But does it ? Does this
claudication, as described in the horse, resemble angina in any
but the most irrelevant manner ? Surely the main feature of

398 ANGINA PECTOKIS paetii

intermittent claudication is claudication ; the horse stumbles or
falls, the limb of the man is for the moment maimed. How are
such attacks to be compared with attacks of angina pectoris in
which, unless it be the last, the heart, coronary anaemia or
no, may be, often is, undisturbed ; or shows at most no
more perturbation than might be caused by a little flatulent
dyspepsia, or by the irritation of a peripheral sensory nerve ?
Obrastzow says * that angina arises thus : the heart quickens
in rate, the sclerosed arteries cannot expand quickly enough to
meet it, ischaemia sets in with a shorter diastole, and so claudi-
cation ; and this is angina ! He calls it " dyspragia cordis
dolorosa " ! Every link in this argument is frail. The heart's
pulsation need not, often does not, rise in rate ; the coronary
circulation is correlated not with the rate of the heart but
with its metabolism and the blood pressure. But Dr. Parkes
Weber, who pleads for " claudication," admits that the pulse
in angina is often unaltered. The horse, as he trots along,
suddenly drops, often with painful cramp of his legs ; then after
a few minutes, as muscular irrigation is slowly restored, he picks
himself up and ambles forward, again to fall in the same way.
The heart of an atheromatous and anginous patient trots along,
and some day may stop suddenly ; but it does not stumble, or
not until in death it stumbles once for all. The heart cannot,
like a pair of hind legs, curl up, wait for supplies, and then start
away again. To suppose a spasm of these vessels is gratuitous.
It is true we cannot say that the heart in angina never
" claudicates," but when it does there is an end of the case :
the halt is the halt of death. And yet Potain used to talk of
angina pectoris as " painful intermittent claudication of the heart "
(italics mine). But what of the fits of angina — the vast majority
— in which there is not even a trip ? Are we to call them painful
arteriosclerotic cramp ? But we have learned that in the heart
muscle cramp cannot be, or rather that in its systole cramp is
normal to it. And claudication is not due to vascular spasm
but to obliterative arterial disease. As to the stumbling
(" dyspragia angiosclerotica "), we have seen how the more
observant clinical physicians have marvelled at the serenity
with which the heart during the passage of the storm, over it
1 Obrastzow, orig. art. in Zentralbl. f. Herz- u. Gefasskrankkeiten, April 1912.

sec. ii NEUEOTIC CONJECTUEES 399

or through it, ambles evenly along. Some years ago I spoke of
the heart as the one impassive agent in a torture chamber, and
the phrase has been accepted. Almost in the words of my earlier
papers, Gouget,1 in a casual allusion to angina pectoris, has said,
"It is obviously very illogical to attribute to intermittent claudica-
tion of the heart a syndrome during which this muscle proceeds
in its function in an absolutely normal manner, without any
modification of force, or of regularity . . . being present thus
impassively at a painful and agonizing crisis." Where then is
the " dyspragia " ? And in these claudication cases we must
not forget that there may be, and often is, an associated
neuritis of the limb. One of Dr. Parkes Weber's patients, in
whom this affection occurred in one leg only, had suffered in
that leg from sciatica. The concurrences of cramp of the leg
with angina pectoris in certain elderly atheromatous subjects,
as recorded by Ortner and others, certainly prove nothing in
respect of the nature of angina, and presumably are mentioned
as analogies only. Many elderly persons are the subjects of cramp.
If I seem to deal somewhat curtly with a hypothesis which has
such distinguished adherents it is in no spirit of disrespect, but
because by some mishap I have failed to comprehend it.

The neurotic conjectures of angina pectoris are ancient
and manifold, but too vague and perplexed to detain us
long. Laennec was a champion of some nervous hypothesis ;
he suspected the vagus. Trousseau compared angina with
an epileptiform neuralgia. Stokes, and after him Bamberger,
speculated on some cardiac hyperesthesia with hyperkinesis.
Lartigue 2 and Lancereaux sought it in the cardiac plexus ;
and Romberg, Williams, Friedreich, and others followed them.
Bulb, phrenic nerve, vagi, intercostals, cardiac plexus, all have
had their advocates and their day ; to-day the vasomotory system
is taking its turn. The clinching argument of these nervous
advocates is that they are right because, such are the com-
plexity, variety, and obscurity of the nervous endowments of
the heart, they can neither be proved wrong nor be expected
to explain how they are right. We will consider first A, the
vasomotor hypotheses, and then B, the plexus hypotheses.

1 In his treatise on "Arteriosclerosis," 1907.
2 Lartigue, M6m. sur angine de poitrine, Paris, 1846.

400 ANGINA PECTOEIS paet il

A. Vasomotor Hypotheses. — On the vasomotor phenomena
in these, as in many other sudden disturbances of functional
equilibrium, I have spoken in other chapters. By perpetual
vacillations of the balance of the circulation, they may play
no inconsiderable, if an accessory, part in bringing about
the discomfiture of a frail ventricle. However, they play a
part in another hypothesis, that of Dr. Francis Hare.1 After
demonstrating the improbability of current conjectures,
Dr. Hare argues that angina pectoris is due to a painful
distension of the mediastinum, and this to intense vasomotor
constriction in very large areas elsewhere. He thinks moreover
that it may be by this congestion that the coronary arteries suffer
injury, and the cardiac plexus irritation. Dr. Hare is coming
nearer the truth ; if he will substitute tension of the investments
of a diseased aorta for tension of the mediastinum, I think he
will find some things become clearer which he now finds
obscure. But we are agreed that " high tension " is no
necessary coefficient of angina. Ord and others have suggested
that angina is due to a hypersensitive or labile state of the
vasomotor centre — to which the cardiac centre is in close
proximity — whereby the systemic arterioles are thrown too
readily into spasm (a condition such as Salis-Cohen's vaso-
motor ataxia) by contingencies, mechanical, dyspeptic, or toxic
(tobacco, etc.). Dr. William Russell, of Edinburgh, has sub-
stantially adopted this suggestion.2 These storms need not be
mortal unless the heart be somehow bad ; and the hypothesis
does not avoid the confusion between functional storm and
grave organic disease (Chap. II.). Dr. Russell does not
describe the effective mechanism, but the mechanical part
of his explanation seems to fall into the category of the
ventricular dilatation hypotheses. Sir W. Osier, who favours
the notion of vascular spasm, regarding it as " the best
explanation of anginal pain," wavers in a spirit of rather
ironic meditation between various modes in which, with one's
eyes shut, one may conceive its interferences ; whether by a
general constriction " increasing the tension of the pump walls,"
or by local (coronary) constrictions " disturbing the tension of

1 Hare, F., Med. Record of New York, Oct. 28, 1906.
2 Russell, W., Brit. Med. Journ., Feb. 10, 1906.

sec. ii VASOMOTOR HYPOTHESES 401

sections of the heart," or by " pain producing resistance to ten-
sion by the muscle elements." In respect of a labile vasomotor
centre taken alone, many of us, who have been only too familiar
with the violent vasomotor oscillations of malaria, yet have not
observed that these, or any consequent morbid susceptibility of
the vasomotor centre, have ever issued in angina pectoris. That
vasomotor constrictions, like muscular effort, chill, or any other
influence on arterial pressure, are frequently the immediate de-
terminants of the several anginal attacks, we are all agreed ; and
it is probable that, as the medullary centres are more irritated,
they become more labile, and attacks more frequent ; but in
respect of the nature of angina, these storms have no more
than an incidental importance. From the point of view of
Nothnagel's assertions concerning these vasomotor factors,
Dr. Mackenzie x has re-examined some of his own cases,
taking a large number of sphygmographic tracings, and a
few blood-pressure observations ; his results I may summarise
in these few words, that in six cases of attacks in bed
there was no sign of vasoconstriction in any one. He inferred
vasoconstriction of any great extent to be an exceptional incident.
In a case in which I was consulted by letter, an old gentleman,
subject to angina but receiving much relief from pain by rest in
bed, complained, while admitting this amelioration, of " heat
rising from the chest upwards, which renders sleep impossible.
. . . There is no rise of temperature." I guessed that irritation
arising in the aorta, less than would generate pain, might, by
setting up a vasomotor dilatation, arouse the brain which should
have slept ; so that his convalescence was retarded.

Migraine is frequently brought into comparison with angina,
and arguments used from a supposed affinity. But this is to
argue incerhim per incertius ; we know little of the pathogeny
of migraine, we do not know even the mode of the pain, and
its vasomotor conditions are very variable ; sometimes they
are constrictive, sometimes expansive, sometimes neutral, but
apparently always secondary. In Sir L. Brunton's own case
I understand that the trunk of the temporal artery is dis-
tended, as it is, enormously, during the attacks in another friend
of mine, perhaps as an effect of constriction in its distal

1 Mackenzie, Jas., Heart Disease, p. 46.

402 ANGINA PECTOKIS part ii

ramifications. An area of constriction cannot be an area of high
tension. In these parallels there is little to help us to explain
the problem of angina.

Tides of vasoconstriction seem to be frequent in tabetic
cases, not only in syphilitic angina and equivocal phases but
also in the gastric crises, etc.1 The link not infrequently noted
between tabes and angina pectoris is of course syphilis (i.e.
intercurrent syphilitic aortitis). Dr. Morison 2 thus sums up
his own experience on this point : " Peripheral vascular spasm
as a prehminary or primary event in the history of an attack in
angina pectoris is, I believe, rare. As a secondary and aggravating
event it may occur, as also may a condition of vascular laxity
due to inhibited ventricular systole." These storms then have
but an incidental importance in the problem of angina.

However, the neuralgic, neurotic and neuritic speculations on
the origin of angina cannot be all set aside as visionary. To say,
as one author says, that the pain of angina is " purely neural "
is either meaningless or a truism. Assuredly we cannot feel
pain without the assistance of nerves ; yet, as Fagge argued,
angina is too brief in its attacks, too immediately dependent on
effort, and too mortal in its effects for a mere neuralgia. Neuritis
of the vagus, no very rare event in syphilis, which has had some
occasional advocates as a cause of angina, cannot of course
hold the field long enough even to come into discussion ; with
the effects of vagus section or irritation the symptoms, save that
of death, have little in common ; and the notion or surmise that
" the angina pectoris of diabetes " (whatever this may particu-
larly be) is due to a neuritis of the vagus,3 being no more than an
unsupported and indeed improbable guess, cannot claim much
attention.

B. The Cardiac Plexus. — Some thought must now be given to
the hypothesis, not first suggested by Baumes (1808), or Gintrac in
1835, but by Wall,4 championed later byLartigue and Lancereaux,
Peter, and Romberg,5 and recently approved more or less by
Groco and Fusari,6 and by Dr. Mott,7 that irritation of this

1 Vide Heitz and Norero, Arch, des mal. du cceur, sept. 1908.

2 Morison, A., Lancet, loc. cit. p. 99.

3 Lancet, July 1904. 4 Wall. In the Med. Trans, vol. iii., 1772.
6 Lecons de clin. mid., Paris, 1880.

6 Fusari, Rev. de mid., July 1886. 7 Mott, F., Lancet, Sept. 16, 1905.

sec. ii THE CABDIAC PLEXUS 403

plexus, by tension or by inflammation, might be the source of
the pain of angina, and also of the reflex by which a healthy
heart might be menaced, and a degenerate heart stopped alto-
gether. On the evidence before us, all I have hitherto been in
a position to urge is that the most frequent lesion of angina
is a penetrating inflammation about the spring of the aorta.
Desportes, Lancereaux, Peter and others, accepting a lesion so
seated, supposed it to act by some implication and irritation
of the cardiac plexus, an opinion at first sight attractive enough.
Wall, quite in modern fashion, supposed a primary affection
of the cardiac plexus, spreading thence to the corresponding
spinal segments and beyond them ; while Desportes supposed
rather a neuralgia of the vagus. Lancereaux's first case was
published in 1864 ; 1 to reinforce it he published a second.2
The first case, in a soldier set. 45, was apparently syphilitic ; the
second, in a man set. 34, was attributed to malaria. In these
cases the plexus was involved in active proliferating inflamma-
tion of the adventitia and inwards, and I shall show that this
inflammation was indeed the cause of the angina. In his attri-
bution of angina to disease of the cardiac plexus Lancereaux is
quoted as if he had described an inflamed plexus only, but
the careful reader will find more than this ; he mentioned
disease of the aorta on its external aspect, about the spot where
the plexus lies against it. His cases were interesting ; one, as
I have suggested, was of syphilitic nature, for he describes the
well-known prominent cushion ("plaque saillante ") several
centimetres wide, composed chiefly of connective tissue of new
formation. The external coat of the aorta all around, but
especially at the level of its adhesion to the pulmonary artery,3
was the seat of " an extremely rich abnormal vascularisation,"
and filaments of the cardiac plexus were embedded in a kind of
plasma on the surface of the external coat (italics mine). The
coronary orifices were narrowed to the size of a fine probe,
but the heart as a whole was " sain." He quotes, but without
definite report of the state of the plexus, two other cases of

1 The full title of his paper is " De 1' alteration de l'aorte et du plexus cardiaque
dans l'angine de la poitrine " (Gaz. med., 1864 ; vide p. 432).

- Lancereaux, Bull, de VAcad. de Med., Nov. 19, 1864.

3 Here I may remind the reader of angina pectoris in mitral stenosis (vide
p. 443), and in pericarditis of the membrane around the great vessels (p. 457).

404 ANGINA PECTORIS part n

necropsy of angina in which the same part of the aorta was
found diseased. Vaquez, who is forced to admit with Josue
and myself that angina may depend on lesion " at the origin
of the aorta," explains it as stretching or inflaming the cardiac
plexus or its branches. Barie rather jumps at the same ex-
planation, or coquets with a " pseudo-angina " ! (p. 953 of 3rd
edition). Yet he admits the symptoms of aortitis to be the same,
and that death may ensue ! Other pathologists have declared the
cardiac plexus in cases of angina to be normal. Dr. Morison 1
has published, with careful drawings, the necropsy of a case of
angina of seven years' standing. The coronary arteries were
calcified; in a twig of the right was "an intra-vascular aneurysm,
internal to the muscular coat," and close upon it was a well-
marked ganglion cluster. The valves were normal, and the
myocardium well preserved. There is no note of the aorta.
The discovery was remarkable, but we can scarcely suppose
these ganglia to be sensory nerve organs. At present, although
Krehl says the functions of the cardiac plexus and its associated
cells, fibres and ganglia are unknown, yet most physiologists, with
Langley and Anderson,2 regard them as in function wholly motor;
and they are probably right. Recently Dogiel 3 made a minute
study of the intracardiac ganglia and of the several fibres of
the vagus, and says the intracardiac ganglia consist of motor
cells. This statement is so important that I give Dogiel's own
words : " Meiner Meinung nach mussen alle Nervenzellengruppe
gleichwoll sie im Herzen von Frosch, Hunde, oder Menschen
liegen als motorische Nervenzentren des Herzen aufgefasst
werden." He quotes Bidder and Lorit to the same effect :
" Sammtliche Ganglienzellen des Herzens physiologisch gleichartig
sind, und stellen das motorische Zentrum des Herzens dar."
Hence the motor capacity of every bit of the heart.4 Between
these and the vagus terminals there seems to be an "interference"
as in the spheres of light or sound waves. If the vagus stimulus
be prolonged the cardiac motor ganglia regain predominance,
as they do if atropine be given. At any rate it appears that

1 Morison, A., Lancet, Nov. 1902, and " Cardiac Pain," p. 23.

2 See also Koch, Med. Klinik, 1912, No. 8.

3 Dogiel, Pflugers Arch. f. Physiol. Bd. cxlii., 1911.

1 See also papers by Kauffmann in Pflugers Arch. Bde. cxlvi. and cxlvii.

sec. ii THE CARDIAC PLEXUS 405

extension of disease to the plexus is unattended by pain.1
F. Marchant and A. W. Meyer,2 make the further important
point that certain ganglion cells on the hinder and upper surface
of the auricles between the openings of the venae cavse, form a
mediate station of both vagi, whence they exercise inhibition on
all parts of the heart. How far any such lesion of the cardiac
plexus might thus be the cause of Dr. Mackenzie's defect of
contractility in angina, if such there be, is a curious enquiry
which we cannot confide to hands more skilful than his own ;
but it is a priori probable that with alterations or destructions,
complete or partial, of the cardiac plexus, there should be
associated some loss of one kind or another in the cardiac
economy, though probably on the motor side only.

As to the notions of paroxysmal neuroses, neuralgias, hyper-
esthesias, hyperkineses, and so forth, they seem to me to be
patter, too unsubstantial either for adoption or refutation ; they
are of the stuff which the author of Nightmare Abbey called
" philosophic gas." Parallels are drawn, as we know, between
angina pectoris, epilepsy, migraine, and other paroxysmal pains ;
and if Sir James Goodhart (loc. cit.) is impelled towards some such
unsubstantial view of angina it is because he is quite clear that
the cause of it does not lie in the heart. But the coincidence of
such affections with angina in the family or person, syphilitic
convulsions being omitted, is, so far as my experience
and reading go, no higher than the mean ; and resemblances
in the salient features are surely superficial. Angina is
paroxysmal it is true, so is whooping-cough ; but its inter-
mittences probably depend more upon mechanical than on
nervous variables, and to a great extent can by mechanical
means be controlled. The vasomotor fringe in all of them
may, probably would, present similar characters ; but of such are
not the deeper affinities on which we shall found classifications.

That a disease comparatively speaking so rare and so peculiar
as angina pectoris should depend upon a perversion so ordinary,
and in its nature so fluctuating, as a retention of uric acid or
other waste, or of some chronically irritating poison in the myo-
cardium, or, as others suppose, poisoning the cardiac plexus, is

1 See Stienon of Brussels, Arch, des mal. du cceur, septembre 1910.
2 Marchant and Meyer, Pfliigers Arch. Bd. cxlv., 1912.

406 ANGINA PECTOEIS part n

but guessing and seems improbable. " Ptomaines from the
bowel " would probably reduce arterial pressures.

To Dr. Verdon's x argument that the origin of angina lies in
the stomach, I have alluded (p. 344), and shall return to it
in the section on treatment. That a windy stomach may
aggravate and even determine a seizure, or death, is common
experience, and therapeutically important ; but this is not the
root of the matter. Like the vasomotor phenomena, this is but
an incident, an incident common to angina and many cardiac
affections. And to compare the fixation of the chest and
diaphragm in angina with that position in vomiting certainly
does not go beyond analogy. He describes a case in which
after a meal a full stomach would not cause an attack until
the patient began to move about. Notwithstanding, Dr.
Verdon has done good service by his emphasis on the gastric
factor in angina ; and, by his boldness in passing the stomach
tube — a perilous procedure with an over -sensitive vagus ? —
has shown not only how gastric colic may start an attack but
how by relief of the stomach it may be dispersed.

The Author's Interpretation. — Angina and Aortitis. —
Hitherto, in the destructive part of this essay, I have found little
difficulty. Some of the competing hypotheses were mutually
destructive, others were inherently perishable. Ipsae periere
ruinae. But now that I have to address myself to construction, I
have myself to give hostages to fortune. In the midst of a tangle
of prepossessions and incompatible or contradictory notions, let us
try to see what nature is displaying to us, and displaying in vain.
It is sure to be dark if we shut our eyes. From what has gone
before we comprehend that angina is frequently associated with
cardiac and other complications which confuse our vision of
the disease in its essential form ; but it is at least as true
of angina as of other diseases, as indeed it is true for all
scientific investigation, that if we desire to get a clear view of
a problem we must, in the first place, select instances as free
as possible from contingent interference. If we are to inter-
pret angina pectoris we must begin our lesson, not with those
records which are over-written, interpolated, or corrupted, but,
1 Verdon, W., Lancet, June 18, 1910, and other papers.

sec. ii ANGINA AND AORTITIS 407

as again in other scientific investigations, per viam exclusionis,
with the simplest instances. Now has this rule been observed ?
Have not authors, on the contrary, sought their test cases, even
by preference, from amongst those complicated with cardiac dis-
ease of one kind or another ? One eminent physician, by way
of a ready entrance upon his enquiry, at the outset put down
" coronary atheroma, myocardial degeneration, aortic disease,
aneurysm, high arterial pressure," and a few more dilapidations,
as parts of his problem ! Involved in such complexities, how
can we see our way to separate the invariable from the inci-
dental antecedents and associations of the process ? To
advance then per viam exclusionis, we shall, on the contrary,
collect from examples of the disease, typical in their clinical
aspect, those in which the pathological conditions, precedent
and associated, were not the most but the least complex ; so
that, if possible, a common denominator may be found. Now
the simplest forms of angina are those which arise — usually from
infections — in persons young enough to be presumably free
from primary cardiac defects. And of these instances there are
a plenty, including data from necropsy, on which to found a
solid hypothesis. I have cited many of them, and many more
can be selected.

I repeat then that for proof, as for disproof, we must rely on
cases selected for simplicity ; cases stripped, so far as may be, of
accretions. Even death is not an essential but an incidental
issue of angina pectoris. If, in the many cases of relative
simplicity whose nature has been happily veiled by convalescence
from our scrutiny, we cannot give a demonstration of the
pathological focus, yet in life or in death the clinical series
is usually unmistakable enough for the discerning physician
who will but use his eyes and forget his prepossessions. He
will convince himself that a disease which not infrequently
passes away, especially in young persons, cannot have its
primary seat in an irreparable lesion of vital parts — such,
for example, as obliterative disease of the coronary arteries
or myocardial decay. Its causes must be compatible with at
least relative recovery, and yet be such as may prove swiftly
mortal. Now in an inflammatory or subinnammatory lesion
occupying the suprasigmoid portion of the aorta, with its

408 ANGINA PECTOEIS part ii

investment, these conditions are fulfilled. Suprasigmoid syphilis
is the most instructive process of the kind which may be ac-
companied by angina. In this infection we find an infiltration of
the coats of the vessel, usually extending, in anginous cases, from
the adventitia (see Aortitis, p. 183). On the inner surface
we may see a cushion-like elevation of the wall, often of more
or less annular disposition ; this, if untreated, will soon extend
downwards to the coronary mouths and to the valve, producing
perilous or incurable mischief. The older the patient, or the
more this kind of damage, especially in the coronary area, the
more probable is sudden death ; the less able is the heart to
withstand a sharp inhibition.

Arterial Pain. — On cardiac pain, whether myocardial in seat
or not, I have dwelt at length (p. 387), and have argued that in
character it is not anginal. Dr. James Mackenzie, expressing the
common opinion, says 1 " the heart muscle could give rise to pain
just as much as any other muscle in the body " — and of such is
angina. Well, instead of speculating on what could be, let us con-
centrate our observation upon what we know. Ridding our minds
then of " could be," and fixing our eyes upon what is, we may
perceive that there is one principal spot, lesion of which is
ordinarily, if not exclusively, found in angina. The spot is the
ascending aorta, especially the spring of the arch a little above the
valve. This susceptible spot was first indicated by Morgagni who,
on a typical case of angina, probably syphilitic, in a woman aged
42, says of the necropsy that the arch of the aorta was diseased
and dilated, and acutely reflects " satis causarum in aortae
vitiis habemus." The observation next in time of which I have
a note is by Wall 2 who, in the necropsy of one of his cases,
demonstrated a lesion at the origin of the aorta above the valve,
and this lesion, taken it is true with disease of the aortic valve
also present, he considered to be a sufficient cause of the angina.
After him, as we shall see (p. 427), Corrigan made a similar ob-
servation, and arrived, independently, at the same conclusion.
But, it may be urged, is the aorta, are arteries, capable of
pain ? The answer is certainly in the affirmative ; and not in
respect of an inflamed vessel only ; though somewhat similar

1 Mackenzie, Jas., Lancet, March 21, 1908, p. 856.
- "Wall, Med. Trans, vol. iii. p. 12. Case XVI.

sec. ii ARTERIAL PAIN 409

dense fibrous structures, such as a sinew, may in inflamma-
tion give rise to exquisite pain. The throbbing of a healthy-
artery, especially of the aorta, when so far relaxed as to expose
its investment to the full force of the beat, becomes, as many
a nervous orator knows, vexing or even painful. If it is
true that arteries, like viscera or sinews, may, if not stretched,
be pricked, cut, or tied without pain, yet in thrombosis, or at the
moment of an embolism, an artery may be intensely painful,
and during the consequent inflammation be exquisitely tender
to pressure. A graphic story is told by Pierce of Bath of
an arterial embolism in the Rev. R. P., who came to Bath in
May 1684. While " very healthful, lusty, and strong, an
intolerable pain seized him on a suddain in the calf of one of
his legs, in so much that, hearing no gun go off, he had thought
that somebody had shot him with a crossbow. . . . the acuteness
of the pain made him sweat and faint, and very sick at stomach."
I read lately of a case in which embolism of the femoral artery
caused a screaming agony ; and a few years ago I heard of a
popliteal case in a cricketer, who turned angrily round to see who
had struck him, and seeing no one very near him was amazed.
The probability is that the pain in these cases is due to stretching
of the outer investment of the vessel above the plug. Balfour
speaks of " those atrocious pains which attend compression of
an artery for aneurysm." In a case, reported by Dr. Bell, of
sudden thrombosis of the abdominal aorta followed in a few days
by paraplegia and death, the first symptom was a sudden and
intense pain in the abdomen and back. The paralysis promptly
followed. For a fuller consideration of such accidents I would
refer to a discussion, " Uber Gejassschmerzen" at the K. K.
Gesellschaft d. Arzte in Wien, 1893, published in the Wiener
klin. Wochenschr., Nos. 46 and 47 of the same year ; and to
cases vividly narrated in Osier's Lumleian Lectures. The
aortic lesion, if angina is to spring from it, must in my opinion
penetrate to a certain depth, or begin on the outward side,
and be, one might suppose, at least of subacute activity,
though, as with fibrous adhesions elsewhere — as about a
joint — the part thus stiffened or adherent may, after the sub-
sidence of inflammation, remain sharply sensitive to tension.
That aortitis, without any cardiac or cardiovascular lesion, can

410 ANGINA PECTOEIS part n

and does set up anginous pain is now denied by none but those
hardy advocates who, against the evidence of fully typical clinical
symptoms, not only withhold this name, but, if it be adverse to
their own postulates, scout the evidence of these parts laid bare
at a necropsy. Jean Heitz admits that chronic aortitis may
produce severe retrosternal pain, and also the peculiar dread,
yet not only declines to call this angina, but warns the
reader against the use in " coronary angina " of baths which
he does recommend for the aortitis. As he prudently avoids
differential criterions he puts the doctor in an awkward
dilemma. Baumler lets himself go so far as to say (incidentally
in a recent paper) that angina pectoris may arise either from
disease of the coronary arteries or of the root of the aorta
(" Aortenwurzel ") ; but a well-known scientific canon constrains
us to think not how little a particular cause can be made to
explain but how much, and to mistrust a multiplicity of causes.
Still, it is demurred, aortitis, or at any rate atheroma, does
not always produce angina, and when it does the reason is
that in the suprasigmoid area the lesion is very apt to
encroach upon the coronary arteries ; whence the angina.
With the part of these vessels in the matter I have dealt
sufficiently (pp. 353-381). As regards the aorta, this first portion
seems to be the most sensitive (p. 416), and the lesion may
break into angina when it penetrates to a certain depth ; down,
as I suggest, to the outer fibrous investment of the vessel. If
Thoma be right in his belief that he had found Pacinian
corpuscles in the walls of the arteries (p. 418), the mechanics
of pain in these structures become clearer to us. We have
remarked that in any part of the body tension of fibrous struc-
tures, such as the periosteal or fascial, is a potent cause of pain ;
a more efficient cause than the tension of muscular structures.
In skeletal muscle cramp gives pain of this kind because it tells
upon the fibrous elements and tendons with their well-known
sensitive end-organs ; but of cramp, as we have seen, the heart
is incapable. So in angina, tension is probably the mechanism ;
and from this point of view we may regard the ascending
aorta as the tendon of the heart. An inflammatory infiltration
may hurt after the manner of a small suppuration within or
beneath a fibrous band, and a succession of deposits or "poussees"

sec. ii CARDIO-ARTERIAL AFFERENTS 411

may bring about several series of attacks ; in acute aortitis this
may be the mode of the seizures. But in the long reiterated
attacks of chronic cases we may have to do rather with the
element of sprain, or morbid tension ; I compare it again with
the drag of adhesions so familiar to us as a cause of pain on
the movement of a joint once inflamed and subsequently tied
by adhesions. Yet what is an old ankle sprain to a sprain of
an aorta, which is not only an arch upon which life is sup-
ported, but also a bearing which is never out of action, a limb
which can never know a moment's rest upon the sofa ! But
here, in order to carry the reader with me to this new point
of view, I must be permitted to make a digression.

This digression is to examine briefly what is known of the physio-
logy of the cardio-arterial afferents ; unfortunately, in contrast
with our knowledge of surface afferents, our knowledge of deep
afferents is slight. In this difficult enquiry I have been happy
enough to obtain the aid of Dr. Hugh Anderson. After the
reading of a paper by myself at the Cambridge Physiological
Club on February 10, 1909, it appeared that, by the clinical
path, I had been approaching certain views which Dr. Anderson
had already attained from the approaches of physiology. What
these are I will try with his assistance to indicate ; but it must
be understood that he is not responsible for my imperfect
description.

Afferent machinery is that which carries impressions from the
surface to an equilibrating centre ; it is an informing in mediate
contact with a distributing system. An afferent unit then is
an outward cell connected by a conductor with such a centre ;
and an abstract diagram of such a system may be expressed
as a sphere coated with sensitive cells attached to a corre-
sponding number of radial fibres converging to a central office.
But this diagram expresses perception only, an apparatus
which effects nothing. For action, that is for meeting the
readjustments, limbs are necessary, and the uniform sphere has
no limbs. For external limbs the sphere must be reformed ;
extended here and there, and shaped to various instruments :
and on the whole the mechanical instruments will be outside,
those of the generation of energy within, though not altogether ;
for instance, the valves of the heart are mechanical limbs yet are

VOL. II 2d

412 ANGINA PECTOEIS part n

within. To make such limbs then, and to arrange that the large
and various parts concerned with adaptations shall lie towards
the world, while those concerned with the generation of energy
shall be stowed within, the outward coat of our sphere must be
drawn out, and tucked in, on as many different ways. As the
animal series develops, continually new and new extrusions and
intrusions must be made for this packing of certain parts inside,
and for room and play to the parts which are to be without.

Now with the outward limbs and their efferent conducting
threads we have not to do ; we are at present concerned only with
those packed inwards, and of these especially with the heart and
great vessels ; parts in their origin diverticula from the digestive
tube, and therefore to be packed inside. Speaking generally,
with every extension of outward limbs — such as arms and
legs — there must have been some corresponding inward move-
ment of the vessels, as of the other organs of vegetative life.
A conspicuous example of this dragging of parts away and
together is seen in the tangle of fibres known to us as the brachial
plexus, a perplexity caused by the dragging outwards of the
upper limb and of these, and other, strands with them. Thus,
to return to our abstract sphere, for every extension of the
surface outwards some corresponding area of it dives inwards.

Now we remember that a large parcel of our sphere con-
sisted of sensory units, each unit being a cell of the surface
attached below to a conducting centripetal fibre ; when there-
fore a sector of the sphere is drawn inwards we shall see with the
eye of the mind that each unit thus affected must be dragged,
cell and fibre, inwards ; and, as the packing in and growing out
become more and more elaborate, we shall find our afferent
units penetrating in and in, carried farther and farther into the
interstices, more and more intricated with other shifting and
crowding parts and strands, until in their disguise we utterly lose
sight of their migrations and origin.

If then we are to recognise those afferent units which have
thus been shifted and hidden within, we must try to track them
in these modifications ; either by dissection or by embryological
methods, or by both together. We must look for a sometime
surface cell, derivatively a cell of the cutaneous system, attached
to a conducting fibre. Now Dr. Anderson has pointed out that

sec. ii CAKDIO-AKTEKIAL AFFERENTS 413

such units, masked as they may be by change of place and
fashion, are to be discovered. The "touch corpuscles" described
by Pacini, and by Vater, or indeed by Malpighi a hundred years
earlier, are endowments of the skin itself as we know it — the
integument still external. But their successors perceived that like
bodies are to be found far below the skin, namely in the tendons
and many other places ; and that each of these sensory end-organs
is a part of a compound unit of the kind we have been con-
templating ; namely, a nest of cells each with its centripetal twig.
Moreover, embedded in the midst of the body, the same apparatus
may be detected even in its unit form, namely, as a single cell
and twig ; and between this unitary form and the enclosed complex
of Vater, many intermediate and not a few transitional forms may
be observed. Now, from what has gone before, we shall anticipate
that these apparatus also, whether in unit or compound form, will
always be associated with the prolongations of connective fibre
to be regarded, both ideally and practically, as processes of the
skin sweeping and twisting, however far inwards, with the in-
packing of the viscera to which they are attached. In this
sense then all sensation, inside and outside, is skin sensation,
and is still of the same nature and mechanism. Conversely, no
part which is not originally of the skin can feel.

Once more ; by the work of Head, Mackenzie and others, we
know how manifold is cutaneous sensibility, as in the kinds of
touch, in temperature, superficiality, depth, and so on ; differen-
tiations which have been developed with the different experiences
of the skin in its many wanderings and exposures. Leaving
on one side epicritical and other qualities belonging to sur-
face as surface, if we follow the processes of the skin into the
tucks which we have been pursuing inwardly, we shall find
that they have dropped, or never become possessed of, the
sensory qualities correlated with surface experience ; their at-
tributes are more rudimentary, and as a matter of fact may be
confined to sense of tone and pain, the one being normal, the
other abnormal. Tone and pain in this use are probably but
degrees of the same quality ; pull, for instance, being the means
of those marvellous harmonies of muscular use so fascinatingly
illustrated for us by Professor Sherrington ; pain being illus-
trated by the same function in excess, as in muscular cramp.

414 ANGINA PECTOEIS pakt n

When within our bodies all organs are moving in harmony, and
so all the pulls balanced, we feel well ; when their functions
are not all in equilibrium the tensions here or there are unequal,
and we feel these discords of pull or squeeze, from slight uneasi-
ness to intolerable agony. Dr. Hertz, in his Goulstonian Lectures
of 1911, made this true and pregnant remark, " I believe that
tension is the only cause of true visceral pain." And, conversely,
wheresoever these pulls and squeezes generate vibrations such
that they are carried to the sensorium, there, even in remote
recesses, the afferent quasi-cutaneous end-organs and their con-
ductors, mediate or immediate, will be found.

Now is this sketch, curt as it had to be, sufficient to place
us at the right point of view to understand how in fact the
heart and great vessels may behave themselves in respect of
sensation and pain ? We have seen that our knowledge of the
deep afferents of these organs is defective, and our opinions
are rather anticipations than knowledge. But with some
certainty we may say that the investments of the heart and
arteries are involutions of the skin, are indeed subcutaneous
structures ; in them therefore, so long as and wheresoever the
need for afferent currents exists, we may assume that the
machinery has not fallen into an atrophy, and will moreover be
of the same general form as in the skin of other parts ; that we
shall find in or about these investments the cells and afferent
fibres, whether single or compound, to which we have alluded
as end-organs, or under the name of Vater or Pacini bodies.
That the need for such afferent impressions does still exist in
these organs, in the heart and arteries for instance in order
that the fluctuations of tension within them may be regulated,
is beyond doubt. The pulmonary circulation is not subject to
very large fluctuations, and on this side of the heart we should
not expect that the afferent mechanism would be very evident ;
it is on the systemic side that we should expect them to be chiefly
manifest and, on this side, particularly at the spots where
tension is most liable to become strain ; namely at the trans-
ference of tension into velocity at the issue from the heart into
the aorta. Here degrees of resistance to the initial velocity would
be of the greatest importance to the well-being of the circulation,
and here therefore regulation most necessary. Here, that is

sec. ii CAKDIO-ARTEKIAL AFFEKENTS 415

at the entrance of the aorta, we should expect to find the most
sensitive area, and the most efficient afferent mechanism. And,
as these bodies are of cutaneous origin and seat, we should first
seek them in the investment of the ascending arch of the aorta.
As Dr. Anderson has pointed out, it is at the neck of the heart
and aorta that the indrawn skin is, as it were, " pinched into
folds." But the search for bodies of this kind in the elaborated
frame of man, or even of the child, when they have been over-
grown by the close interweaving of other structures, is very
difficult ; and we can scarcely be surprised that hitherto they
have eluded much of the search which may have been made for
them. The search must be made in the foetus, and along the
lines of animal evolution.

Bruns and Genner (Marburg) 1 have studied this sensitive area
of the aorta — the pressure tambour as I have called it, the relations
of the depressor to the heart's work, and the aorta's elasticity.
To every rise of pressure in the aorta they found the depressor
sensitive. If in animals the depressors were cut out, there was no
compensation, or but very transient, so that in its absence the
heart was readily strained.2 Now Professor Danilewsky of Cracow,3
in the course of certain researches upon revival in the mammalian
heart, found an application of the electrodes to the root of the
aorta to be followed by arrest of the beats ; therefore this part
has been called the " heart-knot." If, during an electro-cardial
tracing, this part be pierced, the auricular contraction may cease ;
then, as the animal dies, the ventricular contractions wane and
the intervals between them increase. I need not insist upon the
importance of these facts in respect of my hypothesis of angina
pectoris. Again, Keith and Ivy Mackenzie 4 allude to the
" abundance of the nerve supply to the sinuses of Valsalva at
the commencement of the aorta and round the auriculo-ven-
tricular orifices, which they regard as end-stations for sensory

1 Bruns u. Genner, Deutsche med. Wochenschr., Nov. 17, 1910.

2 One curious result of cutting the depressor I may record, though in the
text irrelevant ; namely, that Gigou and Ludwig, and again Bruns, found that
after a while the heart hypertrophies. See for both articles, Arch. f. exp. Path,
u. Pharm. vol. lxix., 1912. Bittor had said (" Blutdr. u. Herzhypert. bei
Aortenskl.," Munch, med. Wochenschr., 1907) that in man suspension of
depressor action was hard to verify, because the heart worked up to it.

3 Danilewsky, Arch, fur Physiologic, 1905, Suppl. Bd. p. 190.

4 Keith and Ivy Mackenzie, Lancet, Jan. 7, 8, 1910.

416 ANGINA PECTOEIS pakt n

reflexes." It is not unlikely that what I may call the angini-
ferous area, though here most sensitive, is not strictly limited to
this part, but may extend along the arch beyond the origin of the
great vessels, and even to the abdominal aorta and cceliac axis.
To apply the electrodes to the root of the pulmonary artery pro-
duced, in Danilewsky's experiment, not an inhibitory but an
augmentor effect. Thus if it be true that angina may originate
in the pulmonary artery (p. 301), we may suppose that no case
on this circuit would, as angina, prove mortal.

This much then we can say, with some certainty, and on
other evidence contained in more than one part of this
chapter, that, whatever the mechanism at the neck of the heart
and aorta, here is a knot of exalted sensibility to tension.
It is my position that angina pectoris consists in a morbid
exaltation of this sensibility to tension, felt in the majority of
cases at this spot, or more or less onwards in the vessel,
rather than in the heart itself ; and that according to
homology the mechanism for this irritation should be seated not
so much in the inner coat of the aorta as in its quasi-cutaneous
investment. By this mechanism every wave of tension should
be propagated and distributed according to its indications,
so that pressures in excess and in defect may be equalised
or compensated. It would appear that, however large, these
fluctuations — and in vigorous bodily exercises we know that
they may be very large — are normally thus redistributed without
troubling the sensorium ; the balance is automatic. It is when
by disease the receptive surface is made abnormally sensitive
that these stimuli force their way, as pain, to the sensorium.
Happily the sensorium does not usually become well aware of
excessive tensions, say of Bright' s disease or of aortic regurgita-
tion, so long as the investment of the vessel remains normal ;
but if the investment of the ascending aorta — and perhaps of
more extensive areas of the compound cardio -arterial vessel — be
by some morbid cause thrown into a hypersensitive state, then
we receive, as it were, heated reports of blood-pressures, and
tension darts into pain, pain which in the coverings of other
viscera, in pleura, meninges, peritoneum and so forth, we know
only too well may be grievous, but which, when arising in the
citadel of life, is terrific. And, for multiplication of the pain,

sec. ii CAKDIO-ARTEKIAL AFFEEENTS 417

when the corresponding sensory centres, and centres again
above and beyond these, by accumulation of stresses have
reached a certain level of tension, any small additional
stimulus suffices to overthrow equilibrium. Hence the
importance in the treatment of angina of a period of complete
rest long enough to calm this central lability. When by the
assault the patient is dismayed, the efferent nerves of the
heart, receiving this false impression, may, as in labyrinthine
disturbances, act with a readjustment as false, but from
the nature of the case with far more serious consequences. If
the action of the heart be unduly augmented no great harm may
ensue, good perchance ; what does matter is the awakening of
the inhibitory efferent, which, as we shall see in another section,
by an over-protective action only too often, in saving the part,
sacrifices the whole.

Unfortunately when from these general considerations we
pass on, still relying upon Dr. Anderson, to apply our anatomical
knowledge of these nerves, we realise how defective this is.
We have reason to believe that afferent fibres pass from the
heart by way of the vagus, and that the depressor branch plays
a specially important part in the co-ordination of the intracardiac
and systemic blood pressures. We know that the cardiac
branches of the stellate ganglion contain afferent fibres, and we
may reasonably suppose that most or all of them are passing
from the heart to the spinal cord by way of the upper thoracic
nerves. Further, Luschka and other anatomists have shown
that the phrenic nerve is connected with the lower ganglia of the
cervical sympathetic and also gives off branches to the great
vessels and to the pericardium.1

But, as I have said, about the distribution and mode of ending
of these nerves there is much doubt. Smirnow,2 who has investi-
gated the sensory endings in the heart by the methylene blue
method, says that many sensory fibres end in the endothelium ;
but that many others end freely as brushes of fibres in the con-
nective tissues. He has also examined the nerves of the heart
after previous section of the vagus, or depressor, and has been
led by such observations to the conclusion that some of the free

1 See also Leonard Kidd's researches on the phrenic nerve (loc. cit.).
2 Smirnow, Anat. Anzeig. Bd. x.

418 ANGINA PECTOEIS part n

endings in the heart are connected with depressor fibres. On
the other hand, Koster and Tschermak,1 using Marchi's
method for tracing the fibres degenerated after section of the
depressor nerve, say that this nerve is distributed to the aorta
and does not enter the heart. Neither Smirnow nor Koster
and Tschermak describe end-organs in the heart itself, and
we do not know in what way the phrenic branch to the great
vessels ends ; but we have noted that Thoma 2 described
Pacinian corpuscles upon the thoracic aorta and other vessels ;
and Rauber 3 found these bodies in man upon a branch of
the phrenic nerve between the pleura and pericardium on the
left side (see p. 454 on pericardial angina). Dogiel reports
that his pupil Schemetkin discovered " sensibler Plattchen "
in the adventitia and other parts of the aorta ; and Stadler
reports these bodies in both the thoracic and abdominal aorta.
More recently Manouelian,4 who accepts my hypothesis, has
demonstrated, in dogs, sensory end-organs on nerve-fibres amid
the elastic muscular and connective tissues of the aorta, whereby

1 G. Koster and A. Tschermak, Archivf. Anat. u. Phys., 1902 (Anat. Supp.).

2 Thoma, Virchows Archiv, Bd. xciii. p. 100, and Bd. xcv. p. 335, writes :
"Another very interesting element in the structural elements of the
adventitia are the Pacini or Vater corpuscles. Their very frequent occurrence
in the parts about the aorta (as also in the mesentery and elsewhere) is well
known. I have been able to discover them not only in adults but also in
children, and in the foetus in large numbers, in the outer layers of the ad-
ventitia of this portion of the aorta and in the connective tissue layers
immediately contiguous. They are seated for instance on the anterior surface
of the aorta, and very thickly in the neighbourhood of the origin of the cceliac
axis and of the mesenteric artery, as also in other vascular areas." When
this article was written Thoma had not traced them in the thoracic
aorta ; but in the following year {vide ibid. Bd. xcv., 1884, p. 335 note)
he reported that, besides the parts of the arteries mentioned in the previous
article, he had discovered the Pacinian bodies " in the thoracic aorta also "
(and in the subclavian and some other arteries).

3 Rauber, Untersuchungen ii. d. Vorkommen und Bedeutung der Vater 'schen
Korper, Miinchen, 1867, p. 4. " As with the skin over the surface so a papillary
sense-membrane ("eine papillose Gefuhlsmembran") extends through the depths
of the body, with manifold interruptions and recommencements, with many
offsets. This membrane must be recognised as an organ of sense." Rauber
then remarks upon the identity of the end-organs in two regions of the body
so different ; and points out that, while those on the skin are sensitive to many
outer influences, those within are adapted especially to pressure perception.
The abundance of sensory end-organs in the mesentery is familiarly known.

4 Manouelian, Acad, des Sci., 16 juin 1913 ; quoted Zentralbl. f. Herz- u. Gef.-
Krankheiten, Sept. 15, 1913; and Ann. Past, xxviii., juin 1914. See also
Hiiber, " Sensory Endings in Viscera," Journ. Comp. Neurol., 1900.

sec. ii CARDIO-ARTERIAL AFFEEENTS 419

he explains the contractions and dilatations of the vessel. And
I see that Bechterew (p. 247) assumes their presence.

It may be well however, before discussing the pains associated
with disease of the heart, to consider what the meaning of the
" free-endings " in the heart may be.

Dr. Franklin Evans, in his minute description of nerve
end-bulbs in the joints,1 says that these are often intimately
connected with the small arteries of the part — in the adventitia ;
and occasional encapsulated bulbs of arborescent endings are
applied to one side of the vessel, parallel to the stream.

In the more primitive forms of animals all the afferent nerves
are connected with sensory epithelium on the surface, after the
diagrammatic type already imagined ; but in higher forms some
of the epithelial cells become detached from the surface epi-
thelium and, retaining their connection with afferent fibres, form
free sensory end-organs in the connective tissue. Simple forms
of such end-organs are represented in the bird by the Grandry
and Herbst corpuscles, in both of which the termination of the
sensory fibres in connection with cells may be clearly demon-
strated. The Pacinian corpuscle of the mammal is also repre-
sented in very young animals by a group of cells among which
an afferent nerve-fibre branches. But in the adult the cellular
origin of a Pacinian body can no longer be detected and the
nerve-fibre appears to branch " freely " in the core of the cor-
puscle. Further, the sensory nerves of the muscle-spindle or
tendon-organ, as shown by Howell and others, appear in the
adult to end freely in knobs upon the muscle-fibres or tendon-
bundles ; but a study of these organs during early development
again points to a termination of the afferent nerves in cells upon
the muscle-fibres or upon the tendon- organs. It seems not
improbable, therefore, that the so-called " free-endings " found
in the connective tissue of the heart may originally have developed
in connection with epithelial cells which have afterwards been
so far altered as to become indistinguishable ; and it is interesting
to notice that Smirnow mentions special endings in the chordae
tendinese resembling those found in the tendons of the amphibia.

If the views here put forward (Dr. Anderson's) be correct, we
must regard not only the Pacinian corpuscles on the vessels but
1 Evans, F., Thesis for M.D., Cambridge University, May 29, 1912.

420 ANGINA PECTOEIS pakt n

also the free-endings in the heart as sense-organs of epithelial
origin. But, whether this view of the origin of the free-
endings be accepted or not, it is important to recall to mind
that we have no histological evidence of any direct connection
of sensory nerves with the muscle of the heart or of the
vessels. / would urge then that any pain caused by undue
distension or contraction of the heart must be assumed to arise
from the tension exerted on the connective tissue investing these
organs, and to be conveyed from the connective tissue by the nerves
that end "freely," or in end-organs, within it. Similarly we are
told, on high surgical and physiological authority, that pain in
the renal area arises from two parts only — the pelvis and the
true capsule.

Moreover, the connective tissue investments of an organ,
such as the heart, which has been displaced during the course
of development from the neck to the thoracic cavity, are derived
from more than one region, and their sense-organs, as well
as the sense-organs in the connective tissue of the thoracic
cavity, would be dragged down in the connective tissue with
the heart. Accordingly, we are not surprised to find that the
phrenic nerve, which supplies the skin in the neck, sends
branches also to the pleura and investments of the great vessels,
as well as to the diaphragm, a muscle derived from the cervical
region.

But though such sense-organs may be displaced far from the
skin from which they were originally derived, the central end of
the afferent fibre connected with each sense-organ will always
retain its central connections with associate cells in the spinal
cord, and these connections it will have in common with the
afferent fibres coming from the parent area of skin. Hence
irritation of an outlying sense-organ, say upon the phrenic nerve,
would excite the conducting group of cells common to it and to
the skin over the shoulder, an area which is supplied also by sense-
nerves arising from the same spinal roots as the phrenic nerve.

On this account, if this common path be kept in a state of
excitement by irritation of an end-organ, say on the phrenic
nerve,1 we should expect to find that slight stimulation of the area

1 I am again indebted to the paper on "The Phrenic Nerve" by Leonard
Kidd, Rev. Neurol, 1911.

sec. ii CAEDIO-AETEEIAL AFFEEENTS 421

of skin over the shoulder would give rise to an undue disturbance
in the conducting cells, and to transmission of exaggerated and
possibly painful impulses ; and, possibly, even without any
additional impulses started from the skin itself, there may be a
feeling of pain over the shoulder because the whole of the con-
ducting cells associated with that skin area had been so excited
by the impulses incessantly reaching them from an outlying
sense-organ originally derived from the skin area, that painful
impulses were started and transmitted to the brain from the
common conducting group, and in consequence were referred
by the brain to an access of painful impulses from the skin itself.
Tidy x says that in aneurysm just above the Valsalval sinus,
right shoulder pain may occur ; and Kidd has seen the same
pain in cases of aneurysm. If the aneurysm be of the transverse
arch, left shoulder pain may occur.

This is, of course, what is meant by the term referred pain,
and by the association between segmental pain in the skin and
internal organs, so ably investigated by Eoss, Mackenzie, Head
and others. In the often quoted paper of Eamstrom, although
it is true that in his summary, and therefore in all reports of the
paper, the author does not mention, and apparently does not
quite realise that, in all his experiments on manipulations of
the intestine, when afferent reactions were awakened he was
dragging on the mesentery ; whether by traction with a blunt
hook, by raising the bowels upon a pad, or otherwise. When
drag was carefully avoided, mechanical or hot or cold touch
called forth no response. It is agreed (Johnston,2 Eamstrom,
Lennander, Mackenzie 3) that the serous surfaces are themselves
insensitive, the end-organs being distributed in their investments
(areolar substructures), endowments in which the mesentery is
peculiarly rich. Eamstrom himself says that when he pulled
upon the mesentery the pain would get worse for 1-2 minutes
after the cessation of the pull, and might not subside for several
minutes. This accords with our clinical experience of angina.
Gray and Parsons 4 speak in the same way of the pain and in-

1 Quoted by Leonard Kidd (loc. cit.).

2 Johnston, Brit. Med. Journ., Sept. 11, 1907.

3 Mackenzie, Brain, vol. xvi.

4 Gray and Parsons, Arris and Gale Lect., Brit. Med. Journ., May 11,
1912.

422 ANGINA PECTOEIS paet n

hibitory effects of a drag on the mesentery, and affirm that to
handle the gut itself with a careful avoidance of any drag on the
mesentery, produces hardly any vasomotor disturbance. This
important contrast they repeat three or four times. They add
that traction on the stomach and oesophagus excites an almost
pure vagus inhibition on heart and respiration, and a fall of
pressure ; with very little vasomotor effect. Strong traction may
stop the heart. In operations on the stomach and under the
diaphragm the splanchnic system is hardly disturbed. Vagus
inhibition predominates, and this in accordance with the effects
of flatulency in cardiac disorder (see Capps and Waters, p. 478).
As Professor Keith says, " mesenteries and visceral ligaments come
into action only when the limits of normal movement are reached"

After this digression let us return to angina pectoris and
aortitis. In the severer cases of infectious aortitis the ad-
ventitia presents to the eye inflammatory swelling ; it is thick
and swollen with exudate, cell proliferation, and vascular
congestion (vide p. 158) ; while the grey translucent elevations
on the inner aspect turn later into syphilitic or atheromatous
spots and patches. No cause of angina comes more clearly
into view than syphilis, and to Wilks and Welch we owe the
description of syphilis of the aorta (and other arteries and
viscera) which has been elaborated, with scant acknowledgment
of their forerunners, by Heller and the Kiel school (Doehle,
Saathoff, etc.) (p. 170). Now syphilis attacks the adventitia,
and thence penetrates inwards as, or associated with, a " meso-
aortitis productiva." On this process, and the clinical features
of this disease so seated, I hope the able description of Dr.
Mitchell Bruce may receive the attention it merits.1

Aortitis of this kind or degree may kill by cardiac inhibition,
especially when it checks an old or diseased heart ; occasionally,
even when the heart and the coronary arteries are intact (e.g. p.
376, Case XII.), it cuts the thread. Now, after many years of
direct observation and of special search in the records, with the
exception of certain rare cardiac cases to be discussed presently,
/ have failed to discover a case of unmistakable angina in which,
whatever the disease of the coronary arteries, the aorta, on
careful examination, was demonstrated histologically to be inwardly
1 Bruce, Mitchell, Lancet, July 8, 1911, p. 72.

sec. ii ANGINA AND AORTITIS 423

and outwardly sound. The notes of the very few cases
alleged in books and essays to present such conditions are
all lacking at this crucial point ; the pathologist, being by
preconception blind to its essential importance, omits or
slurs over in the aorta the investigation he makes minutely
of other parts. In a recent public discussion Sir William Osier x
quoted a case of angina in which " nothing abnormal was
found." This case I shall consider presently (p. 439). Briefly,
the aorta (its inner surface only was mentioned, and of this
only its naked-eye appearance) was said to be smooth and free
from all disease ; but I have heard since that the appearances
were not quite negative ; that the exact words are " except
some slight atheromatous changes in the aorta." The coro-
naries at any rate were normal. Now let me turn to a parallel
case, which points a moral. At a discussion on this
subject at the Royal Society of Medicine 2 Dr. Archibald
Garrod, in combating my aortitic opinions, quoted the case of
a man, aged 40, who died suddenly in a second attack of
angina. After death pneumococcal endocarditis was found,
with recent plugging of the mouth of the right coronary artery.
So far as he could remember there was no disease of the aorta ;
therefore the angina was due to the coronary plug. But
Dr. Garrod is always careful to verify his facts ; and before
the Proceedings were published, in the month following, he wrote
to me to correct his report, saying that " the arch of the aorta
was somewhat dilated and the thoracic aorta very atheromatous " ;
a condition, at aet. 40, probably due either to the pneumococcus
or to syphilis, both of them among the causes of infectious
aortitis. Now, that coronary embolism may produce angina
pectoris I shall not deny, these cases are reserved for the moment ;
all I wish by this citation to do here is to point the moral of careful
observation and careful record. The suprasigmoid part of the
thoracic aorta, which, I repeat, is a sort of sensitive tambour to
regulate cardiac energy by the mediation of the vagus, is the most
prone to produce angina ; the lesion must be acute, subacute,
or issue in tensile adhesion ; and it must penetrate deeper than

1 Osier and Bullard, Medical News, Dec. 15-22, 1909. I have been unable
to obtain this paper.

2 Proceedings, March 13, 1908.

424 ANGINA PECTOEIS part n

ordinary atheroma usually does. To be content with a glance
at the lining only of the vessel, to belittle any patches and
streaks on its surface, sometimes perhaps to overlook even
these, and always to overlook its outer coat, is perfunctory
work. If our fathers examined bodies with less instruction,
it was with less prejudice. In T. Paytherus's case (a port wine
bibber aet. 66) Parry reports not only the state of the heart,
but adds that two inches above the aortic valve the vessel was
atheromatous and doubled in thickness. From without then
the vessel should be examined even more assiduously than from
within, for certainly a periaortitis may give rise to angina ;
here signs of acute inflammation may be found, or in a chronic
case the adventitia, especially in old syphilitic cases, may be
altered : on section the vessel, probably dilated a little, if
no more, will feel dense and gristly to the knife, and may be
adherent. Unquestionably angina occurs in many a man whose
slowly degrading vascular system one would not readily accuse
of activity in any area ; yet, as we shall see presently, I, and
others, have found that even in these slow forms of atheroma
subacute phases of local extension are not uncommon, or
adhesions may drag ; moreover angina, though not unknown in
the aged and decayed, is prevalent rather in senescence.

Of syphilitic aortitis Stadler (loc. cit.) says that one case
in five had suffered from angina, minor or major ; Josue has
accepted my views in their entirety ; and indeed our German
colleagues are now beginning to talk of schmerzhafte Aortensklerose.
Now if I consult the first handbook of medicine at my elbow,
I find among the symptoms of aortitis these : " It may consist
in a weight or oppression, or a severer distress, amounting
to intense retrosternal pain, comparable with crushing by a
red-hot iron bar ; or a vice-like constriction, often accompanied
by much tenderness or superficial hyperesthesia. There is
often also a peculiar sense of dread, as if the last moment were
come (italics mine). From thence atrocious pains may radiate
to the left arm or to the arms."

This aortitic agony Gibson contrasted with that of angina
pectoris as a continuous and not a paroxysmal pain, an opinion
in which I cannot follow him, unless the " status anginosus " of
very intense cases be described as " continuous." He added quite

sec. ii ANGINA AND AORTITIS 425

truly: "There is no considerable dyspnea, but death is often sudden.
Or again, the oppression may never proceed to these extremities,
but continue rather as an anxiety without positive fain, or may
even simulate a hysterical state of mind " (italics mine). Boinet
writes1 : "In aortitis the pain is retrosternal ... is sometimes
compared to a bar compressing the chest . . . sometimes it is
agonizing, extremely violent, piercing, atrocious, with accesses of
painful dartings to the left shoulder . . . often in the left arm,
down to the little finger. In their suddenness, their intensity,
and their gravity, these attacks resemble angina pectoris. . . .
They are sometimes followed by syncope, sudden death. An
attack of angina pectoris may be the first manifestation of acute
aortitis, especially above the aortic valve . . . when it does not
depend upon obliteration of the coronary arteries . . . which event
is observed more particularly in chronic aortitis." The attacks
resemble angina pectoris ! May we not rather ask the learned
author in what respect these attacks differ from angina pectoris ?
Brouardel himself, who had studied aortitis, acute and chronic,
chiefly from a pathogenic point of view, said of its symptoms —
that they vary with the symptoms of the disease and other con-
ditions, but that the most frequent of them is angina pectoris.
And to his opinion let me add the comment on angina of that
no less observant clinician, Broadbent, who wrote on disease
of the aorta as follows 2 : " Angina, answering to this criterion,
is met with clinically in association with aortic valvular disease,
or with aortitis, or with dilatation of the aorta general or
aneurysmal, or with atheroma of the aorta without obvious
dilatation, or with fatty degeneration of the heart . . . but all
these, except perhaps acute aortitis (italics mine), are very common
without angina. Angina is established when the coronary
arteries are implicated." Of course this last reflection had to be
brought in as a tribute to orthodox opinion ; but seeing that
the author had just admitted acute aortitis to be the one state
in which angina occurs unconditionally, and as this disease,
however disposed to implicate the coronary orifices, does not
always attain them,3 and if it does, and even blocks their mouths,

1 Boinet, in Brouardel's Traite de medecine; also Angina Pectoris, 1897.

2 Broadbent, W. H., Lancet, May 27, 1905.

3 See, e.g., Coloured Plate by Dr. Mott in Allbutt and Rolleston's System
of Medicine, 2nd ed. vol. vi. p. 568.

426 ANGINA PEOTOEIS part n

may not empty them of blood, and as coronaries are continually
blocked or choked without angina, the inference of Broadbent's
last clause seems not inevitable. The changes in the aorta
giving rise to angina — the author goes on to say, as Gibson said,
very truly — are often of a subacute degree, so obscure and
insidious as not to reveal themselves by evident symptoms.
Now these descriptions in the current text -books are found
not, as the unwary reader may suppose, under the head of
angina, or of coronary atheroma, but of aortitis ; as any one
who will turn to such works for himself may read.

It has often been objected to me that before we attribute
angina pectoris to changes in the aorta, we must explain how a
disease, comparatively speaking rare, can depend upon a morbid
process so common that few senile aortas are innocent of it. To
retort that the same objection arises in the attribution of angina
pectoris to disease of the coronary arteries, which is almost as
common, does not carry us much farther. We have to try to
discover in the one case or in the other the factor which
determines the particular issue of angina. I have suggested
that this elusive factor may be a more active phase of
aortitis, more especially of aortitis in a certain area (supra-
sigmoid), or of a certain depth of penetration ; and that
atheroma is prone to such phases of recrudescence. Bureau *
describes such phases thus : " Putting aside," he says, " cases
of primary acute aortitis, in the immense majority of cases
aortitis develops itself in aortas previously the seat of the
chronic affection — as in gout, senile degeneration, and the
like." Gibson, in his work on the Heart, expressed the same
opinion, almost in the same words. Broadbent again says
(loc. cit.), " the changes in the aorta usually begin so insidiously
and chronically, that no evidence of them can be detected till
dilatation of the vessel is discovered ; but occasionally, if the
aortitis becomes acute, it reveals itself by symptoms." Sansom 2
wrote, " ' Only atheroma,' do you say 1 Examine it, and you will
see some old and some new patches, in different stages, like an
eruption above the aortic valve . . . some old and yellow, or
calcified, or fibrous, but beside them little gelatinous patches,"

1 Bureau, " Aortites aigues," These de Paris, 1893.
2 Clin. Journ., Oct. 24, 1900.

sec. ii ANGINA AND AOETITIS 427

and so on. Indeed these exacerbations are now generally ac-
cepted by pathologists ; it is agreed that in chronic atheroma
there are subacute periods when gelatinoid patches supervene,
either in contiguous spots, or with a marginal distribution ;
patches themselves to pass likewise into " ordinary atheroma." x
Now these more active atheromatous patches, under such con-
ditions, resemble the primary acute patches of the acute infections ;
and if seated in a particular area, and penetrating to a certain
depth, they will be revealed by similar symptoms — symptoms of
the type which has received the clinical name of angina pectoris.
Marmorstein, in an article on " Des aortites grippales," 2 gives
as a chief symptom of the aortitis, " douleur avec caractere
angoissante et retrosternale." From his article I quote a case
in point :

Male, set. 50. Angina pectoris, with pulse of high pressure.
Aorta dilated to 3 cm. in the right second space, systolic murmur,
hammering second sound, apex thrusting. Died in attack.
Necropsy : dilated ascending aorta. Internal aspect swollen, and
covered with patches — some bony, others moderately hard and
yellow, others soft, grey, or reddish grey. Left ventricle enlarged.
Valves fairly normal and competent, but aortic cusps opaque.
Diagnosis : chronic aortitis with acute poussees ; one acute
gelatinous patch close to orifice of left coronary, and probably the
cause of death." (No allusion to outer aorta, no sections made of
this part.)

I may mention here that in the case of Dr. Forrest's
(p. 514) I find a note that the aortic arch, palpable in the
jugular fossa, was very tender to the touch. Her attacks were
severe and the seat of the pain mid-sternal, often darting into
both arms. This I have noticed more than once.

In the month of May 1908, six months after the delivery of
the lecture on Angina pectoris 3 which is the substance of this
essay, while reading in Sir W. Osier's library I lighted upon a
certain article by Corrigan, extracted from No. 35 of the Dublin

1 The connection of gelatiniform patches with atheroma and with syphilis
respectively is a problem for further investigation ; but it seems clear that
such patches are not peculiar to syphilis.

2 Marmorstein, Rev. de med., 10 mars 1908.

3 To a large medical audience at the Mount Vernon Rooms, Fitzroy Square,
London, under the presidency of Sir Hermann Weber.

VOL. II 2 E

428 ANGINA PECTOEIS paktii

Journal of Medical Science. This distinguished physician com-
menced his article with these words : " I have two objects in view
in these observations : first, to show that inflammation of the
lining membrane of the mouth of the aorta (author's italics) is
capable of producing the group of symptoms to which we give
the name of Angina pectoris, and is therefore entitled to a place
in the list of the causes of this formidable affection ; secondly,
to trace the pathology and treatment of aortitis." The paper is
illustrated by a coloured plate of a heart and aorta laid open,
" showing the diseased portion round the mouth of the aorta ;
the lining membrane being crimson red, turgid, and swollen out by
an effusion of lymph behind it, to the height of at least one-
eighth of an inch." (The author, unfortunately, omits to indi-
cate to which case of angina the plate belongs ; but if, as would
appear, it belongs to Case I., this was of a carpenter, set. 39, and
is obviously and very characteristically syphilitic.) In Case II.
a " gelatinous pulpy effusion under the lining membrane " occu-
pied a space above the valve for a breadth of one-half to one inch.
The valve also was invaded, and " one cusp ruptured, evidently
recently." This case also looks like one of syphilis, but the age
of the patient is not given. The heart in both these cases was
" enlarged," but no histological examination of it is reported ;
nor is the state of the coronary arteries or their orifices alluded
to. Both cases were marked during life by angina of the ordinary
description, and severe in degree ; and the aortas seem to have
resembled closely that shown by Dr. Parkes Weber at my
Fitzroy Square Lecture (p. 187), and afterwards at the Eoyal
Academy of Medicine.

Corrigan adds a chronic case in which after death extensive
disease of the aorta was found. For three years this woman,
set. 47, had complained of " what was supposed to be nervous
spasms" (italics mine) (attacks of pain stopping her while walking,
etc., etc.). On this the author writes, as again and again I have
written (p. 241) : " It is hard to resist the conclusion that had
the fits, erroneously supposed to be nervous angina, been referred
to their true cause, the inflammatory action in the mouth of the
aorta might have been arrested, and life have been saved." The
author's treatment was mainly a course of mercury, pushed
till the gums were sore, and repeated later. The success

sec. ii ANGINA AND AOETITIS 429

of this prescription in more than one instance — a common one
in those days for any kind of " inflammation " — supports the
presumption that some of his cases were syphilis.

Other cases he mentions, some with necropsies, but, either
in detail of diagnosis or of pathology, less decisive ; I need
not follow the author through arguments with some of which
I cannot agree. My purpose is to call to witness the only
modern physician who— so far as I know — had distinctly
attributed angina pectoris to disease of the aorta ; yet even
Corrigan does not attach angina definitely to disease of the
aorta as the pathological counterpart of the clinical series, but
says only that aortitis in the area in question is " capable " of
setting up these symptoms, and is " entitled to a place in the list "
of its causes. Once more I repeat the canon of scientific reasoning,
that causes are not to be multiplied praeter necessitatem.

Broadbent, in another essay,1 describing, as we shall see
presently, a case of " aneurysm at the very root of the aorta,
within the pericardial sac," comments on it thus : " that it is
not always possible to distinguish between anginal pain due to
aneurysm in this situation, and true angina." Then why be
so bent upon evading the obvious inference ? Broadbent's
endeavours to find a criterion for the distinction, such as the
course of its radiations, the degree of dread, and so forth, were
in vain ; these differences we shall all agree are no criterions.
Gibson was very bold ; he settled the matter by seizing upon
the symptoms of aortitis and handing them all over to the
heart. Of aortitis, he says, " the pain is frequently of the true
cardiac (!) type ; that is to say, it has the sternal position (!)
and the tendency to radiate" along the well-known lines.2
Another physician no less eminent is even more ingenious : he
says "the anginous crises produced by the Coronaritis blend ('se
confondent ') intimately with the painful incidents (' les accidents
douloureux,' author's italics) of aortitis " : really a delightful
apology !

The great weight of the evidence connecting angina with
the aortic area is far from being as widely recognised as it
ought to be. Austin Flint urged, as Norman Moore has done,

1 Broadbent, W. EL, St. Mary's Hospital Gazette, vol. i. No. 1, 1895.
2 Gibson, G. A., Diseases of the Heart, p. 826.

430 ANGINA PECTOEIS paetii

that " in angina pectoris, disease of the aortic orifice and of the
aorta is found more frequently than any other changes." The
following case, taken from one of Heller's papers,1 is very instruc-
tive. A man, in the course of a violent effort, broke down one
aortic cusp, and also forced out a pouch above it in the suprasigmoid
portion of the aorta (italics mine). The first, the most violent,
and the abiding symptoms were attacks of angina pectoris, the
pain radiating as usual down the left arm. These attacks beset
the patient till his death six months afterwards. Dr. Norman
Moore 2 has said, " When angina pectoris is present, even
if on a particular examination a murmur be not discovered,
disease of the aortic valve (it would be safer to say, of the aorta)
(italics mine) is almost always present." Dr. Havilland Hall,
who is not without sympathy for my hypothesis, has spoken to
the same effect as Moore, whose clear-sighted maxim is well
illustrated by the following case (from Vaquez and Bordet) :

A man of 48 returned home one morning after a rackety night,
and on lying down was seized by an atrocious attack of angina
pectoris. Face pale, and anxious ; respiration accelerated but super-
ficial. No dyspnea. The attack lasted many hours, and an acute
aortitis was diagnosed. Blood pressures were normal. Auscultation
and percussion gave no assistance, but an orthodiagram, taken a
few days later, revealed that the aorta was uniformly enlarged to a
considerable extent ; and its walls were thickened. The arch was
not raised (see p. 204). (Probably a syphilitic case. — C. A.)

Again, in his Lumleian Lectures of 1909, Dr. Norman Moore said,
" In cases of sudden death with disease of the aortic valves, the
myocardium is sometimes degenerate, but in other cases shows
muscular tissue in which degeneration has not begun " ; and pro-
ceeded to contrast clearly with angina the pain sometimes " felt
towards the apex " in mitral disease, rightly explaining that, even
if severest is more a continuous ache (vide pp. 387and 441). Noth-
nagel, confused as were his ideas of angina, nevertheless cor-
rectly made this same discrimination. Recent researches (Carey
Coombs and others) show that rheumatic inflammation begins,
not in the valve, but in the deeper structures around it. We

1 Heller, Deutsche Arch. f. Hin. Med., 1903.

2 Moore, N., " Hunterian Lecture," Oct. 10, 1900 ; reported Lancet, Oct.
20, 1900.

sec. ii ANGINA AND ANEURYSM 431

know that the a-v bridge may thus be injured (Mackenzie and
others).

Angina Pectoris and Aneurysm. — Let us tarry a while
longer to weigh some further evidence from diseases of this class.
From what has gone before, it may be asked : Now, if angina
pectoris depends upon a flaw in the thoracic aorta, is it found
that aneurysm of this part is attended, in its initiation at any
rate when it is forcing the vessel, by anginal symptoms ? The
answer is that in no inconsiderable number of such cases this is
so ; Dr. Gibson says, " in a large proportion of cases the initiatory
stage is attended with such symptoms." Sir William Osier x
says " severe attacks may occur in the early period of aortic
aneurysm " (a period, by the way, when the coronary orifices
are less likely to be occluded) ; " they were noted in the histories
of 22 out of 132 cases." That such should always be the case is not
to be expected ; the site of the aneurysm, the rate of its growth,
and other variables, determine the contingency. And weight
or oppression at the chest, though consistent with angina
pectoris, may be no warranty of it. The initiation of a thoracic
aneurysm is often latent ; or if at this period pains there be
they may be vague and wandering, or fixed and tedious, rather
than anginous in character. Boring and continuous pains are
more indicative of a later stage, a stage of pressure on neigh-
bouring parts, and of some considerable extension of an aneurysm
which in its initiation may have been silent. Thus Gairdner, in
his essays on Aneurysm, in my System (first edition) and in " Rey-
nolds'," distinguished between the pains of pressure — pains gnaw-
ing and persistent, and " paroxysmal " pains. He quoted cases
of referred pains of this kind, relating them to the districts of Head
and Mackenzie, in paragraphs which I cannot quote at length ;
but, for instance, after many years of study and enquiry he was
prepared to state that " in not a few instances in which the
diagnosis from other facts is well established, aneurysm of the
arch of the aorta leads to symptoms closely resembling typical
angina pectoris . . . with pain and numbness of the left arm
. . . extending sharply from the chest into the neck, face,
shoulders, and down one or both arms." The angina, he adds,
" may precede the discovery of aneurysm by years," and " usually
1 Osier, W., Medical Chronicle, May 1906.

432 ANGINA PECTOEIS partii

vanishes as it is established " (i.e. when the investment of the
vessel has gone under). In one of Osier's cases (loc. cit.) the
angina began in 1893, but in 1894 there were no physical signs :
six years later the angina had disappeared, but definite signs of
submanubrial aneurysm had come forward. Dr. Drummond x
has since insisted upon the same features ; and Dr. Graham
Steell, in accordance with my own interpretation, states that
angina is by no means rare in aneurysms involving the ascending
aorta.2

About five years ago, with Dr. Glasier of Mildenhall, I saw a man,
aet. 26, with angina. Patient graphically described the " grip " about
the junction of manubrium and mid-sternum, and the radiation across
the upper pectoral area to the left arm as far as the elbow. Syphilis
was strongly denied, but we suspected aneurysm. The signs were a
trifle of dulness to the right of manubrium, a systolic thrill strongest
at the base, and a simultaneous murmur following the first sound
after a brief interval. Heart distinctly hypertrophied. Arteries
too palpable for age. In spite of the hypertrophy the blood
pressures always ranged low — about 100-110. We provisionally
diagnosed aortitis and aortic stenosis; possibly a Valsalval aneurysm.
Treatment, chiefly by rest and iodide of potassium, had the effect
only of mitigating the angina. Six months later Dr. Glasier
reported to me that " he died in the night, bringing up a large
quantity of blood. I think there is little doubt that he died from
a ruptured aneurysm." Dr. Hawkins also saw this patient.

Two other recent cases in my own practice of syphilitic
aortitis, running side by side, have gone on to aortic regurgita-
tion ; in one of them aneurysm has formed without angina ; in
the other no aneurysm is discoverable, but the angina is very
definite, indeed rather prolonged and severe. Quincke 3 says
that, besides pressure pains, thoracic aneurysm " may assume all
the well-marked phenomena of angina pectoris." Trousseau, in
his chapter on angina pectoris, which he was unhappily encouraged
by Duchenne and Aran to regard as a neuralgia analogous to
trigeminal neuralgia — his reason being that in some cases he had
failed to discover any disease of the heart — described, notwith-
standing, two severe cases, cases which he himself had distin-

1 Drummond, D., Brit. Med. Journ., Jan. 13, 1908.

2 Steell, Graham, Lancet, Dec. 9, 1911.

3 Quincke, Ziemssen's Cycl., Art. "Aneurysm."

sec. ii ANGINA AND ANEUEYSM 433

guished as genuine angina, which afterwards proved to have
been initial stages of thoracic aneurysm.

A case of another kind I may quote from Dr. H. L. Dixon's
thesis for the Cambridge M.D.1 The case occurred at St.
Thomas' Hospital, under the care of Dr. Acland :

Male, set. 52. Arteries thick and tortuous ; large white kidney
and anasarca. High arterial pressure. Suddenly was seized by a
typical attack of angina pectoris — his first. This was not repeated,
but it was followed by severe continuous pain in the epigastrium,
which lasted till his death three days later. P.M. Hsemopericardium.
§ xii. One inch above the aortic valve was a transverse tear of the
inner and middle coats of the vessel. The blood had dissected its
way into the pericardial sac.

This case may be compared with the well-known record of
Morgagni on the wife of a painter in Padua, set. 40, who
suffered from " violent pains in the chest and arms." Vallis-
neri invited Morgagni to open the body ..." a little above
the semilunar valve there was a narrow ulcer." Lancisi,
in an unmistakable case of angina (" quemdam sub sterno
dolorem usque ad humerum propagatum, et pectoris angustiam"),
reports at the necropsy an aneurysm of the aorta, " sub egressu e
pericardio." Desportes made a like observation, wondering why
the disease in this place should set up angina ; the pain he
compared with that of popliteal aneurysm.

In another essay Gairdner remarks that the small aneurysm
seated near the aortic valve is the kind more frequently associated
with angina ; his words are, " Small aneurysms thus impinging
upon the heart are especially productive of angina." He says also,
" Even small aneurysms, if arising very near the heart, and
especially such as project into the pericardium or compress in
any degree the base of the heart, are much more apt to give rise
to angina-like symptoms " ; and that in the presence of anginal
symptoms the attention of physicians should be very minutely
directed to irregularities of the ascending aorta. To draw again
upon Sir William Osier's stores,2 we read, " There may be
paroxysms of pain, often simulating angina (why " simulating " ?)

1 Dixon, H. L., Act kept., Oct. 8, 1909.

2 Osier, W., Clinical Lecture (in 1901) at Johns Hopkins Hospital on
"Aneurysm of the Descending Aorta." For Rupture, see p. 207.

434 ANGINA PECTOEIS part ii

in small aneurysms at the root of the aorta ; in fact there is a
special group of cases in which angina pectoris is the initial
symptom of aneurysm of the aorta." In Dr. Mackenzie's work
on The Pulse (p. 239), the following case of angina is cited :

Male, set. 40. Tightness across the chest, and pain down
the inside of both arms, especially on exertion. Death sudden.
P.M. a small aneurysm of the aorta immediately above the aortic
valve. Both coronary arteries were healthy ; but there was some
" fatty degeneration " of the myocardium.

Once more, Breitmann,1 in a careful study of syphilis of the
arteries, says, " If, however, the aneurysm is situated near the
aortic valve, the signs may be those of the valve lesion with the
anginal syndrome " (italics mine). Now it is remarkable that
in his descriptions of myocardial syphilis with dilatation, and
of syphilis and thrombosis of the coronary arteries, Breitmann
does not allude to this " syndrome."

A distinguished physician has warned us lest if angina occur
with such an aneurysm we fall into the error of giving it its
own name ! Surely the error would be less in the bestowal
of the name than in the ignorance, too often inevitable, of the
full conditions of the diagnosis. It has been objected that in
aneurysmal angina patients do not die suddenly as in the senile
cases ; but sometimes they do : however, as a rule, aneurysm
occurs in comparatively young men with sound hearts.

Armed with quotations from authors so eminent and con-
siderable, I need not multiply witnesses to the same effect. If
here and elsewhere I am tedious, it is because only by reiteration
can I press my argument home ; with Lisette, " Je dis la meme
chose parce que c'est toujours la meme chose." It is conceded
that aneurysm of the thoracic aorta, and especially of the first
part of it, without any cardiac or coronary disease, may set up
angina pectoris ; the pain being due to the aortitis or strain
which precedes or accompanies it. If this be so, then the aorta
alone is capable of producing this malady, and in a form, to
use Gibson's words, " most typical, so that not the slightest
suspicion may be entertained of the nature of the case ; and
which means early structural change in the wall of the aorta."

1 Breitmann, Gaz. des hdp., 21 iev., 1903.

sec. ii ANGINA AND ANEUKYSM 435

If then to this rule of association of angina with aortic lesion we
find some exceptions, and some I have yet to consider, we shall
presume the variation to depend on conditions for the precision
of which we have not as yet sufficient data ; and until the atten-
tion of pathologists shall be bent to this problem, we shall not
obtain the data we need for the complete morbid anatomy of
angina. I repeat that no notes of such cases are acceptable in
which the state of the first few inches of the aorta in its whole
thickness is not accurately described as to its appearance,
the exact site of any lesion, and its histology. Such careful
reports as this of Dr. Walter Broadbent,1 from which I will
quote a few fines, are rarely to be met with (to Dr. Poynton's
I have referred already, p. 275). The patient 2 was attacked by
acute aortitis and severe angina pectoris, which ended fatally.
Dr. F. Gr. Bushnell cut sections of the aorta and heart's muscle.
" In the aorta there was a perivascular infiltration with leucocytes
round the vasa vasorum of the aortic wall, more marked in the
outer coat." In this case, as contrasted with those of Poynton,
the sections of the heart muscle (duly stained) showed a singular
absence of change, whether in striation or nuclear or other alteration
(my italics). It will be remembered that in many or most of
these cases we have to deal with degenerate, or with syphilitic
hearts ; and as in syphilis this area of the aorta is very prone to
suffer, and thus to be the seat of angina, the cluster of symp-
toms will vary. In one case of the kind indeed, besides the
sinus aneurysm, " atheroma of the aorta and coronary arteries "
is mentioned ; but aneurysms of the sinuses of Valsalva, till
revealed by their comparatively early rupture and fatal issue,
are often latent. Even Sir William Osier,3 whose researches on
this subject are of such importance as to make my incessant
liberties with his name inevitable, in emphasising, as he does,
the closure of the orifices of the coronary arteries as the chief
factor of angina, gives, in my opinion, insufficient attention to the
immediately contiguous part of the aorta. Corrigan, in one of
his cases,4 reports that " an effusion of organised lymph was found
between the fining membrane of the aorta and the fibrous coat."

1 Broadbent, Walter, Angina Pectoris, 1897.

2 Dublin Journal, vol. xii., Nov. 1837.

3 Osier, W., Lancet, May 27, 1905.

4 The case is given more fully in the chapter on Aortitis, p. 427.

436 ANGINA PECTOEIS part II

Precisely, in the very spot I have anticipated ; I ask for no
better evidence. My experience then coincides with that of Dr.
Norman Moore and others, not forgetting Nothnagel himself, who
says that, in contrast with mitral lesions, which are not attended
with anginous pain, "lesions of the aortic ring, on the other hand, are
often painful, and attacks of true angina are common, particularly
when the root of the aorta is involved " (italics mine). I could not
myself have written a passage more convincing of the general
truth of the position I have taken up in the interpretation of
this disease.

We know now that aortic valvulitis may penetrate below
and beyond the valve, and may creep so far as to impair the
neighbouring structures. Dr. Mackenzie, in conversation, de-
scribed to me a case of acute rheumatism, with aortic valvulitis
and angina, in which at the necropsy aortitis was anticipated,
but none, as I understood, was found. Probably the inner
surface only was examined, no sections made, and the invest-
ment of the vessel neglected ; I suggest that the valvulitis had
penetrated into the subjoining parts, perhaps to the pericardial
investment of the aorta. Perisigmoid as well as suprasigmoid
lesion may suffice to produce angina ; this I shall consider later.

We have it on the testimony of Broadbent, and other trusty
observers then and since, that although of course any one or
more of its characters may be absent from a particular case of
" true angina," yet in each and all of them the group is character-
istic of both angina and aortitis. Dr. Lees, at the Harveian
Society's discussion, agreed that a dilated aorta was a very im-
portant confirmatory sign of angina. I reiterate then, is it not
strange, on the general acceptance of aortitis as a cause at least
of " anginiform symptoms," that in necropsies on this disease
a careful description of the suprasigmoid aorta should have
been so frequently omitted — a neglect which in the records of
many treatises on the disease I have had again and again to
lament ? Concerning the coronary arteries, no feature, however
minute, is forgotten ; the state of the heart's muscle is most
carefully reported ; but the aorta is either overlooked altogether,
or we are put off with some such hasty phrase as " aorta athero-
matous." Some of the older authors give us better data ; for
example, of one case of typical angina pectoris, Jurine reports

sec. ii DEFECTS OF NECEOPSIES 437

that the heart was negative ; that the posterior coronary trunk
was indeed calcified in its middle length but its orifice open to
a probe (" stilet ordinaire "), and the anterior artery presented
only an atheromatous patch = 4 mm. " But," he proceeds, " the
base of the aortic cusps was of a cartilaginous consistence."
In one of Jenner's cases the coronary arteries were diseased,
but so also were the coats of the aorta ; for two inches
above the sigmoid valves they were doubled in thickness and
studded with white patches. Exemplary instances of a more
scientific examination of the parts are of two cases I have already
quoted, one by Dr. Poynton, who leans to my view of angina,1
and one by Dr. Walter Broadbent ; in these cases sections of the
aorta were made. In No. 1, F. set. 38 (the "true case of angina"
of Cheadle) (vide p. 275), the sections of the ascending arch showed
extensive patches of acute inflammation. The intima was raised
and pinkish, some translucent patches and a few small areas of
atheroma were appearing ; microscopically the usual infiltrating
proliferative characters were seen, especially around the vasa
vasorum ; fibrous tissues swollen. In his second case the same
minute examination of the aorta was made, and a similar state
was found. I have alluded to the-' morbid sensitiveness of
adhesions, well exemplified in inflammatory affections about
the joints, but about the aorta I find but one description of
this condition, nay, but one reference to it, this was by Hirtz
and Braun.2 In three cases of " classical " angina (syphilitic
aorta) these pathologists described dense adhesions about the
aorta, binding it to neighbouring organs.

M. Huchard's collection of necropsies, laborious as it is, fails
of its full value, by no fault of his, from this imperfection of the
pathological records, especially in respect of the suprasigmoid
aorta. Although Huchard was possessed by the coronary idea,
we do owe him the service of laying the ghost of " pseudo-
angina " ; as this bubble went on bubbling it was well that an
enterprising controversialist was ready thus to prick it again.

Even in records of cardiac syphilis precise note of the
suprasigmoid aorta is often lacking ; yet, as we have seen,
in these cases angina pectoris is far from uncommon, and is

1 Poynton, Heart Disease, 1907, p. 241.
2 Hirtz and Braun, Soc. mid. des hop., 31 mars 1911.

438 ANGINA PECTORIS partii

fairly amenable to specific remedies. In these cases of angina,
if mortal, and a necropsy obtained, as in Dr. Parkes Weber's
case x (vide p. 264), suprasigmoid aortitis is found, with or
without coronary occlusion, but generally with it ; as this is
a chief factor, not of angina, but of death in angina. In-
deed angina pectoris in middle or early middle life is so
frequently syphilitic that this probability should be uppermost
in the mind of the physician, so that by prompt and vigorous
specific treatment not only may the angina be cured, but also
destruction of the aortic valve prevented. Some of these cases
of aortitis, assuredly syphilitic, progress destructively in spite
of specific treatment, but this is nearly always established too
late. A certain case reported by Broadbent (loc. tit.), which
ended more fortunately, was probably of this nature :

Male, aet. 50, angina pains, never very severe. Next a systolic
aortic murmur appeared, and the pulse, sometimes small and weak,
sometimes large and lax, fell in number — to 60 and 54 (pressure
upon or invasion of the auriculo-ventricular bundle ? — C. A.) ; then
came a soft diastolic murmur, not always audible, which at length
disappeared. In six months all symptoms subsided, leaving the
systolic murmur and a parchment-like second (aortic) sound.

Dr. Bruce Porter, of Windsor,2 has described a characteristic
case of the kind which he rightly diagnosed as "an acute
aortitis" issuing in injury to the aortic valve. The patient was ex-
tremely ill, suffering from " anginal attacks." Maximum systolic
pressure about 200. Kept going by morphia and atropin and
nitroglycerine, which had to be increased to ^-^ every hour,
and the morphia to \\ gr. in 24 hours, for " only thus was the
pain in the aorta kept at bay." The physical signs were those of
" general dilatation of the aorta," then of aortic regurgitation,
and ultimately of mitral insufficiency. . . . The patient at date
of report was recovering, having had only three anginal attacks
in the last five months. (No history of syphilis was to be obtained,
but it is difficult to attribute it to any other cause.)

I deferred the discussion of the only case on record —
so far as I know — of angina apparently genuine, and mortal
moreover, in which after death no lesion was found, aortic or

1 Reported to the Royal Acad. Med. in March 1908.
2 Porter, Bruce, Brit. Med. Journ., Nov. 21, 1903.

sec. ii DEFECTS OF NECKOPSIES 439

other (Osier and Bullard) (vide p. 423) ; this case, as reported,
stands against every hypothesis of the disease. I have tried to
get a copy of the original paper,1 but none is to be had.
I take the account, therefore, from Osier's Lumleian Lectures.2
M., set. 26 : "a heavy smoker," and athletic. The pain is
described as " in the heart " ; which is not typical, at any rate
in terms. He had an enormous number of attacks during the
year and a half before his death. It is said that after death
nothing was discovered ; that every part of the heart and its
appurtenances were normal, or practically normal. Now as yet
this case stands alone, it stands without corroboration. Some
fallacy in diagnosis or autopsy there may have been, for the
record is contrary not only to every one of the multifarious
conceptions of angina, but likewise to all clinical experience of
the disease. No young man dies of nothing at all ; in every
death there is lesion or poison. That the man was a heavy
smoker was noted as important ; any one who has seen a bad
case of tobacco angina can guess that it might prove mortal ;
though I have never seen nor read of such a case, with adequate
pathological record. Against the supposition of syphilis an
autopsy even apparently negative seems decisive. As I have
said before (p. 425), the quotation may be inaccurate. However,
until this case receives some corroboration it must stand as
an enigma, and quotable only under reserve. When we look
at the evidence as a whole, are we not compelled to say with
Josue 3 : " All these facts are in disagreement with the coronarian
hypothesis ; on the other hand, they are readily explained by that
of myself (Josue) and Clifford Allbutt. The pain of angina
pectoris arises at the origin of the aorta, and is provoked by
certain changes in this part of the vessel. Our case (a case he
had been describing) favours this way of looking at the matter"?
Is there an Angina of the Heart ? — My argument then
so far is that angina pectoris is due to tension of quasi-
cutaneous investments, not to anaemia of muscular tissues or
strife within them ; and that in the vast majority of cases

1 Medical News, Philadelphia, vol. Ixxvii. p. 974.

2 Osier, W., Lancet, March 28, 1910, p. 840.

3 Josue et Paillard, Bull, et Mem. de la Soc. Med. des Hop. de Paris (Seance,
janv. 29, 1909). For his own previously published views Josu6 refers to the
Soc. Med. des Hop., 3 juillet 1908 ; a paper he kindly sent to me.

440 ANGINA PECTOEIS part n

of ordinary angina this tension is exerted upon the thoracic
aorta, whose ascending portion appears to be more exquisitely-
sensitive to tension than the rest. Furthermore I have been
led to suspect that such tension and capacity for pain may
be felt in the same or a similar manner, and propagate itself
in the same or a similar manner, in this fibrous investment
as it extends forwards upon the aorta or backwards upon
the body of the heart itself. The innervation of this cardio-
aortic area is so nearly uniform that pain of like origin and
character might arise from capsular tension in more than one
parcel of it.

Let us see then if there be a pain, or pains, local or referred,
anginiform or otherwise, which do signify distress at the heart
itself; pains which we may construe as a remonstrance by an
overworked, engorged, inflamed, underfed, or decaying organ ?
On this point I think our daily experience leaves little doubt.
We have all recognised a pain, notably in mitral disease,
which cannot well be regarded as other than cardiac in origin ;
and in mitral disease it may be, I suppose it is, called forth
by distension, or possibly by fatigue, of the heart. Sir William
Osier says 1 : "In most affections of the heart pain is con-
spicuous by its absence. ... Of valvular lesions mitral
disease is often associated with slight pain, particularly in
children with greatly enlarged heart. And sometimes in women
the pain is of great severity and persistence, but it rarely has
the characters of true angina " (italics mine). Pawinski again
writes that the pain of " heart strain" is never anginiform, nor
even violent, but a weary ache ; and he thinks that if in any case,
as in one of Da Costa's, the pain was more like that of angina,
the case was not a simple one, but complicated with heart affec-
tions, perhaps with a pericarditis sicca. This vulgar heart
pain then does not resemble that of angina ; it is not vehement
nor paroxysmal ; it is never attended by the peculiar dread ;
and radiations, usually absent, are never remarkable. It is a
dull, depressing, continuous ache. Whatever its source, this pain
is an intercostal neuralgia, most intense — as is often the case
— in the ramus perforans lateralis. Differentially speaking, Dr.
Mackenzie 2 writes that the aching and hyperesthesia (tender-
1 Osier, Sir W., Luml. Led. p. 841. 2 Mackenzie, Jas., Heart, vol. ii. 3, 1911.

sec. ii AN ANGINA OF THE HEAET 441

ness of skin and muscle) in ordinary cardiac dilatation are around
the apical area, and that as the distension is relieved they pass
off. This pain he refers to the 3-4 dorsal segments, an area a
little lower than the aortic pain of angina (lowest cervical
and 1st and 2nd thoracic ?). Tenderness of the left sterno-
mastoid and trapezius he refers to the paths of the second and
third cervical. Certain cases of sudden coronary embolism at-
tended with pain I shall discuss presently ; in them the pain may
be intense, but more continuous, and in seat often epigastric, or
truly " precordial." Now if we admit, as I think every clinical
observer will be ready to do, that such is our everyday
experience of heart pain, as in mitral disease, or in ill-compen-
sated aortic regurgitation without disease of the aorta, we may
use this feature as a point of comparison with other pains of
cardio-arterial origin. The following patient, brought to me by
Dr. Alexander of Walthamstow, is a very interesting example of
what I think was " pain at the heart," as contrasted with the
pain of angina pectoris (pp. 387 and 430) :

Male, set. 64 ; for about two years had complained of pain defi-
nitely in the cardiac area, rather depressing than severe. When he is
sitting perfectly still it disappears ; when he moves it returns. For
instance, on walking upstairs and undressing it appears, with some
dyspnea, and continues ; when he is settled in bed these symptoms
pass off. There is no peculiar dread nor arrest, he can go forward ;
but, as to walk up a hill brings on the pain and dyspnea, he is fain to
stop for relief. It does not extend nor radiate. Some emphysema
was present ; but the heart could be mapped out to 1 cm. beyond the
mid-clavicular line. The sounds presented a somewhat laboured
systole, and a ringing second aortic sound. Radial pulse thrusting
and sustained ; artery fair for age. The systolic pressure indicated
at first well over 200 mm., but when every means of quietude had
been taken — including emptying the bladder — the reading gradually
fell to 180.

Such a pain, probably of cardiac origin, mimics " the
heartache of melancholia " (Robert Jones), or of other " dis-
heartened " people ; though this semblance may be only super-
ficial. However, such is the pain of the overdone heart, as seen
in Dr. Alexander's patient and in and out of hospitals daily.
In this case the heart was labouring under high blood pressures,
and the pain was associated not with arrest of respiration

442 ANGINA PECTORIS part n

but with dyspnea. This kind of pain is not paroxysmal, and
it does not radiate. A grip or even " squeeze at the heart "
is occasionally described by such patients, but not comparable
with the vice-like compression of the thorax in angina. Some-
times, it is true, the pain of angina also may be continuous and
wearing, but only I think between times, in phases of alterna-
tion with acute attacks. Dr. Norman Moore1 says of the
more equivocal pain that if cardiac, even if not confined to one
spot about the cardiac area, nay, even if " very severe spasmodic
pain is also sometimes felt, which might be mistaken for angina
pectoris," yet if watched it will be seen to be different in that it
is more continuous, lasts a much longer time, often many hours
or days, and is not attended with any sense of impending
death. In the following case from my own notes we find
these two kinds of pain interestingly contrasted.

Male, sent to me by Mr. James of Biggleswade. Burly, rather
obese man of 63. Had lived freely. Pain in the chest two months,
especially after meals and on exertion. It had two seats of origin,
under the left breast — " cardiac region," and about mid-sternum,
but a little to the right of the bone. Both pains aggravated by exer-
tion, but the patient insists on a distinction between them. The
sternal pain was paroxysmal, radiating down left arm chiefly ; when
worse passed also to the right, along inner aspects, not beyond the
wrist. The pain in the region of the heart was a continuous, weary
and depressing local ache, not severe. It was often tedious of an
evening when he was quite at rest, and would grow worse when the
heart became irregular. No dyspnea. No dread. Radials not very
thick, but pressure obviously very high, a thrusting pulse. The
systolic pressure had reached 200 when an accident happened to
my manometer. Chest too fat for precise examination, but enlarge-
ment of heart evident, and pulse hard in carotids and subclavians.
Faint systolic aortic murmur, second aortic sound " tinny." Urine
normal. No casts, no albumen. Sp. gr. 1025. The diagnosis
given was that the heart was painfully labouring in Hyperpiesis,
and the aorta severely strained, perhaps to the degree of a sub-
acute aortitis.

This man had both angina pectoris and heart disease, each
with its several and different pain. Now I must reiterate that
in the pain of angina mitral regurgitation is, generally speaking,

1 Moore, N., Luml. Led., 1909.

sec. ii AN ANGINA OF THE HEART 443

not an aggravation but, as Walshe and other clinical students,
especially Broadbent and Musser,1 have proved, a palliative.
To quote further from Musser ; he stated (among other con-
clusions not relevant): " that when dilatation of the heart super-
venes in a patient, the subject of angina pectoris, the subjective
symptoms may subside ; that angina pectoris may occur in a
patient who had dilatation of the heart when the dilatation is
removed by treatment." The relief is generally attributed to a
coincident fall of aortic pressure ; I have said that my experi-
ence is to the same effect.

That in mitral disease angina is curiously rare is the
testimony of perhaps all observers. But now we have to
meet certain exceptions to this maxim, marginal instances,
rare but signal ; these I propose to discuss with certain
other lesions attended with anginiform pains which may
however be directly of cardiac origin. These instances, on an
impartial view of the facts, I cannot ignore, although they may
have to wait a while for their true interpretation ; they are
instances, I frankly admit, of angina, clinically unquestionable,
occurring with heart lesion, and apparently caused by it. By
their rarity, and the prepossessions of their observers, these
cases have too often escaped a thorough verification ; at present
however they do point to the possibility of an angina of directly
cardiac origin. It is rather remarkable that it should fall to
me to justify the occasional use of the term " primary cardiac
angina " so commonly, but for the most part so erroneously, in
the mouths of our brethren. Regarded on their cardiac aspect
these rare cases seem to fall into three classes :

A. Those associated with mitral disease and especially with

mitral stenosis ;

B. Those associated with thrombosis, aneurysm, or rupture

of the ventricle, often with a focal pericarditis.

C. Those associated with pericarditis.

Anginal Pain with Mitral Disease. — In taking a large survey
of the subject before us, on the one hand we have seen, in the
sphere of the phenomena not directly associated with disturb-
ance of the heart named angina pectoris, some which can
be explained by, and are correlated with, lesion wholly con-

1 Musser, J. H., " Angina Pectoris," Amer, Journ. Med. Sciences, Sept. 1897.

VOL II 2 F

444 ANGINA PECTOEIS part n

fined to the aorta ; on the other hand, looking, as broadly,
at the phenomena of disease of the heart, we see some pains
directly associated with cardiac disease, but as a rule they are
not attended with pain of the mode of angina. Viewed in this
large way the contrast is so striking we may wonder that its
significance has not commanded more attention. But this is
not all.

A. In the only four cases, which I can remember, of
association of mitral disease with angina no necropsy was
obtained ; I had half forgotten them therefore, supposing
them to be of complex origin ; possibly associated with aortic
atheroma. Still occasionally I read or heard of other cases of
the same association ; and Dr. Beddard, who also had seen a
few such instances, more definite than mine, kindly recalled
my attention to this side of the subject. My four cases were
as follows :

The first case was in a certain Mr. F., who was staying for some
weeks at the house of his son, Dr. F., who had kept a careful eye on
his father's symptoms. Mr. F. was an old man with obvious athero-
matous disease of the arteries, and no doubt of the aorta ; and
symptoms of cardiac disorder, of which I have no precise note, had
for some weeks given his son no little anxiety. However, the patient
was said to have had no mitral murmur until a certain day, when
he was seized with a violent attack of " angina pectoris," and the
agony of it persisted so grievously that death seemed imminent.
Now, so far as I remember, the symptoms, save that the pain
seemed more continuous, resembled those of ordinary angina,
with two exceptions ; the first exception was the presence of urgent
dyspnea with cyanosis ; the second was the site of the pain, which
in this case was seated no doubt in the cardiac and epigastric area ;
the patient pressed his hand on the chest below the nipple, and over
the sixth rib. A high-pitched murmur, apparently of mitral re-
gurgitation, was audible, and this, as I was assured, had ap-
peared with the first seizure.

We guessed that some rupture of decayed structures of the
wall about the valve had occurred ; or a thrombosis of a large
coronary branch. This was my opinion, the mitral murmur
being but an event of some myocardial collapse. I may add
by the way that, although the agony could not but alarm the
hardiest patient, yet there was not in this case the peculiar
omen of death. I find no memorandum about pericardial

sec. ii ANGINA AND MITEAL DISEASE 445

friction (p. 461). Of the second case I have no notes made at
the time, but I recall that, with the appearance of a mitral
regurgitant murmur, anginal pain radiating from the heart's
apex set in, but here also with dyspnea and cyanosis. As in
both these cases, which seemed contrary to the maxim of
relief of angina by mitral regurgitation, there was old stand-
ing and severe cardio-arterial disease, they cannot be taken
as crucial ; especially in the lack of necropsy. The third was
more definite, though also without necropsy.

Man, set. 52 ; seen January 1904 with Mr. Agnew of Bishop's
Stortford. A vigorous, burly, fresh-complexioned man, in his youth
an athlete, but latterly stout, and out of condition. Temperament
impulsive ; health excellent. A few days before had an altercation
with a half-drunken workman ; a wrestle took place, and the man
was " chucked out." A little tremulous, he returned to his desk,
and in a few minutes pain of great intensity set in at the chest ; it
began one inch to the left of the xiphoid, and passed up to the right
axillary line. No pain about the apex. Mr. Agnew saw him very
soon, and then were there no morbid physical signs. The pain was
so intense that he had to be kept under morphia ; it was continuous,
and never passed into either arm. He was kept at absolute rest,
and in two days the pain subsided ; when I saw him then he said that
while in bed " he was all right." I found the heart a little dilated to
the right ; the veins of the neck were not swollen, nor the liver,
but there was extensive coarse crepitation over the backs of both
lungs. Also a loud systolic murmur was audible at the apex
(this appeared about seven hours after the attack began) ; it
was audible also behind under the scapula, and at the xiphoid was
very intense and superficial, as if tricuspid ; probably both the
mitral and tricuspid valves were leaking. The pulmonary second
sound was accentuated. The pulse was small and apparently of
very low pressure, rate about 120-130 ; when first seen it was 140.
He died, but no necropsy was obtainable. This pain, as I have
remarked concerning some cases of coronary thrombosis, etc., if
akin to that of angina, scarcely behaved like it.

The fourth case was in a girl of 11, the subject of mitral
stenosis after rheumatic fever. She suffered from attacks to
which the title of angina pectoris could not be refused.

Other recorded attacks of angina with mitral stenosis in
young subjects, some in cases verified by necropsy, are more dis-
tinctive. Schmoll records such a case of angina with mitral

446 ANGINA PECTOEIS pakt ii

stenosis and regurgitation, in a girl, set. 21. x There was no pain
in the arm, but a paresis of the limb. Dr. Knott has published
a similar case. 2 Dr. Samways 3 in getting out a large number
of mitral stenosis necropsies at Guy's Hospital, found there
had been pericarditis in one-third of them ! Dr. Graham Steell 4
has published two " typical " cases, and stated that " the
coronary arteries and orifices were perfectly sound." Both
were in women, of the ages 22 and 24, in whom athero-
sclerosis was presumably absent. The signs were those of
mitral stenosis, and the symptoms, similar in both, were pain
strictly at and round the heart, a dragging pain rather than a
sense of thoracic constriction, but paroxysmal, and radiating
thence, shooting and tingling to the left shoulder and arm, and
left side of neck and face. The attacks usually occurred at
7-9 p.m. and were preceded by fits of dyspnea. After the attack
the spine was tender in the region of 1-3 dorsal vertebrse, and
there was tenderness in other areas in front. The dyspnea
subsided with the pain. The sphygmograph indicated no
variation of curve during the attacks. He adds elsewhere
the pointed reflection that death in these cases does not result
from the angina, but in the ordinary course of valvular disease.
Dr. Beddard was good enough to report to me (in September
25, 1909), two such cases among his outpatients ; in one of
them, a woman, the angina was of such intense severity that
the distress could be palliated only by chloroform inhalation.
Venesection gave no relief. The attacks in her were prone to
recur when the general symptoms were worse, but also at
moments of excitement, exertion, chill, and so forth. Further-
more, Dr. Andrew Elliott was good enough to send me written
reports of two cases, in both of which however the association
was probably apparent only.

I. Female, set. 48, who had had rheumatic fever ten years before,
and now presents symptoms and signs of mitral stenosis, suffers from
very severe typical attacks of angina, with angor, passing at times

1 Schmoll, Munch, med. Wochenschr., Oct. 8, 1907.

2 Knott, Amer. Med. vol. viii., 1904.

3 Samways, D. W., Brit. Med. Journ., Feb. 6, 1898.

4 Steell, Graham, Lancet, Nov. 21, 1903; and Dec. 9, 1911. Also Index
of Treatment (loc. cit.).

sec. ii ANGINA AND MITEAL DISEASE 447

into the status anginosus. At her worst she was often relieved by-
venesection, but was chiefly benefited by nitrites and morphia.

Now in this case the angina may well have arisen from the
aorta, for Dr. Elliott noted a diastolic murmur, with some
aortic characters, heard faintly and occasionally down the
sternum. However, a necropsy was obtained, and in fact
" atheroma of the first degree was found at the bases of the
aortic cusps, and the aortic orifice was slightly dilated. " The
coronaries were normal"

II. The interest of the second case lay likewise in the associa-
tion of mitral stenosis (in a woman, set. 54) with anginoid
seizures ; but these, after some watching, he discerned to be
"spurious." They were "spontaneous" and prolonged; the
patient was restless and excited and highly emotional ; there was
no true angor. Moreover, under treatment upon this diagnosis,
the anginoid features of the case subsided.

But other cases of genuine angina, supervening upon mitral
stenosis, have been recorded here and there ; for instance
by Ortner,1 and by Dr. Otto May (two cases of mitral stenosis in
women set. 31 and 45 after rheumatic fever). Dr. May suggests,
as Dr. Beddard had suggested to me, that the cause of the angina
might lie in strain of the pulmonary artery, probably with the
atheromatous injury of the vessel often found in mitral stenosis.
If it be so, disease on the right side of the heart does not determine
a dextral radiation (p. 301). Ortner endeavours to discriminate
between the characters of the pain and symptoms in these
valvular cases, and in " typical " angina; but his differences are
vague : in many of these stenosis cases the radiations have been
quite typical (not even " confined to the depth of the chest "),
and the symptoms have differed only in so far as they were
blended with those of the valvular lesion. I am disposed, there-
fore, to wait a while until by careful autopsy, with our eyes open
to this part of the problem, we can ascertain whether or not in
these exceptional cases of mitral stenosis with angina the aorta,
outside as well as within, is intact. For, as the left auricle
embraces the root of the aorta, a subinflammatory process may
readily extend from the one member to the other ; or, as in
Elliott's Case I., in Ortner's, and in both of Steell's cases,
1 Ortner, loc. cit. pp. 14 and 24.

448 ANGINA PECTOEIS partii

both heart and aorta may have been infected by the rheumatic
poison.

It is known to students of heart disease that in mitral
stenosis palsy of the left recurrent nerve is no infrequent
symptom ; x but we are still more familiar with it in diseases
of the aorta in which angina pectoris also is not infrequent.
Accordingly, Boinet 2 suggests that, without compression of the
nerve by dislocated parts or enlarged glands, a periaortitis
may account for this recurrent palsy ; indeed in three of the
reported cases chronic adhesive pericarditis is mentioned, and
in one of Herrick's cases 3 the left recurrent was imbedded in a
mass of cicatricial tissue. Fetterolf and Norris conclude that,
by distortion of the parts in mitral stenosis, the nerve is in-
deed compressed between the dilated left pulmonary artery and
the aorta ; but, considering the softness of the parts, and the
normal flattening of the nerve against the aorta, they think that
something more is required to account for the effect, and suppose
from the evidence that the nerve is palsied by a neuritis pro-
pagated from the pericarditic, the glandular, or other local
inflammations which are found in some of these cases. Thus
the carotid pulses may be unequal ; and Muktedir 4 describes
two cases of mitral stenosis in each of which the voice
altered, and palsy of the left vocal chord was demonstrated.
The right pupil was dilated in both. Kraus thinks the re-
current nerve cannot be pinched by the auricle, but is
dragged and atrophied by the downward swing of the parts ;
but if so should not this effect be more common ? Lian and
Macorelles,5 reviewing this subject, coincide in opinion with
Fetterolf and Norris. They quote a case in which they de-
monstrated a corresponding local chronic mediastinitis ; and from
another source one in which after death a perivascular inflam-
mation was found. Now if in mitral stenosis such a process

1 For a careful study of this event see Fetterolf and Norris, Amer. Joum.
of Med. Sciences, May 1911 ; and Conn, G. (of Konigsberg), "Linkseitige Rekur-
renslahmung in folge von Mitralstenose," Arch, fur Laryngol. Bd. xxiv. H. 1,
1910.

2 Quoted by Fetterolf and Norris, loc. cit.

3 Herrick, Tr. Ass. Am. Physicians, vol xxvii., 1912, narrates several
cases with necropsies. Some had had anginal attacks, some not.

4 Muktedir, Deutsche med. Wochenschr., 1911, No. 11.

6 Lian et Macorelles, Arch, des mal. du cmur, juin 1913.

sec. ii ANGINA AND MITRAL DISEASE 449

may arise, it may account also for the occasional coincidence
of angina pectoris, as likewise engendered by a periaortic in-
flammation. All we can say as yet is that mitral stenosis may
be associated with irritative lesions round about. As I have
said elsewhere, we have been too content with a static view of
valvular diseases, and to regard the morbid process as con-
fined to the parts of the valve and orifice. The observations of
Carey Coombs, of the Leipzig school, and of others tell us that
these processes are more subtle and pervasive. Dr. Hare of
Philadelphia has reminded us that Mahomed demonstrated how
prone was what we now call partial heart block to ensue in
mitral stenosis ; an observation which was verified by Galabin.
Recently Mackenzie, Lewis, Herringham, Hay, and others have
illustrated this course of events ; and led us to see how chronic
inflammation may be propagated around the mitral area, and,
as I suggest, may gather occasionally about the root of the aorta,
and be revealed by angina. In malignant endocarditis, again,
a complexity of this kind would be intelligible.

Professor Allan,1 whom I have quoted elsewhere (p. 172),
in his long series of necropsies in cardioarterial cases, includes
instances of stenosis due to syphilitic thickening of the fibrous
rings about the valvular orifices. These may have been cases
of periaortic syphilis.

From these instances at least two points of importance emerge;
namely, that Ortner in these autopsies found the coronary arteries
quite normal ; and, secondly, that if it be true that the subjects
of mitral stenosis may, very rarely, be prone to angina, then
angina does not arise from straining of the left ventricle, which
usually in these cases is underloaded. It is the right ventricle
which labours under excessive stresses. Therefore, in the
absence of more post - mortem evidence, and especially of
closer examinations of the parts around the aorta, we must
suppose that in these, as in the rare instances of angina with
mitral regurgitation, some other factor was concerned of which
we have no information, but which we may guess at.

B. I have now to appreciate some similar evidence that
angina pectoris, or pains not unlike it, may be caused by
aneurysm and rupture of the heart itself, or by sudden
1 Allan, Intercolon. Med. Journ. of Australia, March 1909.

450 ANGINA PECTOEIS pakt n

coronary thrombosis, or very rarely, embolism (p. 370) ; now if this
be so, we may again be constrained to admit the possibility
of anginal pain originating about the heart. In common report
we hear of two modes of sudden death in angina ; the one a
sudden snapping of the thread in an ordinary paroxysm, the other
in a no less sudden, but also violent and protracted, seizure
which is the first and the last. The patient, who probably has
abeady shown signs of decay, is killed by a long and terrible
anginal agony. Two such cases have occurred in the last
twelve months in my circle of friends. These are cases, I
believe, of coronary thrombosis. We must remember that in
the excitement of a fulminant and mortal seizure, precision of
notes is not to be expected ; and it may be that in some cases
the name Angina is hastily attributed to any violent pain in the
chest, whatever the associated symptoms. But in many of
them it is true that a substernal pain of intense agony, with
radiation to the left arm, is recorded definitely enough. Dr.
Parkes Weber has kindly directed me to the records of many
cases 1 in which a sudden block of a large coronary branch was
attended with severe local pain. From these cases, and some
others, I find the distress was associated with a pain, substernal,
epigastric, or submammary, more continuous, it is true, than ordi-
nary attacks of angina pectoris, but apparently of the same nature
(p. 368). In all of them however the agonizing dyspnea and cardiac
failure pointed to a causation different, if not wholly different.
Morgagni says he does not know how to make an end of writing
on these cases (aneurysm of left ventricle, etc.). In older days
these, and such, sudden painful deaths were attributed to
poison ; but Morgagni emphasises lues as a main cause of such
explosions in the arteries and heart (vide Ep. XVI.). A clinical
difference is illustrated however by a case of Dr. Morison's,2 in
a man set. 59, the subject of a fatal thrombosis of the right
coronary artery. During the period of his survival (about 24

1 The principal are Church's case, St. Bart's. Reports, 1896, vol. xxxii. p. 17 ;
Korczynski's, Abstract in Jahresb. ges. Med., Berlin, 1887, vol. ii. p. 219 ; Hek-
toen's, Medical News, Philadelphia, Aug. 20, 1892, p. 210; A. Morison's,
Harveian Soc, Nov. 25, 1909 ; Garrod's, Proc. Boy. Soc. Med., April 1908 (the
same reference also to Parkes Weber) ; J. Mackenzie's, Heart Disease, p. 44,
1908. Cases referred to by His and Beitz, Gesellsch. d. Charite-Arzte, Berlin,
Jan. 6, 1910, are reported in Berl. klin. Wochenschr.. 1910, xlvii. p. 645.

2 Morison, A., Lancet, Jan. 8, 1910.

sec. ii COEONAEY THEOMBOSIS 451

hours), the kind of pain, and the collapse, suggested perforation
of gastric ulcer ; a behaviour not quite characteristic of the
pain of angina, even in its most importunate or tenacious
assaults. The same difference is to be found in the notes of
a case of coronary thrombosis most kindly furnished to me by
Dr. Gr. E. Higgens of Hornsey Eoad, N.

Man, set. 47, seized on a Saturday about mid-day — not during
exertion — with sudden pain about the lower end of the sternum ;
vomited frequently, and complained of dimness of sight. He became
collapsed ; the pulse ceased in the right wrist, in the left was feeble,
rapid, and intermittent. He died on the Sunday evening. His
mind was unclouded till the end. During this last 30 or 40 hours
of life the pain was extremely severe and continuous, so much so as
scarcely to be assuaged by morphia ; it was slightly relieved by
turning into the semiprone position, so as to maintain pressure upon
the chest. The seat of it was the lower sternal and left hypo-
chondriac region. He also suffered (and this is a fundamental
distinction) from extreme dyspnea. An interesting fact in this case
was the accession on the Sunday afternoon of cramp in the left hand,
the fingers being semiflexed and inextensible. The autopsy (at the
G. N. Central Hospital) by Dr. E. H. Shaw revealed only slight athero-
matous changes in the coronary arteries ; but the right vessel, for the
first 1| in. large and empty, was at this farther point completely ob-
structed by an irregular red clot extending almost to the junction of
the transverse and posterior descending branches. There was a small
narrow clot in the transverse branch. The heart was rather large
and fatty, especially the right ventricle.

The patient was seen in life by many observers, who variously
thought his case to be one of angina, or of rupture of the heart,
of a coronary artery, of an aneurysm, or of a visceral ulcer.

There is no reason in the nature of things why anginal pain
should not be as continuous as pain may be ; in origin it is not
rhythmical but contingent ; it does not arise from synchronising
of multiple oscillations, peripheral and central, nor on inherent
nervous capacities but, determined by contingency, passes with
it. Whatever the contingency, be it tide of blood pressure, local
injury, or other urgent condition, if the cause be continuous, so
will the pain be, so far that is as the sensorium can take it up ;
and, until exhausted, it can take up ten stimuli per second : a less
frequency than this is virtual continuity, the shorter negative
phases we fail to apprehend. What distinguishes these em-

452 ANGINA PECTOKIS part ii

bolisms then from angina of the ordinary form is not the
kind of pain — for this, if it be more about the heart, may be
substernal, and quite anginal in seat — but other variables ;
the flutter and lability of the heart, the rapid, irregular, and
failing pulse, the waning cardiac sounds, the dyspnea, the
cyanosis. Hochhaus,1 in a description of four cases of sudden
stoppage of a coronary vessel, points out also that the anginoid
pain is more continuous than in typical angina pectoris ; and
that the pain fades into the background as the heart gives way.
I shall quote from this paper again presently. Angina is not
always present. Sudden embolism of a renal artery sometimes
causes pain in the loin, sometimes not. Embolism of the splenic
artery, no very rare event, has in my recollection never caused
notable pain, presumably because the spleen is a loosely knit and
distensible organ. The conditions of tension in these several cases
are various. Kaufrrnann (in the 6th edition of his Lehrbuch) says
that anginal pain is caused only when a main coronary trunk, right
or left, is suddenly jammed. In three cases of sudden throm-
bosis, reported at Kiew,2 the pain, at times radiating, resembled
angina pectoris very closely ; but " the principal objective signs
were of ' meiopragia cordis ' — disappearing impulse and diminish-
ing sounds " ; the prominent symptoms dyspnea and heart
failure. The chief clinical distinction to remember in coronary
thrombosis is that, if in a large branch, angina may be present
but is inconstant ; while dyspnea and rapid fall of blood pressure,
symptoms which in ordinary angina do not occur, are constant.
The literature of these cases, if we omit the imperfect
records, is not large. Tiedemann opened the subject in 1843 ;
but the earlier writers, ignoring symptoms, or taking refuge in
the "neuroses," hyperesthesia plexus cardiaci, and such guesses
of von Romberg, Bamberger and others, confined themselves
to pathological anatomy. Von Leyden in an able paper 3
pointed out that angina is not an obligate clinical symptom of
this thrombosis, and, though occasionally typical enough, is often
indefinite or aberrant, and associated with dyspnea, dropsy,4

1 Hochhaus, Deutsche med. Wochenschr., 1911.

2 Obrastzow and Strachesko, " Thrombosis d. Kor.-Arterien d. Herzens,"
Zeitschr. /. klin. Med. Bd. lxxi., 1910.

3 Von Leyden, Zeitschr. f. klin. Med., 1884.

4 See also Panum, Virch. Arch. Bd. xxv., as an earlier observer of the subject.

sec. ii COKONAEY THEOMBOSIS 453

etc., especially in the milder cases with temporary survival ; but
that in all sudden blocks of large branches dyspnea, collapse,
and heart failure occurred. Von Ziemssen wrote later to the
same effect.1 With Morgagni's case 2 no symptoms are recorded.
Mayer points out that, as it may be associated with throm-
bosis, so angina may be caused by aneurysm of a coronary
artery.3 Obrastzow and Strachesko, of Kiew, record angina in
three of their cases, thus :

Man, set. 49. Angina ; block of left coronary ; sclerosed aorta ;
myomalakia and patch of pericarditis. In Case II. thrombosis : no
angina ; intense dyspnea ; rupture. In Case III. thrombosis :
angina ; (but as the aorta was much diseased, and with
" atheromatous ulcers," the pain may have originated there).

In most of these sudden coronary blocks the angina
appears in the form of " status anginosus." English observers
have been more vague in correlating anatomy with symptoms ;
and both English and foreign observers have too often
forgotten to record the condition of the thoracic aorta. In a
recent article Herrick of Chicago 4 divides the cases into four
classes : (1) Sudden death, in pain ; (2) angina, with death in
a few minutes ; (3) non-mortal attacks, with slight angina (ob-
struction of a small branch) ; (4) graver forms, mortal after some
longer period ; of these he gives six cases, and one necropsy :
Symptoms ; angina often severe, feeble quick pulse (sometimes
retarded), feeble cardiac sounds, dyspnea, cyanosis, pulmonary
congestion. In the necropsies pericarditis.

Dr. Parkes Weber has published 5 one case of angina
pectoris in which thrombosis of the right vessel was found ;
the obstruction however was an old one, and, as the reporter
pointed out, might have existed before the angina began ; for
new blood vessels had formed about the seat of the plug. The
patient was a diseased man of drunken habits, and " there was
also atheroma of the aorta." Still after all there remain not a

1 Von Ziemssen, Bert. klin. Wochenschr., 1901, S. 253.

2 Morgagni, De sed. 1. ii., Ep. 24, 16.

3 Mayer, Deutsche Arch. f. klin. Med. Bd. xliii.

4 Herrick, Summary in Arch, des mal. du cozur, mars 1913. See also Gaz.
des hop. de Paris, Seance 29, Janvier 1909.

5 Parkes Weber, Trans. Pathol. Soc, London, 1896.

454 ANGINA PECTOEIS part n

few striking cases of the coronary thrombosis and myomalacia,
not all of them attended with patches of pericarditis, in which
nevertheless attacks of pain occurred to which the name of
angina can hardly be denied. In respect of the pains and
their degrees, the time element, a gradual or a sudden occlu-
sion, makes much, perhaps all the difference. I will consider
the bearing of these cases on my hypothesis of angina after
dealing with angina and pericarditis.

C. Pericarditis and Angina. — In a case of heart rupture with
angina, recorded in an interesting article by Dr. Sidney Phillips,1
a patch of pericarditis was found over the seat of the rupture.
There were two attacks of angina, the second mortal. The pain
of pericarditis, often stabbing or boring like that of other serous
membranes, is in ordinary experience referred to the " cardiac
area," not in the careless use common in descriptions of angina
pectoris, but in a proper sense of this phrase. That there are
cases of pericarditis — somewhat rare, but significant — in which the
pain is like that of angina pectoris, has been known for some
years to careful observers, such as Sibson,2 Byrom Bramwell,
Andral,3 Peter,4 and others.5 They might have spoken more
plainly, and said that pericarditis is occasionally associated
with angina pectoris, for an analysis of these exceptional cases
may help us to interpret this stealthy disease. Andral writes :
" Ces douleurs rappellent a s'y meprendre celles de l'angine de
poitrine " (italics mine). In the earlier records, as for in-
stance in one of Fothergill's necropsies,6 our forefathers were
puzzled by the discovery in some cases of angina of pericardial,
and even of pleural, inflammations. The remarkable case of
angina recorded by Haygarth of Chester 7 proved on autopsy to
be one of mediastinal suppurative inflammation, apparently
involving the base of the heart and the great vessels.

1 Phillips, S., Lancet, January 28, 1897.

2 Sibson, A., Reynolds' System, 1877.

3 Andral, Clinique med. tome iii., 1834.

4 Peter, Lecons de clinique medicate, 1880, tome i. p. 419. (Seizures
radiating into the left arm.)

5 See also Steell, Graham, on "Pericarditis" and "Angina," Med. Chron.,
Nov. 1913 ; a paper which came into my hands too late for this essay.

6 Fothergill, Lond. Med. Obs. vol. v. See also Haygarth' s case, Med.
Trans, vol. iii.

7 Haygarth, in vol. iii. of the Med. Trans., 1772.

sec. ii ANGINA AND PERICARDITIS 455

Dr. Graham Steell writes : 1 " The combination of peri-
cardial friction sound with angina pectoris is seen often enough
to leave an impression on one, and is occasionally noted by
others, as by F. Roberts in Allbutt and Rolleston's System, vol.
vi. p. 47, by Gibson in Reynolds, and by Walshe." Steell relates
four cases. Case I. illustrates the fugitive course of the sound,
although the pericarditis proceeds; the third illustrates "exactly
typical angina " with pericardial friction, ending in recovery.
In No. 4, of pericarditis, " the diagnosis of angina was (clinic-
ally) clearly established." Gallavardin 2 says under Pericarditis :
" Its pains can in certain cases put on the character of angina
(Andral, Sibson, Peter) . . . and the patient may suffer from
the (peculiar) angoisse."

Now as to the facts ; in anaesthetised animals to pinch or
stretch the pericardium sends up the blood pressure (Kidd,
Mathison), an effect lessened but not abolished by section of the
phrenic ; the pericardium appears to have a further sensory
supply. The pain of pericarditis may extend from the cardiac
area, and, as we shall see, may perhaps reach the left shoulder,
even while the inflammation is confined strictly to the cardiac
surface. Erasmus Darwin (loc. cit.) noticed in pericarditis that
the pain might travel to the left shoulder, a feature which he
attributed to direct nervous conduction. This possibility I have
discussed on another page, and I shall return to it. But my
present purpose is to dwell more definitely upon angina pectoris,
in the strictest sense of the word, as an effect of pericarditis.
Sansom wrote, concerning pain in heart diseases, " Pericarditis
may be painless ; but usually there is considerable distress, which
is referred to the heart, but it may extend to the left shoulder
and arm. . . . In rare cases it is paroxysmal, and has the characters
of angina pectoris " (italics mine). Sturges,3 in one of his cases
of pericarditis, a girl, aet. 5, reports that " she suffered a sort of
anginal attack." Dr. Samuel West 4 writes on pericarditis,
" Cardiac pain of the acute kind at all resembling angina is very
rare, and is met with only when there is acute cardiac dilatation,
but by no means always then." The qualification seems to weaken

1 Steell, G., Med. Chron., Nov. 1913.

2 Gallavardin, Mai. du cceur, 1908, p. 212.

3 Sturges, 0., "Lumleian Lectures," Brit. Med. Journ., March 10, 1894.

4 West, S., Brit. Med. Journ., Oct. 26, 1907.

456 ANGINA PECTORIS pakt n

his opinion of the cause (p. 386) ; not to mention the difficulty
in pericarditis of discerning degrees of cardiac dilatation. Con-
versely, in no disease indeed is acute dilatation of the heart more
common than in acute rheumatism, yet with it " pain resembling
angina is very rare " ; there is room then for great hesitation
in assuming the cardiac dilatation and the angina to be cause
and effect. Dr. James Mackenzie again, in a private letter,1
kindly invited " my attention to rare cases in which the pain of
pericarditis has the same distribution as in angina pectoris." I
welcomed this further testimony to facts which had not escaped
my attention, and which in my Cavendish Lecture (vide p. 160)
I had already made some endeavour to explain. Dr. Byrom
Bramwell 2 also has described a case of angina associated with a
pericarditis, which in this instance seems to have been syphilitic,
as follows :

Workman, set. 49, well built and nourished. History of syphilis
and alcohol. He was attacked by angina pectoris, but for a day
or two nothing abnormal was to be found about the heart ; then,
however, a distinct pericardial rub became audible. The pericarditis
lasted for a fortnight, after which time the patient made a complete
recovery (italics mine). N.B. — An instance, among many, for those
who deny recovery in angina. See also Kernig's and Ferrio's cases
(pp. 459-460).

Dr. Bramwell confessed that the interpretation of the case
remained obscure to him.

Teissier,3 in cases of the pericarditis of Bright's disease,
reports " angoisses retrosternal quelquefois tres vives " ; but
with dyspnea also. Barie writes to the same effect.

In his Morison Lecture for 1904 (p. 35), Gibson said, " In
pericarditis anything approaching the typical symptoms of fully-
developed angina pectoris is undoubtedly rare ; occasionally
however a case presents itself with the characteristic distribution
and special features of a true anginous seizure." Why not put it
in plainer language, and say that in some rare cases of pericarditis
we meet with angina pectoris. Weintraud 4 under " Pericarditis "
says that patients often complain (" berichten die Kranken

1 Dated March 19, 1903.

2 Bramwell, Byrom, Diseases of the Heart, etc., 1889.

3 Teissier, Bull. med. 12 avril 1911.

4 Weintraud, in Eulenberg's Lehrbuch, ii. 323.

sec. ii ANGINA AND PEKICAEDITIS 457

oft ") of a severe pain behind the sternum and through to the
back ; or radiating up to the neck, and sideways into the arms.
In its fuller manifestations (he adds) this pain corresponds to
typical angina pectoris ; so that presumably the slighter but
similar manifestations are of the same nature. A short time
ago I read in an article by an eminent German physician, whose
name has escaped my memory,1 that the pain of pericarditis
ranges from a slight stitch or oppression up to the most intense
(" intensive ") attacks of angina. Now it is remarkable that all
these writers on pericardial angina — so far as I remember, all
of them — refrain from the customary tribute to the coronary
arteries. Why is this courtesy withheld %

In a paragraph on pain in acute rheumatism of the heart,
Weill et Nouriquand 2 say that beside the " simple gene pre-
cordiale," spontaneous or called forth by pressure, less commonly
(" moins frequemment ") intense pain radiates beyond the cardiac
area, with pallor and anxiety. They point out that these pains
are sometimes comparable with those described by Peter and
Letulle, and attributed by them, as by Lancereaux and some
earlier clinical authors, to neuritis of the cardiac plexus. They
allude to the opinion that acute myocarditis may be painful, a
speculation into which however they decline to enter ; they con-
tent themselves with the demur that, " keeping strictly to the
exclusive domain of facts," in the necropsies of such cases they
have found nearly always a recent, generally slight, pericarditis.

The controversy must be decided by post-mortem evidence,
yet, if pericardial angina is rare, autopsy in such cases is still
rarer ; but it is generally understood that a partial dry peri-
carditis may occupy the parts where the great vessels leave the
heart. In the article on Aortitis, I have alluded to Pawinski's
very important evidence, and to Auscher's evidence 3 from a very
interesting case of " posterior basic pericarditis," with angina,
to indicate that the cause of angina in pericarditis may lie in the
extension of the inflammation to that tract or collar, thus invading
the periaortic structures.

1 In the Deutsche med. Wochenschr., May 19, 1910.

2 Weill et Nouriquand, " Cceur et rheumatisme visceral," Paris medical, ler
juillet 1911.

3 Auscher, Bull. Soc. Anat. Paris, fevrier 1896.

458 ANGINA PECTOEIS part ii

Auscher's case was as follows :

Male, set. 61. Of sober habits ; never suffered from syphilis
or rheumatic fever. No tobacco. For a few months previously
had been subject to severe and typical angina pectoris ; he described
the pain as of a red hot bar squeezing the chest violently, an interior
pain. One of the attacks ended in syncope. After admission to the
hospital he had had one attack, diagnosed clearly as angina pectoris ;
and a distressing sense of oppression was often felt. A double
murmur was heard about the base of the heart which was attributed
to aortic disease with regurgitation. Nine months after discharge
he was readmitted for rapid phthisis, and died. (As no farther
mention is made of it, the angina presumably had ceased.) At the
necropsy the heart was found perfectly healthy, the aortic and other
valves normal, and the aorta " supple and elastic." " Les orifices
des coronaires etaient irreprochables," and these arteries were " sur
toute leur longueur souple et permeable." Sections showed also
that the walls, both as to vessels and muscular tissue, were normal.
The integrity of all these parts was " nettement demontre." Then
what was found ? What was the explanation of the angina ?
Around the base of the heart and the root of the great vessels, and
on the corresponding portion of the parietal pericardium, were
definite signs of old chronic pericarditis, and upon these areas was
an opaque false membrane. This is a crucial instance of angina
with sound heart and sound coronaries, but with inflamed aortic in-
vestment.

Pawinski's x evidence again is that these latent inflammations
of the pericardium, with more or less restricted highly fibrinous
exudates, may attack this part of the sac, the part which invests
the roots of the great vessels. He records eight cases of his
own which were marked by anginal pain of intense degree,
especially at the onset. In some cases in which the pain was
most violent, the pulse began suddenly to fail — " a sudden fall of
the heart's action (' Herzthatigkeit '), with a weak and irregular
pulse " (vagus symptoms ?). Indeed these stenocardial effects
he relies upon as symptoms of this one of the latent forms of
pericarditis, suggesting that neuritis of the plexus cardiacus may
be the most important source (" Quelle ") of " stenocardia." He
denies that an explanation can be found in coronary disease and
myocardial anaemia, for in his cases it was the pericarditis which
called forth the pains peculiar to angina — " die Angina Pectoris

1 Pawinski, Deutsche Arch. f. klin. Med. Bd. lviii., 1897.

sec. II ANGINA AND PERICARDITIS 459

eigenthiimliche Schmerzen" — without the coronary arteries being
involved, or in any way concerned ; as we saw in the syphilitic
case recorded by Merklen (p. 375). In one of these, a case of Peri-
carditis sicca, Pawinski noted physical signs of dilatation of the
ascending aorta. Now, had such attacks occurred in old persons
with diseased arteries, they might well have proved mortal by
inhibition ; however, in all Pawinski's mortal cases death was due
to other causes. I may here refer to Perez' case without repeating
it. Von Romberg 1 writes likewise : " Sometimes (in peri-
carditis) the anxiety is greater, and is accompanied by pain
radiating into the neck and arms, especially the left arm,
resembling angina pectoris ; unpleasant symptoms which may
precede the more objective phenomena by a day or two."

As further evidence of the same kind, I would cite also an
interesting paper by Luigi Ferrio,2 of Professor Bozzolo's clinic.
This paper I had procured for other reasons, but in it I noted
also some remarks, apt in this place, on the propagation by con-
tinuity of inflammation to the aortic valve from that part of
the pericardium which encloses the roots of the great vessels.
As probably in the following case :

J. M., set. 17. Acute rheumatism ; ten days after admission, a
recrudescence of fever with pericarditis and intense pain, " alio sterno
e nelli parti adjacenti" ; soon afterwards the aortic valve was attacked.
Paracentesis pericardii, withdrawal of turbid serum with flocculent
fibrin. Relief, and ultimate recovery.

Boinet 3 likewise says, "Acute or subacute aortitis also may
result, rarely it is true, by propagation of inflammation by
contiguity in pericarditis and in endocarditis ; especially in
rheumatism.

Pawinski says that the angina does not occur with pericard-
itis in other parts of the sac, an opinion which, as we shall see,
is open to some doubt, or qualification. I may note, notwith-
standing, that it is in pericarditis about the origin of the aorta
that angina is most apt to appear. I note also that irritation of
the pericardium sets up vagus inhibition (extrasystoles, etc.).
Cocainise the pericardial area and the vagus ceases to respond.

1 Von Romberg, Krankht. d. Herzens, 1906, p. 372.

2 Ferrio, L., Gaz. degli osped., Sept. 24, 1905.

3 Boinet, in Brouardel and Gilbert's System.

VOL. II 2 G

460 ANGINA PECTOEIS part n

Let us now turn to the reverse of these events, to a possible
propagation of subacute inflammation from the aortic area to
the pericardium : five such cases are recorded by Kernig ; 1 of
these I will give a scanty summary.

I. An elderly general officer, subject to angina. After a severe
attack his temperature rose, and a pericardial rub was heard at
the base of the heart. II. Physician, set. 47. After great effort,
severe attack of angina ensued, with rise of temperature and peri-
cardial friction. Symptoms passed off in ten days. Convalescence
satisfactory, and return to full work. III. Army officer, set. 56.
Severe first attack of angina (lasted 6 hours). Two or three days
later some rise of temperature and a pericardial rub. Three weeks
in bed. On rising from bed, sudden death. IV. Merchant. Mt.
68. Angina. Then a bad attack lasting 24 hours. Two days later
rise of temperature and pericardial rub. Feverish for a fortnight ;
then complete recovery from all ailment. V. A similar case nar-
rated to the author by a colleague.

At the Pesth Congress in 1909, and again, I think, at the
Berlin Congress of 1912, Professor Sternberg of Vienna read
an interesting paper on this aspect of the subject, entitled
" Pericarditis epistenocardiaca." 2 In opposition to Pawinski,
Sternberg and Kernig insisted, rather topsy-turvily as it seems
to me, that the anginous symptoms came first, and that the
pericarditis followed them ; i.e. a bacterial or other infection
attacking the myocardium causes the angina, and the pericarditis
is but an epiphenomenon. Sternberg produced two cases, with
a necropsy in one of them. This was of a man of 47 (age at
death 51) with a long story of syphilis in self and wife. He
had nasal disease with asthma, and for some years symptoms
of disease of the arteries and heart. On April 26th he had an
attack of angina. On May 23, 1906, occurred a second very
severe attack of angina pectoris, and within 24 hours a pericardial
rub was heard. Temperature 39'2. His stenocardial attacks
seem to have persisted, as a report in 1907 speaks of them as
less frequent. After this a period of amendment was obtained,
but then a gradual dissolution set in, with much asthma and
cardiac failure, amongst which sufferings little is said of angina.

1 Kernig, St. Pet. med. Wochenschr., 1892, and (with five new cases, but no
necropsy) Berl. klin. Wochenschr., 1905. See also Bramwell, B., Diseases of
Heart and Arteries, 1889.

2 Protocol, published Wiener med. Wochenschr., No. 1, 1910.

sec. ii ANGINA AND PERICARDITIS 461

Of the necropsy it is sufficient to state that a chronic partial
aneurysm of the heart was found associated with old peri-
carditis ; the aorta exhibited the well-known syphilitic destruc-
tion, and the coronary arteries also were extensively diseased.
So that although the acute seizure attended with pericarditis
determined one of the attacks of angina, or coincided with it,
yet without it there was quite enough specific mischief in the
aorta to account for this event. Upon a case so complex no
decisive argument can be founded. The second case was in a
man of 74, in whom an attack of pericarditis occurred with
angina. He made a good recovery. Sternberg's opinion is, as
I have said, that in all such cases the pericarditis follows the
anginal seizure, at an interval however so short — a few hours —
that from the ear alone it would be impossible to time its
onset precisely ; in any case not before the tough tunic was
stretched by exudation into its interstices.

From a survey of the cases with necropsy, and a reading of
the rest by their light, it would seem that the chief features
of Sternberg's cases (loc. cit. p. 368) are a sudden block of a
coronary artery — whether by an embolus or by thrombosis
— with Ziegler's myomalakia, and disposition to aneurysmal
pouching ; upon this rides a superficial pericarditis, as on the
pleuritis of a pulmonary infarct. In Sternberg's opinion the
formation of aneurysmal dilatation relieved the angina ; with
it the tension may have yielded. He called the stenocardial
(thrombosis with hypersemia ?) the first stage ; the pericarditis
marked the second ; the third was the latent stage of apparent
recovery ; and the fourth, the decay of the cardiac muscle.
But on current notions the third and fourth stages ought to
have been those of the stenocardia.

After the publication of Sternberg's paper appeared that,
to which I have alluded, on the same subject by Professor
Hochhaus of Cologne,1 but dwelling more especially on the
diagnosis of sudden coronary block (p. 450) ; he reports
instances of such diagnosis during life by Hammer, Cursch-
mann, Obrastzow and others.2 Hochhaus describes three

1 Hochhaus, Deutsche med. Wochenschr., Nov. 9, 1911.

2 See Krehl, Erkrankungen d. Herzmuskels, Wien, 1901. Also Zeitsckrift /.
hlin. Med. Bd. lxxi. He. 1 and 2, with bibliography.

462 ANGINA PECTOEIS paet n

cases, all with pain of a more or less anginiform character ;
but as in two of them pericarditis was present as well as aortic
disease, and in one of them a history of angina in its ordinary
form, I will concentrate attention on his third case. This
was of a woman, set. 69, who was seized with the symptoms
which I have indicated, including severe substernal pain — a
group of symptoms which, so Hochhaus argues, seems to suffice
for diagnosis of this accident. Considerable aortic atheroma
was found after death ; and the coronary arteries were exten-
sively thrombosed (both with old silting up and several recent
acute plugs). Now in this case the pericardium was smooth
and bright ; so that pericarditis is no necessary mean in throm-
botic angina. The myocardium however, besides necrotic
changes, presents in these cases, especially about the apex,
hsemorrhagic swellings and acute fibrinous exudations into its
substance, and these changes in Hochhaus' case were well marked.
I have discussed these problems with Professor Hochhaus, and I
admit that this instance again, most carefully described, seems
to be almost crucial ; I can no longer hold that the source of
angina pectoris is exclusively aortic, though it is possible that the
atheroma of the aorta, long latent, sprang into life and set up
angina at this critical moment. No periaortitis is recorded. In
these cases then the intense anginiform pain appears to have
been generated, not by any extension of inflammation from the
pericardium to the root of the aorta — vera causa as this is — but
in the heart itself. The interpretation of the pain however in
my opinion still lies in differential tension of investment, in an
engorgement and distension of the affected portion of the peri-
cardium by the sudden hsemorrhagic and fibrinous exudations.
This stretching of investment, and perhaps of fibrous attachments,
evokes pain in the same way as at the root of the aorta it is
evoked by the distension of systole, or by rupture with sudden
escape of arterial blood between the coats of the vessel. But,
as we might anticipate, the pain is more continuous. It is to
be noted that in all (?) these cases there is pain about the heart
itself as well as in the sternal area ; and that the angina is a
feature not, as would usually be assumed, of the chronically
enfeebled heart but a transient feature of the initial phase
only. Dilatation of a whole ventricle is not thus differential,

sec. ii ANGINA AND THE PEKICAKDIUM 463

is less sudden and is not unnatural ; still dilatation is not rarely
attended by a sickening ache. I have said that the agony of
mesenteric embolism is presumably to be explained in the same
way ; that is by the tension and drag on the mesentery, which
is rich in sensory nerve endings, and by the thrust of the
sudden secondary engorgement and effusion.

But nearly all these records are defective in lucid clinical dis-
tinction between continuous pain in the cardiac area, which we
know does occur in some cases of sudden coronary embolism,
and the paroxysmal sterno-brachial pain of angina ; also they
lack definite delineation of the several areas, the mind being
occupied with the ruin of the wall of the ventricle. Moreover in
most of these cases, besides the pain, there were many signs of
heart disease and heart failure ; they suggest that under these
conditions a coronary plug and myocardial destruction do not
suffice to produce angina, that they are not its cardinal factors ;
that to set up angina the tough pericardial investment must
be suddenly and differentially stretched, by exudation, or by
some local surge of the blood. Kauffmann (loc. cit.) says indeed
that beyond the plug a strong hyperemia sets in, even to
hemorrhagic with other exudations, sometimes to rupture.
Ordinary pericarditis in such subjects, without the factor of
aneurysmal pericardial distension — as for instance in Bright's
disease, — even with coronary disease thrown in, does not set up
angina unless it embrace the root of the aorta. I reiterate
that in many cases of angina with pericarditis, as for example
in Auscher's well-known case,1 in some of Pawinski's, and
many others, the coronary arteries were intact.

Hampeln2 has carefully surveyed a long list of cases of rupture
of the heart and aorta, and found the characteristic difference
between them to be the predominance of anginal pain in the
aortic cases ; pain in the cardiac cases being often absent,
or ill -marked. (See Aortitis, p. 206.) Now we have seen
that a rupture of the ascending aorta, stretching the invest-
ment of the vessel by the dissecting blood, causes pain
analogous to that of periostitis. Dr. Humphry informs me

1 Auscher, Bull, de la Soc. de VAnat. de Paris, vol. x., fev. 1896 (see p. 458).

2 Hampeln, St. Petersburg med. Wochenschr., 1899. A paper of which I have
seen only abstracts in other journals.

464 ANGINA PECTOEIS paktii

that in a recent case of his own, in a young man in whom
after a violent effort symptoms of severe angina pectoris
ensued, at the autopsy a clean rupture of the aorta a little
above the valve was found, the blood having dissected up the
coats. The heart was quite normal, and the aorta, though a
congenitally slender vessel, was free from disease. There was no
syphilis. There are on record not a few of these splits of the
aorta with angina, and in most of them, before autopsy, a
diagnosis of angina pectoris was made. D'Antona has pub-
lished x an interesting summary of these sharp-edged ruptures,
with two cases of his own ; in one of these, in which the pain
was intense, the coats were split asunder by the dissecting
haemorrhage. (Similar cases (e.g. Pallasse's case, p. 207) and a
further discussion of this subject are to be found in the chapter
on Aortitis, p. 206.)

In all these rupture cases the adventitia shews itself remark-
ably tough, and is not torn ; it is the last strong guard of the
integrity of the vessel. Now these aortic ruptures are analogous
to the forcing of the visceral pericardium in the coronary
thrombosis of which we have just been speaking.

Aneurysm of a coronary artery seems to arise only in the
course of embolism (Kirkes and Wardrop Griffith) ; 2 if angina
be present it would probably depend not upon the aneurysm,
which of itself might not cause much tension, but on some
associated local condition.

Now if for the moment we consider the facts of the common
association of angina pectoris with aortic disease, especially with
its acuter inflammations and strains, facts of which we have
all this plenty, we must be struck with the convergence of their
evidence towards a conviction of their causal dependence.
Even in respect of angina arising in the heart itself I have
shown that in this area we have been too wilfully bent upon
seeing nothing but the coronary arteries or myocardium. In
Auscher's case of pericarditis sicca attended by three attacks
of severe and typical angina pectoris, when six months later
the patient died of phthisis the remains of false membrane were

1 D'Antona, Arch, per le sci. med., 1911, vol. xxxv. fasc. 4.

2 Griffith, Wardrop, Brit. Med. Journ., Feb. 22, 1901 : with a good list of
records.

sec. II ANGINA AND THE PEKICAKDIUM 465

found on the roughened surfaces of the visceral and parietal peri-
cardium investing the origin of the great vessels ; and I repeat
the author's declaration " that in spite of the typical angina
and parietal pericarditis around the aorta " . . . " F orifice des
coronaires etait irreprochable . . . " ; that these vessels were
beyond reproach " dans toute leur longeur," and on section
proved in histological structure to be normal. Is not this
crucial ? Gallavardin's anxious flutters between loyalty to
Huchard and the coronaries and the evidence of his own acuter
observation are diverting. In one breath he says with emphasis
that angina does not arise from a " coronarite veritable "
but nearly always from an aortitis propagated to the orifices
of the coronaries ; nay, he quotes Bard and Morvan, and
under the influence of Josue and myself admits that we must
remember " c'est l'aortite qui importe surtout, non la corona-
rite " ; yet he is perpetually harking back to the old notion,
and losing his way. He tries to find some controversial refuge
in a neuritis.

On the other hand, as I have said already we are
all agreed that by sufficient slowness of approach, a kind
of tolerance, which may be illustrated from many kinds of
disease, may be established. This immunity of whatsoever
structures, coronary or myocardial or aortic, if the disease be
but slow enough, is well illustrated by the following case,
recorded by Dr. Parkes Weber.1

Male, aet. 61, syphilis, and gumma of liver. Extensive atheroma
of the aorta, which at its root seemed to involve all the coats. At
some places the pericardium was adherent, as if by a panarteritis
rather than by an atheroma of the intima ; and at one spot was
found an aneurysm the size of a cherry. The coronary orifices were
blocked. Yet there was no history of angina.

The conclusion then to be drawn from these further clinical
and pathological records is, that if angina arises during an
ordinary pericarditis it is due to an extension of it around the
collar of the great vessel ; that if it arises on embolism or swift
thrombosis of a coronary vessel it must be of a main or large
trunk, and the pain due to tension of the investment of the

1 Weber, Parkes, Path. Trans., 1896.

466 ANGINA PECTOEIS part II

heart either by pericarditic products or by the engorgement of
the peripheral area beyond the plug.

Death by Inhibition. — But how then, on this aortic
hypothesis, comes angina pectoris to be so fatal ? In this
vessel are not dilatation and disease common enough, and, if
part of the machinery of death, nevertheless not lethal in
this dramatic sense ; how indeed can aortic disease, without
rupture of the vessel, prove thus suddenly fatal ? This difficulty
however we have to meet in any current interpretation of
angina. How is it that an attack of pain at length kills suddenly,
and by a heart-stroke, although time after time physicians have
watched the invasion to the very door of death without a totter of
the heart ; or with no more perturbation of it than is seen in many
a transitory disorder which, apart from the signals of angina,
would not give us even momentary alarm ? Is it not still more
incomprehensible that often, while the patient is in so hard a
grip that he cannot start back even from death's door, his pulse
may be going on its way with indifference, and not be moved
even with a secondary and sympathetic affection ? Thus I was
led to surmise that in angina pectoris the fatal shock must be
something secondary and quasi-accidental, and then I thought
of an inhibition of the heart by reflex action, by a kind of
" shock."

It is thus that the swift bolt of angina, often as silent as swift,
striking a man down in his path, has possessed all who have
known it with a kind of awe. The physician perceives at once
that this swift passage is by the heart ; hence Parry's name of
Syncope anginosa, and that of Sternodynia syncopalis (Sluis, 1802).
That this death is due to the vagus, stung by the anginal pain
and acting often upon a decrescent heart, is the part of my
hypothesis of angina (1894) which already has found some if
not general acceptance.1 In order to understand how death

1 There is a legend, apparently originating from von Bezold, that Rufus
of Ephesus and Galen knew of the influence of the vagus upon the heart. Rufus
(after Erasistratus) certainly described the nerves springing from the brain,
but of this special effect of the vagus I can find nothing. To say there is no
such statement in Galen is more than I dare assert ; Galen is a copious person ;
but I do not recollect any such passage. Before the brothers Weber (1846),
Willis and Lower (end of seventeenth century) showed that to cut the vagus

sec. II DEATH BY INHIBITION 467

happens in angina pectoris — for at first sight death is not, I
repeat, a likely issue of aortitis — let us consider, briefly as it
must be, some relevant points in the mechanism of cardioarterial
sympathies and concerts. In the first place we shall distinguish
between the vago- sympathetic and the vasomotor mechanisms, the
centres and the branches of which form distinct and partially
independent systems. The superficial and the deep cardiac
plexuses lie, as to the former between the pulmonary artery and
the aorta, and as to the latter and much larger portion, on the
posterior part of the root of the aorta ; these portions are how-
ever so intimately connected that for present purposes they
may be taken as one.

The vago-sympathetic group consists, as the name implies,
of contributions from sympathetic and vagal sources ; and
from this subcentre fibres are distributed to all parts of the
heart and contiguous vessels. It contains afferent fibres which
pass to the spinal cord by the posterior roots and thus attain
relations with consciousness. There are probably afferents from
the whole of the aorta, and from other arteries — reflex or auto-
matic, local or general, — but little is known of them. The
sympathetic contains vasoconstrictor fibres. Moreover, as will
be illustrated presently by some observations on the pleura,
there is a connecting link between the cardiac and pulmonary
plexuses, so that irritation in the one is felt more or less vividly
in the other. The centre for these plexuses in the bulb is
distinct from that of the vasomotor system, although a heightened
activity in either may be felt by the other. Furthermore, as we
shall see presently, these centres are in close concert with the
respiratory centre in the bulb, and have with it harmonious
periods of activity and relaxation (see also fifth nerve, p. 297).
There are of course vasomotor centres in the thoracic cord also,
with connecting fibres to the sympathetic.

The vasomotor connections of the heart, for the later elucida-
tion of which we are indebted to Professor Langley's researches,
are supplied from the sympathetic system. At present we
may confine ourselves to its splanchnic division, and to its

quickened the heart ; and ten years before the Webers Volkman made ex-
periments on the vagus with an electric stimulus, and included it in his
compression experiments.

468 ANGINA PECTOEIS part n

regulation in respect of the heart by the depressor nerve whose
action, passing first in an afferent direction, then causes a dilata-
tion of the splanchnic reservoirs, whereby at need peripheral
resistance is lowered, and the heart is relieved of stress. The
vagus and depressor nerves are no doubt both in incessant touch
with the heart and the aortic tambour, as the hand of a good
horseman is in continuous touch with his horse's mouth. For
inhibition, if we think of it, is not an occasional interference with
vital function but a primary condition of it ; without it energy
would be dissipated as soon as conveyed ; there would be no
storage of energy. Indeed inhibition is not unknown in the
sphere of chemistry, as with orcein and resorcin. Biological in-
hibition may depend likewise on some chemical phase. Sir
David Ferrier has spoken of the depressor, " the afferent nerve
of the heart par excellence, as in reality the sensory nerve of the
aorta." 1 We know how Ludwig and Cyon demonstrated the
two roots of the depressor, one from the vagus in the neck,
the other from the n. laryngeus superior, which goes to the
cardiac plexus. To irritate the central end causes a fall of
pressure and retards the pulse ; but if the vagus be cut only
the former effect is seen. The depressor is thus partly vagal,
partly vasomotor, chiefly splanchnic, but with some peripheral
distribution. It is a safety valve for cardiac distension. Here
also I must refer again to Koster and Tschermak's experiment of
isolating the aorta and demonstrating that distension of its first
portion is followed by a fall of blood pressure.2 Schumacher,3
who was working independently of Koster, showed also that it
pertained to the first portion of the aorta. But we must
remember not to apply too readily to man results obtained upon
animals ; there are grounds for analogy, or even homology,
but probably not for identity. Professor Sherrington also4
speaks of the aorta, as for many years I have done, as the
receptive field for the depressor whose terminations in the wall
of the vessel have been demonstrated ; and its most adequate
stimulation is a distension of this wall, whereupon by relaxation

1 See also Koster, " Ursprung d. N. depressor " Neurol. Centralblatt, 1901,
p. 1032.

2 Koster and Tschermak, Pflugers Arch. Bd. xciii., 1902.

3 Schumacher, Sitzungsber. d. Wiener. Akad. d. Wiss. Bd. iii. Abt. 3, 1902.
* Sherrington, C. S., Brit. Med. Assoc, 1909.

sec. ii DEATH BY INHIBITION 469

of vascular tone arterial pressure falls. But such stimulation
does not cause pain — at any rate, not directly.

If the pain of angina excite both the vagus and the vasocon-
strictors, it appears — e.g. under adrenalin (Schafer, loc. cit.) — that
the vasoconstrictive action predominates ; although the vagus
may still be in action. When it is severed the blood pressure rises
enormously. I do not know that it is always true to say that this
double effect of the pain makes for more embarrassment of the
heart. An intraventricular rise of pressure may call forth a
stronger cardiac response, such as not only to resist the nursing
vagus but also by rise of tension to stimulate the depressor.
These considerations apply only to immediate effects. In the
long run, section of the depressor (in dogs), by increasing the
call on the heart, brings about a genuine hypertrophy both of
heart and aorta x (media and intima) ; and in hyperpiesis the
vagus seems to get used to habitual excesses of blood pressure.
I cannot agree with Bittorf that this ease is due to lesion of
the vagus terminals. But all depends upon the capacity of
the particular myocardium, if old or young, sound or unsound.
Bafningly complex are all these coefficients. If the vagus is intact
the pulse is slowed, as we may note occasionally during attacks of
angina (Vol. II. p. 332) ; but the prolonged fall of pressure is not
due to this — a longer diastole means at first a larger contraction
volume — but to dilatation in the splanchnic and probably
some other areas also.2 So if, momentarily, this and the vagus
diastole may mean plus output, this soon ceases as less venous
blood is returned. If the splanchnic nerves are divided, the
corresponding area fills with a large bulk of blood, which is
thus removed from the active circulation. A further and
perilous relaxation of the splanchnic system in shock and
collapse is, up to a certain point, too well known to detain us
in this place. Again, if the restraining influence of the cardio-
inhibitory nerves is removed by division on both sides the
heart begins to gallop. But, although we cannot but argue
severally about these divisions of the nervous endowments of the
heart, yet in life their connections are so complex and intimate

1 Brims u. Genner, " Einfluss d. Depressors auf die Herzarbeit," Deutsche
med. Wochenschr., No. 37, 1910.

2 See Bayliss, Journ. of Physiol, vol. xiv., 1893.

470 AHGINA PECTOEIS part n

that to alter the balance in any one of them operates as a com-
pound effect. This integration is true especially of the augmentor
nerves which, broadly speaking, on their excitement serve to
increase the output of the heart even, within limits, against a
rise of peripheral resistance. The functions of the vasomotor
and vagal divisions are however more independent than that of
the augmentor ; and, under experimental observation, the normal
inhibition of the heart by the vagus, mixed nerve as it is, may be
made plain. For instance, during experimental rises of arterial
pressure which, forasmuch as its own arteries are not, or are
but little, subject to waves of constriction, are felt at once in the
medullary centre, the curb upon the heart becomes instantly
perceptible ; its work is diminished and, caeteris paribus, the
pressure falls to its former level. So dependent is the circula-
tion upon its nervous adjustments that Balint,1 in some experi-
ments in dogs and cats, found that to destroy the aortic cusps
produced no drop of function, and gradually the heart became
hypertrophied. So again, the fatty heart produced in dogs by
phosphorus does not make at once for functional failure ; yet in
dogs, even with a sound myocardium, to cut one vagus, and
still more to cut both, ends promptly in heart failure.

It seemed necessary thus at some length to reconsider the
sphere of action of the vagus in order that my hypothesis of its
potency in angina might be better understood. The function
of the vagi, conservative as within limits it is, may nevertheless,
as Goltz, starting from the original observations of the brothers
Weber, in 1845, proved on cold-blooded animals, have a mortal
issue ; especially when the heart is old or enfeebled. A like
effect was then obtained by experiment in warm-blooded animals
on stronger irritation, not of the substance of the viscera but of
their investments. When the vagus is cut this effect is pre-
vented. However, by virtue perhaps of its mixed character,2
the vagus thus vexed does not usually stop the heart, not even
if the irritation be continued ; the vigorous heart escapes from
its governor, and in a strait refuses to spare itself at the cost

1 Balint, Deutsche med. Wochenschr., Jan. 6 and 13, 1898 (quoted by Dr.
J. H. Sequeira).

2 Some experiments suggest that the vagus may contain some accelerator
fibres, the action of which is usually masked (see Laidlaw and Symons, Journ.
of Physiol, vol. xli., 1910).

sec. ii DEATH BY INHIBITION 471

of the life of the system. Indeed ordinarily, if the stimulus
cease, the inhibition of the heart beat is followed by a rebound.
Hence the extrasystoles not infrequent in angina. Cushny and
Edmunds 1 have shown that the vagus effects its purpose by
lowering cardiac conductivity (heart block) ; and in a more
recent study of the subject, Hering of Prague 2 confirms this
opinion, with further detail, some of which concerns us here.
But, as Dr. W. T. Ritchie says,3 the lowered conduction gradually
ceases, even if the stimulus be continued. I have sometimes
speculated on the effect in the heart of sudden change of motion
into heat, which might aid the accelerators in this " escape."
That in pyrexia the heart is accelerated we know, but here other
causes of acceleration come in. James and Williams 4 note that
in the electrocardiogram a heart under vagus preponderance
shows only a prolonged diastole ; and it is in the later part of
diastole that the vagus tells most effectually. It is in this phase
of angina, not " in systole," that death takes place. A fall of
pressure, as by mitral regurgitation, or by means of a drug,
caeteris paribus, disarms the vagus, and averts death by in-
hibition ; and this in angina we commonly see (p. 443), and
even bring about, as by the nitrites.

I have said that during an attack of angina, sometimes
plainly sometimes less distinctly, the pulse may alter to the
touch ; it may hesitate or fluctuate, usually by retardations
suggestive of effort or check (p. 332). To Dr. Mackenzie's
remarks on pulsus alternans in angina I have made some
allusion (p. 334) ; it is important to distinguish this falter
from the controlling influence which I am discussing. And
both these conditions are to be distinguished from the
retardation of heart block. Dehio, twenty years ago, and
Kronecker 5 also, discussed this last kind of retardation as a
loss of irritability or conductivity ; Gaskell,6 Roy, and others

1 Cushny and Edmunds, Amer. Journ. Med. Sci., 1907.

2 Hering, H. E., Munch, med. Wochenschr., 1910, No. 37, and Zeitschr.
f. exp. Path. u. Ther. vii. pp. 363, 1909.

3 Ritchie, W. T., Quart. Journ. Med., 1912, vol. vi. p. 47.

4 James and Williams, Amer. Journ. Med. Sci., Nov. 1910.

5 Kronecker, Arch. f. Anat. u. Physiol., 1883, p. 263.

6 Gaskell, Journ. of Physiol, hi., 57, 1880 ; and Phil. Trans., 1882, p. 1017
(" that the excitability of the ventricular muscle is at the time not absolutely
the same throughout ; certain portions respond only to every second impulse.")
See also for recent research Mines, Journ. of Physiol, vol. xlvi., 1913.

472 ANGINA PECTOEIS part n

have discussed pulsus alternans as an expression of differential
or fractional muscular states, and of remainder blood in
dilated, and not dilated, cavities respectively. Then Hering,
verifying Gaskell's explanation, emphasised the distinction
of pulsus alternans from extrasystole which might simulate it.1
But Dehio was, I think, the first to use atropine as a means of
analysis, so as to distinguish vagus from myocardial lag ; this
valuable test often enables us to discern in a particular case
how much of the retardation may be myocardial or Purkin-
jean,and how much, if any, due to vagus, and therefore transitory.
Under atropine the dissociation of auricle and ventricle may be
ended, or at least modified ; the auricular rate may rise while
the ventricular remains unchanged ; and conversely, as Thayer
and Peabody have demonstrated,2 to stimulate the vagus in
heart block — as by pressure in the neck — may throw out ven-
tricular beats and slow the auricular even without notable pro-
longation of the a-c interval. But if the heart block be wholly
myocardial, if, that is, the dissociation be more or less structural,
atropine may make no difference. We shall see under the head
of Treatment why I am labouring these points, and how it is that
this action of atropine is of great practical importance. But Spiess
and Magnus- Alsleben 3 of Basel, who produced pulsus alternans
in rabbits by " glycoxylsaure," concluded that, generally speak-
ing, pulsus alternans consists not in partial asystoles but in a
universal hyposystole. And they found also that, under these cir-
cumstances, the vagus might even prevent a pulsus alternans ; for
on section of the a-v bridge, so as to isolate the ventricle, the
pulsus alternans ceased at once (" trat prompt auf "). As Thayer
and Peabody say, at times during an attack of angina one may
feel alternating waves of vagus influence ; waves which may or
may not sum with other factors to modify the phrasing, auricular
or ventricular. And I have seen, on accelerating the rate by
atropin, that with this acceleration pulsus alternans may become
perceptible, although apparently not continuously present. Pulsus
alternans then is no simple state of myocardial affection, but is
a complex of variables, and not necessarily persistent.4 So in

1 Hering, Prdger med. Wochenschr., 1902.

2 Thayer and Peabody, Arch. int. mid., March 1911, vol. vii.

3 Spiess and Magnus- Alsleben, Zeitschr. f. exp. Med. Bd. ix. Heft 2.

4 Wenkebach (Unregelmassige Herztatigkeit, 1914) has submitted pulsus

sec. ii DEATH BY INHIBITION 473

angina, if there be any degree of the Stokes-Adams condition,
what I have called a phrasing of the pulse may be observed ;
moments of summation of stimuli, a full consentaneous contraction
with dissipation of waste, and then a falling away of this integration.
But even when dissociation is present the a-c interval may still be
normal (Wenkebach, Gossage, and others). Once more : pulsus
alternans may occur with little or no default of the heart in cases
of high aortic pressure. At moderate pressures the elastic vessel
in easy diastole and systole takes up and neutralises variations
of output ; but when the wall is very taut this play approaches
to zero, and thus unyielding does not take up these variations ;
now every output, plus or minus, is reported in the pulse, and
such an alternation is not uncommon, and need not, I think,
signify a failing heart. Of course, during brachial compression,
in obedience to psychical causes or to respiratory tides, radial
beats may come through unequally.

Hay and Moore1 also have demonstrated, by Mackenzie's
method, how salient may become the influence of the vagus in the
Stokes- Adams condition; and there is other evidence to prove that
myocardial degeneration does not impair the control of the vagus,
that on the contrary such a heart is stopped by it more readily.2
Dr. Mackenzie says that " if any one function of the heart
is depressed the vagus is prone to seize upon it, and to increase
the depression " ; and again " depressed cardiac functions are
more susceptible to vagus stimulation." Dr. Gaskell also
showed, what is of great importance in this study, that after
vagus stimulation the restoration of cardiac function is gradual,
the beats increasing in strength slowly as the anabolic and
fortifying effects are realised. This, as he says, is gradual
function ; but if the vagus be hit by what I may call a snap-
shot the heart is checked without recompense, the sudden sharp
stimulus to the vagus having more of the depressor effect and
less of the anabolic and restorative effect than consists with
more gradual interference. And herein may lie some explanation
of the reflex vulnerability of old or diseased hearts, — that in them
the anabolic restoration is still slower of attainment ; nutrition

alternans to clinical analysis, and considers that Mackenzie's view of it as a
foreboding of death needs qualification (see case, p. 265).

1 Hay and Moore, Lancet, Nov. 10, 1906.

2 See Dr. Anderson's Cat Experiments, p. 475.

474 ANGINA PECTOEIS part n

is sluggish, and osmosis and surface tensions are in the older
tissues less vivid. Dr. Lewis * agrees that in prolonged a-c
interval (partial heart block) the vagus effect may be in-
stantaneous : the next ventricular contraction is suspended,
and no response may be obtained till several auricular systoles
have passed. We may note by the way that the a-v bundle is
said to be nourished chiefly by a particular branch of the right
coronary artery, a point to be observed in cases of death with
partial coronary obliteration.

Thus, under many known and some unknown conditions the
heart, as in the familiar Goltz experiment of tapping a frog's
abdomen, fails thus to escape. It is then in its first impres-
sion that the vagus influence is most critical ; as its influence
is protracted counter influences gain ground ; thus, if the
heart is sound enough to hold on, it gets driven forward.2
It is said that as the heart is escaping from vagus inhibition
the curve is, or often is, anacrotic ; 3 a minus cardiac impulse
being, in respect of this phenomenon, equivalent to plus aortic
resistance. In the frog experiment the vagus influence is sudden
and maximal, conditions which even for a healthy heart may
become irresistible (vide Reich, p. 483). Still, the healthy heart
of young subjects, as in the angina of syphilitic or rheumatic
aortitis, manages nearly always to escape in time — its readjust-
ments are both elastic and ready ; with the deteriorated or
even with the merely old heart it is not so. As the active
youth slips his foot and promptly saves himself, but the stiffer
joints and unready muscles of the elderly man fail to respond in
time and he falls before he can save himself, so it is with the
heart imperceptibly altered by age, or enfeebled by coronary or
other disease ; it cannot save itself, it topples, regains a step per-
chance, loses it again, and drops. Thus occasionally in a sound
patient by extreme agony, by an agony such, let us say, as the
passage of a calculus, a blow on the testicles, or a sudden and
intense emotion, the heart may be inhibited to fatal arrest ; as

1 Lewis, T., Quart. Journ. of Med., Jan. 1911.

2 Lewis, T., Practitioner, Feb. 1907.

3 Von Frey has shown that an anacrotic curve may be noted as the heart
is escaping from vagus inhibition, and that, as Roy and Adami and Lewis had
proved, such a curve may be one of only relatively excessive peripheral resist-
ance : i.e. of heart weakness.

sec. ii DEATH BY INHIBITION 475

again it may be by a specific effect of chloroform upon the
vagus. In the vagal nucleus, says Sir David Ferrier, a pin-prick
will arrest the heart. It is said indeed that firm pressure upon
the eyeballs will inhibit the heart, even to syncope, enfeebling,
retarding, or even arresting the radial pulse ; and that in animals
(dogs) the heart may thus be stopped in diastole. It is more
than probable that, in the degree of deterioration which an aged
or diseased heart may have undergone, its chances of escape from
an irritated vagus are proportionately diminished. Besides, we
shall see presently that in angina the vagi become hypercesthetic
(Wenkebach).

Dr. Hugh Anderson, to whom I desire again to express my
thanks, showed to me a very instructive experiment bearing
on this point. From a cat he removed the third — accelerator —
cervical ganglion ; so that the heart was delivered over to
contrary influences, as of the vagus. Now it appears that if,
taken in the hands, this animal be waved up and down, the vagus
is stimulated to action. In a young cat thus operated upon and,
on recovery from the operation, waved up and down, the effect
of the vagus may not be conspicuous ; the heart may lag a little
but it is not much affected, and never arrested. But if the cat be
an old one — one however in which on autopsy cardiac degenera-
tion may not be manifest, its life is in perpetual danger; to
wave it now reduces the ordinary cat pulse of 120 perhaps to
40. And not only may the waving kill it, but it is in peril of
death from ordinary contingencies. So liable indeed is the
animal to die suddenly that further observations often come
thus to a premature end. For, while the vagus resents its
stimulus promptly, reflects it as instantly, and on the removal
of the stimulus as promptly releases the check, with the
augmentor and accelerative influences it is otherwise. These
agencies come into action gradually ; they have a long period
of latency, a slow approach to the maximum, and a long
persistence after removal of the stimulus (Gaskell and others).
Thus experiment verifies what clinical experience had abundantly
illustrated, that under inhibitory influences an old heart, even
though to the eye of the pathologist it may not betray disease,
may yet stop while a young one escapes.

But this is not all ; in angina the vagus is morbidly sensitive,

VOL. II 2 H

476 ANGINA PECTOEIS part n

as one may say — worried. We may be surprised in angina to
find this nursing nerve become so ascendant, and so menacing,
seeing that in other diseased states — in ursemia for instance — it
may retard the heart but does not arrest it. Some light is thrown
upon this point by a letter of Professor Wenkebach to myself, in
which he writes that in angina he has found the vagus extraordin-
arily sensitive.1 In a few cases, during tranquil intervals, he has
very cautiously tested it by weak pressure on one side only, and
has found the effect to be prompt and excessive. As an afferent,
it seems in this disease to be baited to a degree of dangerous
activity. Indeed he thinks that the heart of an anginous
patient might be stopped by a tight neckband. In such states
close observation of the vagotonic motions of the pupils of the eye
might assist us, especially during deeper respirations. Sir Edward
Schafer 2 also points out this further peril of sudden death.
The inhibition may be deferred, but in two or three minutes
" suddenly show itself and prevail over the accelerators,"
when the auricles may cease to beat, and the ventricles
contract with a slower and somewhat irregular rhythm ; points
which remind us of no infrequent experience in angina pectoris.
To meet this abatement the accelerators and augmentors,
acting upon both auricles and ventricles, renew the rate and
force of the beats, and output is increased, even against some
rise of blood-pressure. This effect, he adds, is " precisely similar
to electrical excitation of sympathetic branches proceeding to
the cardiac plexuses." I may repeat that, while the accelerans
reinforces both systole and diastole, the vagus slows diastole only ;
hence its occasional mistakes. In clinical practice we perceive
darkly how complex are the conditions at work, excitatory and
inhibitory influences blending variously and inconstantly as
preponderances, quotients, or resultants ; and subject meanwhile
to preventions of access not only by antagonisms but also by
temporary or permanent changes in tissue conductivity. 3

1 I find the same observation is made in certain cases of heart disease
by Robinson and Draper, Journ. Exp. Med., Jan. 1, 1812, vol. xv. 1. As
these pages are passing through the press Professor Wenkebach has published
these clinical tests, with graphic illustrations, in his new work on the whole
subject of irregular cardiac action, Engelmann, Leipzig u. Berlin, 1914. He
accepts my hypothesis that sudden death in angina is by vagus reflex.

2 Schafer, Sir E. A., " Functions of Suprarenal Capsules," Brit. Med. Journ.,
June 6, 1908. 3 See Sherrington, Proc. Roy. Soc, Dec. 1908.

sec. ii DEATH BY INHIBITION 477

To turn now to the vasomotor or depressor division ; here we
find that the relief to the heart is by a direct relaxation of pres-
sures on dilatation of the vessels of the abdominal viscera,
which may become heavily engorged ; accordingly here too the
heart's work falls in output as well as in diastole. Within the
normal play of our reciprocating engine, as Professor Sherrington
has so admirably demonstrated in the skeletal muscles, inhibition
diminishes tonus in antagonists ; if then we regard the vaso-
constrictors as antagonists of the ventricular muscle, we may
anticipate the explanation of reciprocal working on vasomotor
governance to be analogous to that in the voluntary muscles.
" Two antagonists may be in action together, but their activity
decreases and increases in reciprocal proportions ; hence the
smoothness and accuracy of trained movements " (Sherrington).
Hirsch and Stadler think the depressor, which by twigs from
the jugular ganglion is a sensory nerve of the aorta, does not
exercise this continuous reflex, but regulates rhythmical efflux on
systolic call only. There are of course other depressor nerves also.
How readily a lysis of the circulation may come about through
the depressor I need not stay to explain ; indeed it is the less
necessary to do so as in angina pectoris I do not suppose this
to be the usual mode of dissolution ; in this disease death is
ordinarily by the alternative peril of vagus arrest. Von Dusch,
it is true, spoke of death in angina by paralytic dilatation of
the heart, but quite conjecturally.

Francois Frank, in Marey's Laboratory in 1876,1 showed
how irritating vapours, when applied to the nasal and laryngeal
mucous membranes, would retard the heart through the vagus ;
observations which were repeated and enlarged by Brodie and
Russell.2 These observers proved that almost any afferent nerve
of the body, under appropriate stimulus, can retard or arrest
the heart. They showed then, what is now well known, that the
stimulus of a rise in arterial pressure will, caeteris paribus, retard
the pulse. And we know also that cortical irritation may have
similar effects. Dr. Jex Blake has repeated these observations.3

In the Laboratory of Experimental Therapeutics in the

1 Frank, Francois, Acad, des Sciences, \ dec, 1876.

2 Brodie and Russell, Joum. of Physiol., 1889.

3 Jex Blake, Brit. Med. Joum., Jan. 21, 1911.

478 ANGINA PECTOEIS part n

University of Chicago, Drs. Capps and Lewis x have illustrated
these processes in a very interesting way. In my early Leeds
essays on empyema, I was led by experience to deprecate the use
of intrapleural antiseptic injections, because under such inter-
ferences, and apparently in consequence of them, syncope or even
death had happened.2 In some of my own cases under such
washing alarming faintness had occurred. Many records were
published later of these perilous events on washing out the pleura
or otherwise interfering with this cavity, especially near the
root of the lung ; e.g. by Cayley, Goodhart, Raymond, Vallin
(who repeated Capps' and Lewis' experiments), and others.3
As such injections often seem desirable, these warnings were
received by physicians with some reluctance ; and the deaths
recorded in certain cases were attributed, not to this operation,
but to thrombosis or some other accident. As years went on
however more and more cases were added to the lethal list, and
the practice of injection began to wane ; but, although Dr.
A. E. Russell had in some measure anticipated these results,
and had thus explained a case of sudden death on an exploratory
puncture of the chest by cardiac reflex,3 I think that the
Chicago research was the first definite experimental proof of
the chain of causes. Russell did not find the pleura so sensitive
as did Capps and Lewis, but these observers noted its response
especially when the pleura was inflamed. Dr. Johnston 4 has
since demonstrated the fine nerve ramifications, which he
regards as the paths of pleuritic pain, in the suprapleural
connective tissue investment. But with the lessons hence to
be learned in the practice of thoracentesis, impressive as they
are, I am not immediately concerned ; my purpose is to direct
attention to the cardio-inhibitory effect of certain peripheral
irritations, especially of the susceptible thoracic areas, and in
them of investing tunics.

1 Capps and Lewis, Amer. Journ. of Med. Sciences, Dec. 1907, and Arch.
of Int. Med., Dec. 1911. See also Brodie and Russell, Journ. of Physiol.,
1900 ; and Cadman, Journ. of Physiol., 1900.

2 See Editorial, Lancet, Sept. 28, 1912, but I had published this warning,
based on experience, long before " Dr. George Carpenter in 1893."

8 Vide A. E. Russell, St. Thos. Rpt., 1899, and Clin. Journ., Sept. 8, 1909.
But in 1864 Roger had recorded an eclamptic attack which occurred during
operation on a case of empyema (p. 480).

4 Johnston, Brit. Med. Journ., September 11, 1909.

sec. ii DEATH BY INHIBITION 479

Capps and Lewis began by quoting the experience, now perhaps
generally accepted, that in surgical operations about the pleura
" there still remains a considerable number of cases of sudden
death, in which no anatomical lesion (such as embolism) can be
found post-mortem to explain the collapse." Of the connection
between the cardiac and pulmonary plexus I have already
spoken : now Capps and Lewis tested the cardiac response
upon this route, and demonstrated that, although on irritation
of the normal pleura none, or but little, of such an effect may be
perceptible, yet in inflammation of the pleura a potent effect is
manifest. The effect is usually of the cardio-inhibitory kind ;
the heart is slowed, and the pulse tracings make wide excursions
between systolic and diastolic pressures ; the respirations also
are usually slowed, and for the moment may be arrested ; a point
in angina to which, under the head of Symptoms, I have referred
(p. 313). By atropine, or by division of the vagi, they could pre-
vent these effects. But occasionally the influence stole rather
along the splanchnic vasomotor division, when the pulse curves
betrayed a rapid decline of both systolic and diastolic pressures ;
the respirations became shallow and often rapid, and the ab-
dominal viscera engorged. This even more dangerous effect they
could prevent by intravenous injection of adrenalin. By care-
fully watching operations for empyema in man, and by noting
especially the effects of scratching the inflamed parietal pleura,
sometimes the one and sometimes the other of these effects was
observed ; sometimes the pulse became slow, even to inter-
mittency ; sometimes pressures and output fell together, and the
pulse dwindled to nothing. The afferents, as we have just seen,
are distributed, as Lennander demonstrated for the peritoneum,
not to the serous surface, but to the areolar tissue immediately
beneath it.

In a few instances a vasoconstrictor action, occasionally to a
well-marked and persistent degree, was observed ; but this was
quite exceptional ; such constrictive rises of pressure, if recorded
at all, were transient. Why in the many cases the vasomotor
result should be relaxation, but in a few constriction, is obscure ;
but it is notable that the constrictive effect was more frequently
observed in the cardio-inhibitory cases. In this respect we
may recall to mind that in most cases of migraine, or in sue-

480 ANGINA PECTOEIS part ii

cessive stages of a single case, such alternations of vasocon-
striction and dilatation are likewise to be observed. As we have
seen concerning the peripheral pleural surfaces, the inhibitory
effects were obtained vividly only when these tracts were in-
flamed, and the vagus annoyed ; but as the root of the lung was
approached the cardio-inhibitory effect became so much the
more that it would manifest itself promptly even without any
inflammatory factor: there the stimulus was approaching the
pulmonary plexus, and the pulmonary is connected with the
cardiac plexus into which the vagus enters. Brief cardio-
inhibitory effects, single prolonged heart strokes such as I have
noted occasionally in the pulse of angina (p. 332), could be
called forth almost at will, by stretching the root of the lung,
or the pericardium ; or by scratching the thoracic portion of
the vagus. Section of the vagi in the neck, or an injection of
atropine, would stop the cardiac effects, but did not exclude a
splanchnic dilatation ; so that a valuable differential test of
the nature of the cardiac effect was thus obtained. In 10 per
cent of operations on the pleura and lung, Korte and Lenhartz
noted some degree of cardiac inhibition — a transient retardation
of pulse and respiration ; and Brodie and Russell demonstrated
that irritation of the pulmonary efferent fibres of the vagus at
the root of the lung arrested ventricular contraction and respira-
tion with fall of blood pressure.1 Indeed in 1864 Roger had
made observations of the same kind on an eclamptic attack
which occurred during an operation on a case of empyema.

Startling effects then may follow even a simple pleuritic
operation. Brunque and Zesas 2 collected reports of 21 deaths
on incision, on lavage, or even on simple puncture (a case of
embolic hemiplegia was omitted). Gunshot and other accidents
causing costal osteitis, or tapping for a cancerous effusion,
have had syncopic, eclamptic, or mortal effect. How important
a bearing these observations have on my interpretation of
death in angina pectoris, the reader probably already appre-
hends.

On hypothetical grounds, in more than one previous paper on
the crisis of life in angina pectoris, I have recommended artificial

1 Brodie and Russell, Journ. of Physiol, vol. xxvi. p. 92.
18 Quoted in an editorial note, Semaine mid., 27 nov., 1912.

sec. ii DEATH BY INHIBITION 481

respiration ; and Brodie and Russell have shown that this
operation tends to quieten reflexes from irritated viscera.
During Capps' and Lewis' experiments the thorax was laid open.

The next illustration of this kind of inhibition which I will
produce, and many more are at our service, is taken from the Ad-
dress in Surgery at the Meeting of the British Medical Association
in 1904. Sir William MacEwen then referred to certain observa-
tions which he had made upon a sympathy between the pudic and
respiratory tracts, a response being obtained instantaneously.
When the pudic periphery of a patient, under anaesthesia, is irri-
tated, a prolonged, almost tetanic, respiratory gasp may be
produced ; and on each single repetition of the irritation a
stridulous inspiratory effort follows. In the majority of cases
the heart yields, if at all, so slightly to this vagus reflex, that to
the finger on the pulse the reduction is scarcely perceptible ; in
some instances however the cardiac sympathy is more ready ;
coincidently with the stimulus the pulse weakens. In a few
persons this effect is still more remarkable and ominous ;
evidently by the faltering of the pulse and the livid pallor of the
face it may become perilous. And here again these phenomena,
if not very notable while the tissues are normal, are rapidly
enhanced under an inflammation ; as may be observed in the
parallel case of an inflamed joint, irritation of which under
anaesthesia may set up spasm of the corresponding group of
muscles and rigidity of the limb.

Sir William Go wers, in the "Vaso- vagal Essay "to which I have
often referred, says, " In man, I think, a cause of adequate pain
has not been known to produce syncope if the patient were under
the influence of an anaesthetic " ; and he surmises therefore that
the afferent impression may be not on the vagus centre, or not
there only, but rather on the sensory regions of the cortex, and
thence focussed down on the cardiac centre in the medulla, as
in cases of sudden intense emotion. For my present argument
this question is not urgent ; but I may remark that, whatever
the mechanism, no such protective effect of the anaesthetic is
notable in operations on empyema, on the brachial plexus, or
(as regards those which I have quoted) on the pudic area ; nor
in my experience is complete protection notable in experiments
upon animals, even when under the deepest anaesthesia. Quite

482 ANGINA PECTOEIS partii

recently Crile and Cushing, under the awkward title of " Anoci-
(Innoci- ?)-association," have done much to elucidate this subject.
Morphin and atropin seem to afford substantial protection.

But, leaving this point undecided, I would reiterate the in-
ference which seems to be enforced by all these observations ;
namely, that when the peripheral tissues which accept the irrita-
tions are inflamed, such reflexes are much intensified. Now it is
in such an irritable state of the aorta, and especially of the supra-
sigmoid portion of it, whether in acute aortitis, or a subacute
extension of chronic syphilitic or of atheromatous disease, that
we may suppose this peripheral area, and probably the vagus,
to be in an exalted state of susceptibility, highly obnoxious
to impressions, and highly conductive of afferent currents, and
that the corresponding centre has become abnormally irritable.
As Professor Barker has said (B.M. Assoc. 1909), and as in
Dr. Anderson's cats, " syncope is very likely to follow slight
violence, even without operation, in old or decrepit people," the
enfeebled or old heart being more susceptible to inhibition, and
less able to resist it. As with voluntary muscles (Sherrington),
fatigue and certain drugs — e.g. chloroform — are conditions
favourable to inhibition. Moreover, according to circumstances,
certain stimuli {e.g. toxic) may promote either excitation or
inhibition, whereby unforeseen reactions may ensue. Besides
the surgeons mentioned, Mummery 1 has thrown light upon
the perils, in the course of an operation, of dragging upon
or wounding certain nerves ; perils which may be even
mortal. Now from our present point of view it is important
to note that the brachial plexus is a way peculiarly open to
this dangerous reflex ; even to sever its strands, as for example
in an operation for cancer, may cause sudden pallor, and
failing of the pulse even to disappearance at the wrist. Usually
the effect is but momentary ; the colour soon returns to
the lips, and the pulse improves : but the issue may be less
happy ; the pulse may fail to get back, and the arterial pressure
may drop lower and lower to death, a death which may be
wrongly attributed to the anaesthetic. Mr. Mummery published
a chart of pressures during an operation in which traction
on the brachial plexus caused a fall in pressure from 150
1 Mummery, Lancet, March 25, 1905.

sec. ii DEATH BY INHIBITION 483

to 50 ; the pressure rising again quickly to 100. To crush the
testicle or the paw of the dog, although under an anaesthetic,
thus abases the blood pressure ; at the first moment there is
a transient rise, then the fall follows. As one step farther,
Reich x has given a full study of operative interference with the
vagus itself. He showed that clean section only paralyses it ;
but crushing or dragging, or even the touch of forceps or bistoury,
re-excites it, so that in critical cases he recommends preliminary
resection of the nerve of the side. From his summary, in six
propositions, only the fifth concerns us here: that crushing of the
vagus is followed by inhibition of cardiac and respiratory action,
which in man may be mortal. For example, Dr. Falkner Hill
of Manchester sent me notes of two events of this kind during
an operation for extirpation of a malignant thyroid. The
anaesthetic was 1| per cent chloroform, with ether and oxygen.
In spite of due support of the jaw, it was dragged down, when,
the patient's condition having till then been quite normal, the
heart and respiration stopped. Restorative measures were suc-
cessful, and a new start was made without any chloroform
admixture ; but, on another unavoidable traction, the same
events recurred, with a mortal issue. From my therapeutical ex-
perience in angina, I suspect that atropin would prevent these
accidents ; but, for operation purposes, to block the afferent path
by morphia seems generally to be efficacious. In comparative
experiments on animals, Reich found the human heart more
susceptible to excitation of the vagus than the animal ; it
proved to be impossible thus to cause the death of an animal.

Now as chloroform is in common use for the relief of protracted
assaults of angina, it is a serious matter for us to know if this anaes-
thetic, or chloral, may be a treacherous ally. I am by no means
sure that, in so nice a balance of forces, chloroform is a safe
remedy ; in the abstract it is not ; in my experience morphin
is no less efficacious, and, moreover, avoids irritation of the nasal
afferent surfaces. In a paper read to the Royal Society (Proc.
R. Soc. 1906) Dr. Embley of Melbourne stated that, in the dog,
chloride of ethyl stimulates the vagus, and, as the drug becomes
more concentrated, the heart halts under vagus inhibition ;
yet not fatally. As in the animals observed the hearts were
1 Reich, " Beitrage z. klin. Chirurgie," quoted The Hospital, Jan. 7, 1908.

484 ANGINA PECTOKIS paktii

healthy, we were prepared to hear that in each case the organ
escaped from the influence. Now in the dog chloroform " pro-
duced an equal effect in one quarter the concentration in air " ;
not only so, but inhibition was succeeded by paralysis of the heart,
and arterial pressure fell and fell until respiration ceased. Dr.
Embley stated that he had witnessed cardiac syncope under
chloroform in two cases in man ; though happily in both recovery
set in, with sudden return of the pulse in fair volume, and of the
living colour to the face. A sound heart, he added, can generally
free itself from vagus arrest, but a feeble heart may fail to catch
hold again on life. Morat and Doyen, Brodie and Kussell, testify
also to these effects ; and the comprehensive study of this
subject for many years past by Dr. Waller is too well known
to every reader for me to do more than allude to it. In this
paragraph I am alluding only to early and sudden deaths,
often under light chloroform anaesthesia ; deaths indirectly due
to chloroform at later stages, deaths due to intoxication of the
cardiac muscle, or to " acidosis," do not belong to my subject.
Now let us apply these results to disease and to angina
pectoris. Perhaps all the arteries have their degrees of sensi-
bility, but the suprasigmoid portion of the aorta, and probably
other parts of it likewise, especially perhaps the cceliac portion
of the abdominal aorta are normally endowed with a peculiar
afferent sensibility to blood pressures. In such a part, let us
suppose a sore spot, an acute inflammation, or a subacute ex-
tension of a more sluggish process creeping over it or into
it. As we have seen, such a condition of receptive tissue
is extraordinarily quick to promote and to multiply reflex
phenomena, and to accumulate stresses in its controlling
centre. If such a reflex be focussed upon a sound heart,
in a youth with rheumatic aortitis, let us say, or in a man
in the prime of life with influenzal or syphilitic aortitis,
the heart, although touched unpleasantly or even critically,
will generally escape. As we have learned concerning the
cardio-reflex effects obtainable in even healthy animals by irri-
tating or dragging upon the central end of a divided nerve,
such as the sciatic, so the stories are many of sudden death in
young and healthy adults from some swift and poignant pain.
And if we suppose the heart to have become enfeebled by

sec. ii DEATH BY INHIBITION 485

decay, due perhaps to a failure or perversion of blood supply,
or to age, even then it may escape once and again, but sooner
or later will probably be overthrown. In such observations
and experiments as I have quoted we see that the critical
moment for the heart in angina, as in light chloroform anaes-
thesia, may lie in a first touch ; let the organ have time to
call up its reserves and its compensatory mechanisms, and it
may be able to fight on, and to fight through. Dr. J. H. Abram,
in a context of other significance,1 describes two cases of gall-
stone which he saw in consultation ; the first patient had a
sound heart and recovered ; the other had a diseased heart, and
died suddenly in the attack. And this, I think, is our experience
in angina. Notwithstanding, in such an hour of trial, even in a
young person with a heart presumably sound, we shall not be
too confident ; too often in such persons, and under such con-
ditions, the results have been mortal. On consulting the authori-
ties— such as Frerichs, and Rolleston — I find a considerable re-
tardation of the pulse (50 or 40) in a gall-stone attack is not
uncommon, especially at the outset. Frerichs has noted falls
of rate to 28 and to 21. Weitzand 2 in such circumstances
injected atropin, on which the pulse ran up to 120. Professor
Saundby and I, after injecting atropin in a case of agoniz-
ing enterospasm, observed the same acceleration. On the
other hand I have published a case of death in the agony of
passing a gall-stone in a healthy young woman ; at the
necropsy the stone was found in the common duct, but the
rest of the body, heart included, was perfectly healthy. Mr.
Pinching of Gravesend, on seeing my published note, kindly
informed me of a similar event in a woman set. 57 : the
gall-stone had advanced one-third of the way towards the
duodenum. No other cause of death was discovered. Conti 3
likewise has noted the reflex effect upon the heart of passing
gall-stones. He dwells also on other subdiaphragmatic causes of
cardiac syncope, and, accepting my hypothesis of inhibition
as the cause of sudden death in angina pectoris, discusses a con-
sequent " reflex palsy of the vagus," " with weakening heart,

1 Abram, J. H., Liverpool Med. Chir. Journ., March 1902.
2 Weitzand, Arch. f. exp. Path. u. Pharm. Bd. xxxiv.
3 Conti, Biv. crit. di clinica medica, 1904.

486 ANGINA PECTORIS part n

tachycardia, and even angina." On the other hand, he speaks
also of vasoconstrictor conditions with dangerous rises of pressure.
But he uses the name angina pectoris very loosely, and the whole
article is rather vague and speculative. I am far from saying
that death does not occur in the way Conti describes, but it is
in the extremer stages of protracted angina ; the usual course
seems rather that the vagi fail by fatigue, then the accelerans
gets the advantage ; the beat rate quickens but the pressure
and output fall, the heart dilates, and pulmonary oedema follows,
often with such intensity as to become widely audible before
dissolution.

I have alluded to Dr. Morison's interesting observation of
the same inhibition in a case of angina pectoris with aortic
regurgitation. While listening to his patient's heart during the
attack, as the vagus inhibition subdued and expanded the
ventricle, he heard the regurgitant murmur falling in intensity
almost to disappearance. The pulmonary second sound, on
the other hand, was enhanced, as in ordinary mitral disease.
This observation disposed him to regard a diminution in calibre
of the radial artery in angina as a syncopic rather than
a constrictive change. This may be so occasionally : as we
have seen vaso - constriction is not always present. Some
sphygmographic tracings have shown the vagus effects on
systolic contractions : these at first are slower, but unimpaired ;
then comes a fall of aortic pressure with more residual blood ;
then the help of a quicker rate until, as the heart recovers its
balance, the output enlarges again, the rate falls, and after the
relief the heart's vigour is restored.

I have alluded to the case of an insane woman in the West
Riding Asylum at Wakefield who in a sudden paroxysm of fury
staggered and fell dead. The heart was histologically sound,
and death was put down to " dilatation " under the suffoca-
tion of fury ; but subsequently I have suspected it was by in-
hibition, i.e. descent in diastole, larger contraction volume, and
longer pause. Relaxation or contraction of the dead organ at
the necropsy does not tell us much.

As regards the relation between the vagus and vasoconstriction,
I will repeat the words I have already quoted from Professor
Schafer, who has told us that " vasoconstriction in the normal

sec. ii DEATH BY INHIBITION 487

state (e.g. under adrenalin) is stronger than vagus reduction ;
but that the vagus influence may be deferred, and then suddenly
show itself (italics mine) ; when the auricles may stop, and the
ventricular rhythm persist slowly and irregularly." x Thus in
practice we find the vagus influences on the heart and the vaso-
motor function masking each other, while centripetal excitement
of cerebral centres, indirect stimulus of the heart by rising blood
pressure, and depressor function are in perplexed variation.

Now I have said more than once that in angina death is
apt to occur on the first falter. It is not during the long
battles that death is most imminent ; on the contrary,
patients come alive out of the most terrible attacks, or terrible
successions of attacks. As Sir Lauder Brunton says,2 " he
is often arrested by no very severe pain." And Dr. Parkes
Weber 3 testifies, " in angina pectoris it is often not the patients
with the best marked attacks who die first." And we may add
that if the patient dies during protracted seizures, he is liable
to fall not on a climax, but at the outset of the particular sally
which proves to be his last. If the heart be advanced in decay,
some travelling bubble of wind, some sudden turn or emotion
disturbs aortic pressure, the reflex trigger is touched and the
heart drops to its rest. When such an event happens at the out-
set, it may be difficult, or impossible, to distinguish the death,
as one of angina pectoris, from the lapse of ordinary cardiac
syncope. In the fiercer assaults, death is often by way of
ordinary heart failure.

There are on record, it is true, many cases of superficial
or torpid suprasigmoid aortitis in which, as in many severe
cases of syphilitic panaortitis, no anginal symptoms mani-
fested themselves at any phase of the process. As we see in
many an analogous impairment elsewhere, a very slow change
may compass its own toleration ; the nervous strands or endings
may be not goaded but benumbed. Thus a strong man who, if
suddenly throttled, would fight for life with demoniac energy,
by very slow increments of cyanosis may sleep into dissolution.

As in middle-aged, but still healthy and vigorous, cricketers

1 Schafer, E., Brit. Med. Journ., June 6, 1908.

2 Brunton, Lauder, Encycl. Medica.

8 Weber, Parkes, Lancet, Jan. 18, 1908.

488 ANGINA PECTOEIS partii

the consentaneity of eye and muscle becomes impaired, response
by little degrees delayed, and little by little the component
elements of function dissociated, rhythm more labile, and balance
less automatic, until the sum of small increments becomes
critical, so with years even in health disturbances are less and
less readily neutralised or compensated. In a healthy state of
the vessel the aortic reflex works well within the margin of
safety, but we have seen how in a subinflammatory or irritable
state this reflex becomes so exalted that each anginal seizure
paves the way for an increasing frequency of reiteration ; yet
we still have to ask how far the integrity of the balance of
the medullary centres is subject to, or susceptible of, higher
control from above ; and if in some cases we may have to suspect
a morbid coefficient in centres superior to the bulb ? The aortic
tambour, a regulative apparatus working through its nervous
endowments, not only governs systemic pressures, but also serves
to control the pressure-constant for the bulb itself ; so mutually
dependent are these beautiful adjustments. For instance, in
arteriosclerosis we may suppose a discord of function to be
brought about in the cardiac centre by a deterioration of its own
blood vessels ; or by a fretfulness generated and perpetuated
by summation of vexings of some tributary afferent surface,
such as to drive it beyond control ; or again by some loss of
control from above. In conditions of this kind patients may
drift into manifold states of peril ; but these are obvious specu-
lations which need no emphasis.

It was by considerations such as these that I was led to
propose (at Yarmouth in 1894) that in the usual sudden death of
angina pectoris the heart does not fail of its own intrinsic decay,
but is stopped by reflex inhibition. Although a few physicians, Sir
William Osier and Dr. Morison for instance, have mentioned this
solution of the problem with approval, it is far as yet from general
acceptation. Von Romberg, in the last edition of his book on the
heart, makes no allusion to my view of the part of the vagus
in death in angina ; though he does suggest that it may be by
shock — that is by paretic vasodilatation in the splanchnic area,
an alternative which, as I have said above, may have to be
borne in mind, but as an exceptional mode. Without by any
means denying that in some instances death in angina may come

sec. ii DEATH BY INHIBITION 489

about by splanchnic shock, I remain of opinion that in the large
majority the mode of vagus inhibition prevails. However the
following case, taken from my private files, presumably illustrates
the alternative of " shock," and the widely various suscepti-
bility of individuals. " Mr. C. S. consulted me," so his family
physician wrote, " for neurotic symptoms, especially pointing
to vasomotor instability, with unequal vascular tone." When
I came to examine his abdomen he proved to be very
sensitive to taps just below the epigastrium. Of this he had
been conscious for some years, so that he carefully avoided
such taps or pressures, as they " made him feel very queer."
His wife told me that one day thoughtlessly she gave him " a
playful little backhander there " when he promptly fell down
in a faint. This was a remarkable exaggeration of our common
sensitiveness in this region ; and in " abdominal angina " at
any rate this may be one mode of death ; but these cases are
rare, and the opportunities of observing and verifying the
precise way of death still fewer. The notion is current, and I
think with some truth, that " sudden death runs in families " ;
if so, the tendency may consist in part in such hypersensitive
reflexes. In his work on La Mort subite (1895) Professor
Brouardel, among many cases of sudden death due to fright
or other sudden emotion, narrates the following : — A labourer
in full health was trying to lift a load, when another coming
up to him said, " Get out, let a better man try," at the
same time giving him a light blow on the stomach ; the
poor fellow dropped down dead immediately. No mark of
violence was found at the necropsy. Of another man, he reports
that in a fracas he was struck upon the testicles ; he cried out,
and fell dead. No lesion was found. Several other such verified
cases he mentions also, in which sudden death followed blows
on the epigastrium, larynx, and so forth ; or sudden emotions,
or injuries, too slight to be directly dangerous to life. A
severe blow upon the chest may cause death by arrest of
the heart ; yet at the necropsy no disease be discoverable.
Boinet says : " Chronic aortitis moreover may end in sudden
death. Often the patient succumbs in a full attack of angina
pectoris ; more rarely he dies of a mere syncope, without
appreciable cause, after some days of discomfort and precordial

490 ANGINA PECTOEIS partii

pain. Potain and Rendu attribute it to an ischsemia of the
coronaries, other authors suppose an anaemia of the bulb.
Degeneration of the heart, alleged by Mauriac, seems improb-
able." Dr. Bence Jones' patient, whose case is narrated in my
Cavendish Lecture (p. 147), died thus suddenly without appreci-
able cause in the heart. When the heart and its own arteries
are diseased, the organ becomes unable to withstand a per-
turbation which a healthy heart would overcome ; and when
angina pectoris, even of some severity, has proved to be con-
sistent with the prolongation of life for some years, or again
when it has ended in recovery, we may guess that the factor
of survival was a healthy, or comparatively healthy, cardiac
mechanism able to resist extremes of reflex inhibition.

CHAPTER VII

DIAGNOSIS

In a full discussion of Symptoms and Causes Diagnosis
has been so far anticipated that little may remain for a
special section. For instance, in spite of what we are told
about the difficulties of discrimination between angina pectoris
and the host of spurious " vasovagal," hysterical, and other
" functional " disorders, I venture to repeat that if the physician
will concentrate his attention upon the definite features
and processes of angina pectoris, not allowing his fancy to
play fast and loose with spurious imitations of a malady so
grave and so sinister, his difficulties will vanish. I cannot
reiterate too tediously that time after time grave errors of
diagnosis arise from temporising with angina, from watering it
down on the supposition that there are gradations between
the false and the real. What we have to decide is whether
the patient be from first to last the subject of a turbulent
disorder or of a mortal disease.1 We are concerned with "trade
and traffic in riddles and affairs of death." As Lancisi says of
genuine and spurious aneurysms, no dissimilar contrast, it is of
vital importance that, as with the Lydian stone, we shall be
content with nothing less than the closest analysis. Of all maladies
there are occasional cases which, at one interview at any rate,
are hard to read ; of angina pectoris such cases may now and
then present themselves : for instance, as Nothnagel's vaso-
motor series occasionally appears in true angina, there is a peril
in too ready an assumption of spuriousness. Nevertheless I do

1 Since these words were in type Lyman Greene, Colorado Med., October
1912, writes : " I would especially emphasise the importance of minor anginas,
and protest against the confused use of the term ' pseudo-angina.' "

VOL. II 491 2 I

492 ANGINA PECTOKIS part n

not hesitate to say that in angina pectoris such moments of
doubt are not more but less frequent than in other diseases of
equal gravity. How much greater, perchance, may be the
difficulty of arriving at a positive opinion — let us say in early
cancer of the stomach, Addison's disease, tuberculosis, or typhoid
fever. In initial stages, or even in later stages, if a disease
manifests itself in some disguise, when for instance Graves'
disease goes far without giving rise to either goitre or exophthal-
mos, or when in an old man a pneumonia or an effusion creeps
on silently without giving rise to pain, cough, or obvious dyspnea
— I need not multiply such examples, — under conditions so
equivocal no doubt the physician, puzzled, or careless, may
fall into error. In other cases, as Dr. Mitchell Bruce has
pointed out, two or more possible sources of a case of angina
may have to be unravelled. And when, under the influence of
modern teaching, we confuse with unquestionable angina cases
of spasmodic dyspnea, and cases of mere counterfeit, we
may well lament that the diagnosis becomes difficult. Thus
it is that some authors find themselves compelled to stipulate
that there is no " true angina " without the radiating pains and
the fear of death ; but I repeat one might as well argue that
epilepsy is not epilepsy unless aura, loss of consciousness, and
convulsions be all present ; or that Graves' disease cannot be
said to exist until goitre, exophthalmos, rapid pulse and fine
tremor have all put in their appearances together. Yet in such
dilemmas, if we examine ourselves, have we not too often to
confess that when we erred, or vacillated, it was for lack
of thoroughness, of accuracy of observation, or of perception
of the relative values of the signs and symptoms inter se ? But
in the inquest of angina pectoris no soft options are tolerable.
Curschmann, who took a naive pride in his unquestionable
powers of diagnosis, described a certain case of spurious
angina x as one which agreed in all respects with the genuine
disease (alle Symptome ivie bei echter Angina). These
symptoms were pain and tightness at the heart, severe (heftiges)
palpitation, oppression to the degree of syncope, radiating pain
in the left arm (italics mine). Now I may ask any experienced
physician if this group of symptoms is characteristically that
1 Curschmann, Lehrbuch d. Nervenkrankheiten, 1909, p. 832.

sec. ii DIAGNOSIS 493

of genuine angina ? Indeed the author himself proceeds
to say that, as they occurred in a hysterical young woman
without syphilis, he was sure of the true diagnosis. Of course
he was ; then why worry about it ? The chief difficulty is, as
Rauzier says,1 to recognise at times the partial dependence of
such symptoms on organic disease ; as in my case of the house-
maid with aortic stenosis (p. 189). Rauzier publishes two such
cases, and wonders if the pain and distress had in them a core
of true angina or not. Now both presented a double aortic
murmur.

Too well aware of the black list of my own errors, or short-
comings, in clinical diagnosis, I venture notwithstanding, " ut
homunculus unus e multis," to feel some assurance that
under the head of angina pectoris we ought very rarely to go far
astray. Cases of difficulty, of suspense, there are, as we shall
see ; but these equivocal instances are not of the counterfeit class,
and cautious effort tests, during tranquil intervals, are generally
crucial. However, among the spurious cases I may refer to a kind
mentioned by Sir William Osier 2 in his Lumleian Lectures which
may be very equivocal. Certain highly susceptible persons, if
brought face to face with a case of angina, and constrained by
anxiety and sympathy, may, under some potency of suggestion,
reproduce in themselves the features of the disease, as it were in
a glass. That the counterfeit may be very close the author's
cases prove to us. I have not had this experience ; but I
remember such a " suggestible " person, highly strung under the
trial of our final M.B. examinations, who, when questioned by a
physician concerning asthma, extemporised an attack of this
disease ; and on another day when questioned by a surgeon on
renal colic threw himself into this attitude of suffering. The
examiners, not without excuse, resented what they supposed to be
mockery; and I, who knew my man, had some difficulty in appeas-
ing their wrath. Thus in a neurotic patient of either sex, especially
if near or under middle age, it may be difficult, at one interview,
to discount some extravagances of blood pressure and a thoracic
oppression due only to " nervousness or vasomotor storms."

1 Rauzier, Province mid., Feb. 3, 1912 ; quoted Arch, des mal. du cceur,
Sept. 1912.

2 Osier, W., Lect. II., Lancet, March 26, 1910, pp. 839-840.

494 ANGINA PECTORIS partii

I must content myself here with repeating axiomatically that
angina pectoris after middle life is usually atheromatous ; under
the age of 45, if not the mock disease, it is usually either
syphilis, rheumatic fever, or influenza.

Concerning the touch of the minor form of the malady, as in
latent epilepsy so in angina, the story of the attacks may be
so unskilfully narrated, so defective in data, so casually alluded
to, or so overlaid by other and more imposing disorders, as to
escape even the attentive medical critic ; yet such cases should
cause no more than transient hesitation. For instance, in
the case of a certain middle-aged lady I felt some hesitation,
until it came out that the patient had twice been awakened
in the night (4 or 5 a.m.) by substernal pain and oppression,
without dyspnea, compelling her to sit up in bed ; this was
almost though not quite decisive. Rarely can it happen that
a broad and discriminating review of all the facts would
fail to build up a decisive opinion : a review of the patient's
age ; of his temperament ; of the state of his tissues and
especially of his vessels and aortic mechanism — as tested for
instance by the dimensions of the aorta, the position of the sub-
clavian and innominate, the quality of the second sound, and
the effect of exercises in calling out, or failing to call out, a
systolic murmur at the base ; the persistent range of his blood
pressure ; in a patient of or under middle age the possibility, or
even the stigmata, of syphilis — such as scars, old iritis or choroid-
itis, Robertson's pupil, loss of knee-jerks, Wassermann's re-
action, or the history of some other toxic cause of aortitis, such as
influenza ; a startled check or warning grip as contrasted with
a gasp and sob as of a cold douche ; or again a coherent story
with constancy of symptoms as contrasted with a flustering
story of incoherent complaints.

Perhaps of my own list one of the more difficult cases to
analyse was this :

Miss B. S., set. 35. Has had much worry ; two and a half years
ago she fainted away. Then, and for some time after, had attacks
of severe pain in the side, a hand's -breadth below the breast
(7th-8th rib). Then the pain moved to the left arm, with a suffoca-
tive feeling and panting. " Always having it." (A " suffocative
feeling" and panting are more suggestive of the so-called false

sec. ii DIAGNOSIS 495

angina.) The pain starts at the inner left wrist, running up the
inner forearm ; sometimes it is at the anterior axillary bend of
the fifth rib, sometimes in the lower intercostal region. During
and after the attacks there is severe hyperesthesia of the whole
left arm and thorax. The attacks are quickly relieved by amyl
nitrite. They are never brought on by exertion, but follow annoy-
ance or fatigue. When free from attacks, can walk up stairs or
hills. No anaemia. The systolic pressure rose to 140, but prob-
ably 10-15 degrees due to nervousness (we had not time to await
the calmest moment). Heart and vessels all seemed normal. No
neuritic or neuralgic " points." The patient was quickly cured by
change of scene, judicious hydropathic methods, and strong sugges-
tion. There was no history of influenza or other infection ; syphilis
was inconceivable, and no signs of it were to be detected.

Pains, heaviness or numbness, or combinations of these in the
left arm are quite commonly associated in neurotic women with
the still better known submammary pain. Vasomotor false angina
is often relieved by nitrites, especially by amyl nitrite, though
not so regularly as we might have expected.

Dr. Byrom Bramwell1 tells us he has seen cases in young
persons in which, had they been older, the diagnosis of angina
pectoris would assuredly have been made ; but in which complete
and lasting recovery (and the age) " showed that the angina
was functional." For, he adds, "it was impossible to differentiate
functional and organic forms." My distinguished friend does
himself an injustice ; no one is better able to discern these vital
distinctions ; but his judgment, if I dare say so, may have
been warped by some systematic prepossession ? In the study of
angina I am disposed to say of not a few of my distinguished
colleagues, as was said of Patmore, " that he did not so much
follow the light, as plant the light where he chose." I have
shown, I hope, that in young cases, syphilitic or otherwise
infective, angina pectoris often does pass away.

As an instance of differential interpretation of pains, I will
call attention again to Dr. James's case (p. 442).

It is often hard in aortic disease of the heart to say whether

some pains are of angina or not. If not, if they be due to

fagged heart, the pain is more about the lower area of the

side, but is apt to rise into the left upper breast ; a pain of

1 Bramwell, Byrom, Brit. Med. Journ., Jan. 15, 1910.

496 ANGINA PECTOKIS part n

cardiac distress does not seat itself under the sternum. Extra -
systolic leaps and bounds of the more violent degrees sometimes
cause pain about the heart, but, so far, the sign is rather good
than bad.

Then there may be, and, if so, more significantly in the
stealthier cases, the peculiar sense of arrest without dyspnea
(we have seen that if there be dyspnea the heart or lungs will
prove to be diseased also) ; the unaccountable touch of warn-
ing, something less perhaps than a meditatio mortis, but yet
significant or sinister out of proportion to the degree or duration
of illness, a feeling in my observation quite alien from the
conflicts, desperate as they may be, with paroxysms of asthma,
of cardiac or renal dyspnea, of laryngeal spasm, of pulmonary
infarction, of tabetic crisis, or " nervous crisis," and so forth —
encounters in which the patient may win or lose, but which at
worst are not an instinctive horror but a rational alarm, a battle
with an open enemy. That ominous touch it is which often
speaks to the wise just when a hint is wanted ; namely in those
light, swiftly transient, early apparitions of angina whose inter-
pretation may not be clear ; the touch of the tipstaff, the sense
of an uncanny call, is frequently there. I have cited the case
of a patient who suffered from anginal pain in the centre of the
hand (see p. 293) ; in that case sure diagnosis was perhaps at
first impossible, but the patient's own foreboding was true
enough.

Pain then seated in the area commonly called " cardiac "
or " precordial " is, as we have agreed, a common sign of cardiac
disorder — valvular or functional ; but neither in seat, nor
character, nor aggravations does it resemble angina pectoris.
I have quoted Dr. Mackenzie's contrast of this " precordial
pain," dull and persistent if at times rather paroxysmal,
with that of angina. This lower intercostal pain may how-
ever strike up the left side of the chest into the neck.
Intolerance of pressure or percussion in this affection is more
conspicuous than in angina ; it is most conspicuous perhaps in
functional cases.

In another case, recently under my notice, the pain was again
the principal feature, not only in the diagnosis, but in the patient's
description ; in the earlier attacks the sensation in the arms

sec. ii DIAGNOSIS 497

was rather one of discomfort and weakness than of pain. This
sensation first came on after long and enthusiastic dancing,
when he felt much exhausted. The discomfort of the arms
extended " down the flesh of both arms down to the wrists."
In later attacks the arms became exceedingly painful, the pain
being now brought on by ascents, though occasionally it would
come on during rest. One or two of his worst seizures awoke him
soon after midnight, the pain in the arms, and latterly down to
the fingers, being " terrible." On ascents or other exertion the
pain or distress was entirely in the arms, and his description was
of something more distressing than ordinary pain. On exami-
nation, which as the chest was fat was not very easy, the cardiac
impulse in its normal site, even in the prone position of the
patient, was perceived with difficulty, and the first sound
wanted quality. Percussion was negative. Nothing seemed
definitely wrong about the base of the heart or the aorta. He
had lived rather freely and had a very anxious business ; he
smoked, but not to excess ; tobacco did not seem to be the
cause. He denied syphilis, but I have blamed myself for not
insisting on a specific course of treatment. I have said that when
he saw me the pain in the arms was the predominant, if not the
only, symptom, yet some attacks — and, oddly enough, the earlier
ones — had been attended by an " exhaustion " in the chest ; in
the later, either the "chest symptoms" had passed off or were lost
in the agony of the arms ; although again it is remarkable that
" a sense of something more than mere neuralgia or rheumatism "
was borne in upon him. Not long afterwards the malady took
on the usual form, and a year or two later he died in a
seizure. Another patient tells me, in spite of some dubious
reassurances of mine, that the pain from which he suffers is
no ordinary pain ; and, as time goes on, I am more and more
convinced that he also is right. Yet his heart to all direct
appreciation is healthy, and once during an attack of the pain
presented, to my perception at any rate, no aberrancy. Now
however the patient is checked while walking, and often has
to sit down, or lean against some support. And I note that he
walks by preference along a road where there are seats.

Even concerning the common radiating pains, error is not
out of the question ; generally by imputation of angina to

498 ANGINA PECTOEIS partii

intercostal neuralgia which, as we have seen, may be paroxysmal,
and attended with much nervous perturbation and with cardiac
disorder; or to the more tenacious pains originating in certain
intrathoracic (especially aneurysm) or spinal diseases, for which
however we have the tests of painful spots, the more continuous
duration, the comparative independence of bodily and emotional
movement, or signs of other meaning, such as those of mediastinal
growth, and so forth. In such cases the X-ray picture would
come to our aid. In an aberrant case, or in one of angina
minor, the response of the pain or oppression to ascent, even a
gentle acclivity, often affords a crucial point of diagnosis. Dr.
Dockray's patient (p. 294) could move about the house without
pain ; he could even turn the winch of his printing machine with
impunity, which was curious ; but to walk up even a moderate
ascent, especially if soon after a meal, pulled him up at once
and inexorably.

On the other hand, it is unquestionably true that in many
cases, and in many attacks, of angina, only too genuine and severe
in kind, even in a status anginosus, there may be no death omen.
However this symptom is one for which, if not spontaneously
mentioned to me, I am rather reluctant to enquire.

Parry, in his descriptions of angina pectoris, dwelt rather too
much upon syncopic symptoms, and so was led to propose the
name of Syncope anginosa. Still there are cases no doubt in
which, especially if the attack be known only by description,
there might be some hesitation between angina, petit mal, a
Stokes- Adams syncope, or an ordinary fainting fit.

The more eccentric seats or courses of anginal pains I have
indicated already ; the practised observer is generally prepared
for them, partly by their behaviour, partly by their associa-
tion with some warning ; and I must not reiterate more than
is convenient {vide p. 296). Rendu x has published a good
example :

A man, set. 40, of robust appearance, was attacked by influenza.
After this he began to suffer from peculiar attacks, consisting in a
kind of crisis arising in the little finger, extending up the arm, and
finally becoming more marked, accompanied by feeling of oppression

1 Rendu, Journ. de mid., June 10, 1896.

sec. II DIAGNOSIS 499

in the chest and agony, with, on some occasions, syncope. After a
short period in hospital these attacks became somewhat better, but
then for a while recurred daily. There were no physical signs of
disease, either of heart or lung.

In discussing the diagnosis in this case, whether it were a case
of angina pectoris or not, Rendu was rather inclined to withhold
the diagnosis of true angina pectoris, because there were no signs
of cardiac affection ; because he supposed angina to be very
rare before the age of 40, and because the pain began peripher-
ally. The previous history of influenza was also, in his opinion,
in favour of a " neurosis." The case ended in recovery. I
think Eendu was clearly wrong, in any case his three reasons
were insufficient. The case was published not long after the
commencement of the virulent outbreak of influenza at the
end of the last century, before its occasional attack upon the
aorta was recognised (p. 268). A few years later Rendu would
probably have come to a different diagnosis ; for he has done
good service since in describing the aortitis and its symptoms
which may follow rheumatic fever (vide Aortitis, p. 155).

Neuralgia of the phrenic nerve might cause some suspicion of
angina ; in one case of diaphragmatic pleurisy in an elderly man
I was for a while in doubt. Phrenic nerve pain is referred
to the insertion of the diaphragm into the costal arch, passes
upwards on the border of the sternum, and between the scaleni
in the neck ; the respiration is cramped and shallow, and racking
cough, hiccup, and even vomiting may appear.

Of physical signs I say nothing ; often there is none (p. 345).
Charles Sumner was examined by many leading physicians in
the States and in Europe, and in every case with negative results.
Perhaps the area of the aorta was not carefully mapped
out. But the not infrequent association of angina pectoris
with aneurysm must not be forgotten ; in the presence of both
to rest satisfied with a diagnosis of either would be un-
workmanlike. In such cases pressure signs, radiography, and
other means may assist us to a complete diagnosis. The
spinal pains of a posterior aortic aneurysm are more continuous
than those of angina ; at first they are little more than
a weary ache, and are usually alleviated by changes of
posture. But aortic aneurysms in the supravalvular area,

500 ANGINA PECTOEIS partii

associated with angina or not, may escape the most rigid
scrutiny, even by the X-rays. We must never forget that
diseases may run in company. I may make a reticent allusion
to the report of a certain well-known case of " gastric ulcer
simulating angina pectoris." The explanations of the pain by a
perigastritis affecting the solar plexus, splanchnics, and dorsal
nerves were quite ingenious ; but then it came out that a short,
soft murmur of aortic regurgitation had been heard ! We
have seen that many of the older writers swept under the
title of angina a motley collection of cases of " gout of the
heart," " gout of the stomach," mesenteric arterial thrombosis,
cardiac and pulmonary embolisms, acute pancreatitis, and so
forth ; as pathology then was they could hardly avoid the
confusion : we must try to do better.

A right interpretation of the uneasiness of abdominal angina,
even if the physician be on the alert to recognise the characters
of this form of the malady, may for a time be difficult. I
think in the following case the diagnosis of " typical abdominal
angina " was questionable, that its symptoms belong rather to
the well-known group of mesenteric atherosclerosis with con-
sequent atrophic and other disorder of the bowels (p. 310).

Female, aet. 42, suffered for years from crampy recurrent pains
of colicky nature. Atherosclerosis present in high degree. Blood
pressure enormously high, heart enlarged. Died of an apoplectic
stroke. P.M. : Extreme sclerosis of abdominal aorta and its chief
branches. Kidneys " intact." x

Tobacco-smokers, gouty persons, coffee-drinkers, and some
nervous persons are liable, especially in later life, to attacks of
cardiac irregularity, especially during and after meals, with epi-
gastric distension, oppression, or even pain, a series which, with
some degree of arteriosclerosis in radial artery and aorta, may
simulate epigastric angina very closely. Ortner says (loc. cit.),
and I agree with him, that it is not sufficiently realised that a
race of extra systoles may cause oppressive pains, often sub-
sternal or epigastric, and sense of tightness. These are the
riddles which call for all our discernment, and a diagnosis on
one visit may be scarcely possible ; but in a few days the

1 Rossbach, Munch, med. Wochenschr., 1910, No. 19.

sec. ii DIAGNOSIS 501

recurrences of arrhythmia during rest, and without the epi-
gastric pain, the comparative ease, when the stomach is empty,
of walking slowly even uphill, the ability, even at worst, still to
go forward, if with some discomfort, the effects of diet and
remedies and so forth, will enable us, after some care and
watching, to come to a decision. Eructations of wind mean
little in this diagnosis ; they accompany all such conditions. In
one ambiguous case of this kind I was assisted to the correct
diagnosis by a note of Broadbent's, which I have found useful
in not a few cases — that cardiac arrhythmias, of the extra-
systolic kind, coming on at rest after getting into bed, are
of functional origin. It has been pointed out that a globus of
wind, or spasm in the oesophagus or at the cardiac orifice of
the stomach, may simulate slight anginal attacks. Mr. Verdon
says it is more than a simulation (p. 344). Dr. Hertz, in his
interesting " Goulstonian Lectures," * described this kind of
discomfort and fulness under the sternum in the middle line
as caused by rapid inflation of the small balloon introduced
for experimental purposes into the gullet. However, speaking
very generally, obvious perturbation of the heart, palpitation,
arrhythmia, or even acceleration is against a diagnosis of angina.
On the other hand, a " gastric or abdominal case," whether a
true angina or not, is by no means safe ; and such patients,
usually elderly men with abdominal and other arteriosclerosis,
should be warned against exertion after meals, or while dyspeptic
or flatulent ; and we shall not forget that gouty plethoric persons
are apt subjects for angina.

Akin 2 cites this case, of a man, set. 56 ; gouty, and a large feeder.
On walking after full meals would feel an oppression, and a little pain
under the ensiform cartilage. Also was short of breath. He would wait,
belch, and then go forward. Pulse 90, tense. Aortic second sound
accented. Urine contained a little albumin, but no casts. So far
the case may not have been anginous, such symptoms are common
in disordered hearts ; yet at a later date angina supervened. Here
the dyspnea might have thrown the physician off the diagnosis.

At the Belfast Meeting of the British Medical Association a
case of sudden (cardiac) death was reported in a young man per-

1 Hertz, Lancet, May 6, 1911.
2 Akin, Journ. Amer. Med. Assoc. ; Kpt. Lancet, June 20, 1909.

502 ANGINA PECTOKIS partii

forming some feat of athletic emulation. At the post-mortem no
disease was discovered, but his stomach was found crammed with
cherries. I believe the line of interpretation of such cases, as of
the so-called angiospastic or angiosclerotic abdominal pains, will
he towards tension upon the mesenteric and other visceral invest-
ments and connections. These tracts are very rich in Pacinian
bodies. In one such case these bodies were found diseased.1 And
in old persons, as Dr. Hugh Anderson's experiments (p. 475)
show, even in cases in which no definite degenerative changes
may be demonstrable, the heart is far more touchy ; so that
death on mesenteric tension is not surprising. Lastly, throm-
bosis of a coronary branch might occasionally, as Pal says,
simulate the abdominal form of angina rather closely (vide p. 311);
the pains, if any, may strike into the left arm. Or the collapse, con-
tinuous epigastric or lateral pain, oppression, and rapid irregular
pulse may simulate a visceral perforation (see case, p. 451).
I will conclude this paragraph with short notes of the following
case, in which my own diagnosis was at fault.

An active and healthy elderly man was walking quickly to keep
an appointment, when he was startled by a distressing sensation in
the epigastrium, " as if a half-brick had rolled over in his stomach " ;
he pulled up, and then walked slowly to his meeting, and thought no
more of the matter. For some months before, however, he had noticed
a disposition to intermittences of the heart ; doublets, triplets, quad-
ruplets, and so on ; or with more arrhythmia : and for the first time
he had had a slight attack of gout. Eight or ten weeks later he took
a long cycle ride in a hilly country, and much enjoyed it ; the next
day he walked some hours on the moors, and returned fatigued ;
but after a rather full tea, started for the railway station, a mile dis-
tant and uphill. Almost at once he felt again the same oppression in
the epigastrium ; this returned incessantly as he walked, so that he
reached the station with difficulty. He was directed to live carefully,
and to avoid exertion ; still the oppression would return on slight
efforts. In London he could not manage to walk from the steps in
Waterloo Place to Piccadilly Circus without bringing on at least a
touch of it. One day he was unexpectedly called upon to walk up a
short, steep rise to a house where he was to call ; as he cautiously
began to ascend a pain seemed to rise under the sternum, and to spread
over the front of the chest ; it was not severe, and was unattended

1 Case quoted, Huber, C, " Sensory Nerve Fibres in Viscera," Journ. Comp.
Neurol, 1900.

sec. ii DIAGNOSIS 503

with inward dread, only with rational apprehension. It returned
a little as he essayed to walk on, still he managed to reach the house,
and felt no more of it. The diagnosis of angina seemed then in-
evitable ; he was put under strict rest and diet, and some anti-
gouty remedies were administered. In a few weeks the whole trouble
vanished ; and gradually the patient returned with impunity to the
active life which some years later he still continues. The malady
proved to be no more than may be indicated by such a title as
"gouty dyspepsia"; and the pain in the expanding thorax seems
to have been but a part of other muscular pains about the chest,
back, and loins, which likewise were interpreted as " gouty." (Com-
pare case, p. 259.)

There is not much fear of error between " abdominal angina "
and abdominal aneurysm. Dr. Nixon x read for me notes of 179
cases of abdominal aneurysm ; in none was the pain anginoid ;
even when paroxysmal it was more after the kind of renal or
other colic, or radiating down some nerve, such as the sciatic.
Generally it was a boring pain, often severe ; the seat usually
lumbar. Death was practically always by rupture, when
the pain was indeed more after the manner of angina pectoris.

To discriminate tabes, whether in abdominal or thoracic
angina pectoris, as an alternative, or associated disease, will rarely
be difficult ; but we must remember that in uncomplicated
syphilitic angina the pupils may have ceased to react to light,
or the patellar and Achilles' tendons to the tap. In one of my
cases of syphilitic angina without tabes, the light-stop sign was
present. There are many differential signs by which the
diagnosis may be made, and the " crisis " of tabes distinguished;
but we shall never forget that aortic disease, due to the same
virus, often brings about a combination of angina and tabes,
with a possible aneurysm in addition. It is conceivable of
course that upon some hapless sufferer both an anginous and a
tabetic crisis may fall together. So far as my small experience
of such mixed cases goes, the paroxysmal "gastric" pain of tabes
itself is intercostal, not substernal in seat ; and, if the heart be
disturbed, it is rather by palpitations, which are not characteristic
of angina pectoris. The pain of " gastric crisis " usually ranges
about the area of the 7th, 8th, and 9th dorsal nerves, but we know
of no reason why tabes should not attack the same spinal
1 Nixon, St. Barthol. Reports, vol. xlvii.

504 ANGINA PECTORIS paetii

segments as those concerned in angina, and might thus set
up the same referred symptoms. Some such interpretation might
hold for a case of tabes published by Vulpian,1 in which, although
angina pectoris was diagnosed, at the necropsy, the heart and
aorta proved to be normal. A peripheral neuritis of cardiac nerves
is alleged by many writers on nervous diseases (Oppenheim,
Pitres, Vaillard), but with little or no definite evidence.

The experience of a particular case reminds me that the
possibility of confusion between an attack of angina minor, or
sine dolore, and petit mal should be mentioned, as contingent
vasovagal or other circumstances might make a single attack a
little difficult to unravel. Still, with both alternatives present
to the mind, the diagnosis could not remain long in doubt.

The factor of tobacco cannot be tested except under a rigid
abstinence of at least six weeks. I have suggested that in tobacco
cases some cardiac arrhythmia is always (?) present (p. 247).
Some cases attributed to tobacco were probably infectious angina.
Appendicitis seems to be capable of anything ; but embolism
of the mesentery, pancreatitis, gall-stones, plumbic, neurotic,
and other belly-aches, are very unlikely to simulate even ab-
dominal angina. Still there are cases, such as one reported by
Ortner,2 and another by Stengel,3 out of 25 cases quoted from
Max Bruch of Vienna, in which atheroma (probably with
thrombosis ?) of the mesenteric vessels, with cramp-like pains,
colic, tympany, and constipation, simulated the abdominal form
of angina pectoris.

Here, in its formal place, the radical distinction between
angina pectoris and paroxysmal cardiac or ursemic dyspnea
must again be emphasised. Although to confuse these states
seems scarcely venial, yet among records of angina pectoris
we may continually detect admixtures of cardiac cases, of pul-
monary oedema or infarction, and of high-pressure dyspnea. Not
long ago I read these published words of a justly esteemed
teacher, " A man walking uphill one day was seized with sudden
breathlessness, so that he had to sit down, in fact he had a very
bad attack of angina pectoris " ; well, so it may have been, but

1 Vulpian, Rev. de rned., 1885.

2 Ortner, Volkmann's Sammlung.

3 Stengel, Toronto Meeting Brit. Med. Assoc, 1906 ; vide Lancet, Sept. 15,
1906.

sec. ii DIAGNOSIS 505

the " fact " of dyspnea was a contrary fact. Probably the case
was just heart disease ; at any rate it was complicated with
heart disease. On the paroxysmal dyspneas of renal disease,
and of Hyperpiesia, I have written at length (pp. 315-316. Com-
pare also Elliott's Equivocal Case II., p. 447). I can only repeat
that the assumption of the name of " angina pectoris," or of
" angina sine dolore," for these seizures is without excuse.

With Mr. Harris of Ely I once saw a man, of 79 years of
age, in whom attacks of anguish led to a suspicion of angina
pectoris (" sine dolore "). The heart was arrhythmic, and the
auricle probably fibrillating. The physical signs suggested
myocardial degeneration. The " fear of death " was a part
of a heavy depression of spirits, and we decided that the case
was not one of angina, but of heart disease and melancholia.
He improved for a time, but at a later date died in the ordinary
course of heart failure.

The following case is a good instance, I can scarcely say of the
difficulty of diagnosis, for in my opinion there was none, but of
divergence of medical opinion ; divergence engendered of the
looseness of phrase in respect of angina pectoris. A man,
about 60 years of age, of despondent but not unhealthy aspect,
complained of pain in the region of the heart. He laid his hand
upon the submammary region of the left side. The pain,
though variable, was not paroxysmal ; it came and went
in a capricious way, observing no moments of exertion or
emotion. At some hours of the day or night, however
quiescent the patient, it would appear ; as at other hours it
would recede. Though he complained of it with morbid
importunity, for he was convinced it was due to disease of the
heart, and would kill him, yet there was no organic horror. The
site, character, and behaviour of the pain, the temperament of the
patient himself, and the other symptoms all pointed to hypochon-
driasis. However, as ill-luck would have it, there was a systolic
murmur at the apex of his heart, a murmur unaccompanied
by any signs of cardiac alteration, or of irregular distribution
of the blood, and due no doubt to sclerosis. He could lie down,
and continually would he, curled up on bed or couch without
the slightest embarrassment of the breathing; and, in his dejected
way, could walk up and down stairs, or out of doors, without

506 ANGINA PECTOKIS part n

renewal of his discomforts. Nevertheless he was pronounced by
two physicians to be suffering from angina pectoris. He was
sent to me by a third physician, a man of large and ripe experi-
ence, who demurred to the diagnosis. I also assured the patient
that his case was neither one of angina nor of any active
cardiac disease ; there were no signs of circulatory disorder, and
the pain had neither the seat nor the manner of anginal pain.
The patient, disappointed by the mildness of our diagnosis, went
off to yet another consultant, who promptly accepted the more
dignified anginal interpretation. The patient threw up his
business, the worst step he could have taken ; and, as I heard
more than once at later dates, succumbed, not to angina, nor
any mortal affection, but to hypochondriac invalidism. Such
are the consequences of the parrot-like repetition that anginal
pain is "in the precordial region." We repeat it till it imposes
itself upon us as truth.

Another interesting example of a like error was narrated a
few years ago by Dr. Shadwell,1 in a discussion at which I had
been describing some cases of influenzal angina. A lady patient,
three days ill of influenza, was sitting up in bed gasping for breath,
she became " livid " (not pale), " her hands and feet were cold."
At first Dr. Shadwell thought these attacks " remarkably like
those of angina pectoris " ; but, as a good diagnostician, he pro-
ceeded to detect and to verify certain tender points in the course
of one of the intercostal nerves on the left side and on the spine,
and finally discerned that the case was one of intercostal neuralgia.
Dr. Shadwell assured us that his case, which was one of the
spurious kind with intercostal neuralgia especially apt to arise
in women after influenza and similar enfeebling maladies, might
well have been taken for angina pectoris. Dr. Shadwell was
probably right, yet he might have hesitated before the evidence,
since firmly based upon clinical and pathological records, ^f
genuine angina pectoris as no very rare sequel of influenza.
If the pain is precordial, if the patient lays his hand
under the breast and across the apex of the heart, the heart
may perhaps be affected, even gravely affected ; but the
presumption so far is against angina pectoris. The pain may be
" referred " from some other viscus, or be a " mere neuralgia."
1 Shadwell, Brit. Med. Journ., May 13, 1905.

sec. ii DIAGNOSIS 507

Intercostal and other neuralgias are not definitely aroused by
movement as are anginal pains. They are more " spontaneous,"
more capricious, more wearisome.

Dr. Head and Mr. Mummery have pointed out that pain radiat-
ing downward to the shoulder and arm, and even paralysing the
arm and hand, may spring from so eccentric a source as a lower
back tooth. Balfour recorded an alarming attack in an elderly
gentleman of " cardiac pain " with failing and accelerating
pulse, which happily resolved itself into an attack of shingles.

Coffee, tea, and tobacco poisoning will not be forgotten ;
doubts of this kind, as I have said, can be cleared up only by a
six or eight weeks' abstinence from the suspected article. The
tobacco oppression does not arrest the patient with the same
imperiousness, he can walk on, indeed he is often restless or
agitated ; still it may be impossible in a middle-aged man with
some arteriosclerosis to come to a decision until tobacco has
been laid absolutely aside for six weeks. For occasionally, in
its slighter degrees, when the cardiac arrhythmia rarely absent
in tobacco cases may be scarcely notable, a substernal
oppression hard to distinguish from angina minor may occur.
Sir W. Osier x says that tobacco angina may prove mortal ; my
own impression is that not a few cases of so-called "tobacco
angina " are angina proper ; e.g. of syphilitic or otherwise in-
fective origin, and that the mortal cases are of them.

On the subject of spurious " anginas " perhaps more than
enough has been said (Chap. II.) ; I will not refrain from
repeating Balfour's sarcasm that the name " pseudo-angina "
is useful only " to hedge the diagnosis." Not that the
false anginas are always " hysteria " or " temper." The
criterions formulated by Huchard, though too formal, may be
useful in practice ; the diagnosis lies not in this item or in that,
but in the sum of the series. We have seen that agitation is
not unknown in cases of angina only too genuine, the patient
may even pace the room, and show other movements of
distress (p. 328). We have all seen such patients quickly sit up
in bed, or even spring to the floor. One of my patients in his
worst moments rolled in the bed to and fro, swaying his arms
and moaning ; but attacks so cruel as to break through the awe
1 Osier, Sir W., Lancet, April 9, 1910. See however p. 246.

VOL. II 2 K

508 ANGINA PECTOEIS partii

of the disease are, I think, always on other grounds indubitable.
The pain or oppression of the " Vasomotor " cases is often
severe, but the pain is commonly in the lower intercostal area,
with precordial anxiety and hyperesthesia, and attended
with sighs and pantings. Or it may occupy the upper
chest, usually the whole upper breast ; it is more diffused, not
definitely sternal, the whole thorax is bursting ; and in the
arm the pain, if any, may not observe the ulnar or any definite
district. The hyperesthesia of angina pectoris, according to
Mackenzie, is deeper, and may be elicited in the absence of
complaint by pinching up a muscle — pectoral, sterno-mastoid,
or trapezius. I have seen superficial skin tenderness now and
then soon after an attack of angina, in one case very distinctly.
Quickened pulse, palpitation, or arterial throbbings suggest
" neurosis." Sometimes the mock angina in its returns of dis-
tension, or fulness with panting, observes a periodicity which is
not seen in the briefer apparitions of the true disease. In most
cases the eye, temperament, and history of the patient, and the
state of the arterial tree, are decisive. Still vasomotor oscilla-
tions often appear in genuine cases, perhaps in few are wholly
absent ; moreover such phenomena may precede and give
warning of a genuine seizure, and such a double process in an
elderly woman might for a while be difficult to disentangle.
Polyuria is a feature of both maladies. It is not my experience
that spurious angina brings about arteriosclerosis. I once
saw a case — with Mr. Cory of Soham — of very slowly established
pulmonary thrombosis after pneumonia in which for about a
week the pallor, oppression, and fear might for a moment have
suggested angina sine dolore ; but the more or less continuous
course of the incident, the hampered respiration, and other
features were distinctive ; although until a few seconds before
the sudden death the pulse was regular at 84, and normal in
quality. Of my own experience, I must repeat that, although
I have been in the way of seeing a good deal both of cardio-
arterial and of nervous disorders, I cannot recall any case of the
so-called " pseudo-angina " which could have deceived a careful
observer, in possession of all the data, unless it were perhaps
one of the rarer tobacco cases, or possibly one of arteriosclerosis
or aortic disease with a fringe of neurosis but no angina.

sec. ii DIAGNOSIS 509

It would be unbecoming in me, however, to assert on my
limited personal experience that there is never room for waver-
ing between " organic " and " functional " cases. For instance,
some years ago I heard to my regret that a gentleman well known
to me, at any rate by reputation, had been obliged in the prime
of life to retire from an important position on account of angina
pectoris. He had access to the best medical advice, and no
doubt availed himself of it, and acted upon it. A few years later
I learned that after an interval of complete rest he had entered
again upon an active life, and was in good health. I wrote
therefore to a common friend of his and mine, an eminent phy-
sician, now taken from us, to enquire if the case had been one
of angina pectoris, perhaps an infection, ending in recovery.
Our friend, who had been consulted in the case, replied to the
effect that he had found " no evidence of any infection, nor
indeed of arterial disease, nor of high blood pressure ; but
rather of atony," and that he himself had opposed the verdict of
angina. His opinion at the time was that " the case was one of
overwork, neurasthenia, and perverted metabolism." We may
not unreasonably suspect that even in this case also, difficult
as it may have been, the diagnosis of angina pectoris was not only
wrong but not justifiable on the facts. Still genuine angina may
occur in neurotic subjects (vide Case 241), with epiphenomena
which might divert the observer from the fundamental diagnosis.
This lamentable mistake has occurred more than once within
the circle of my own experience.

The stealthy growth of aneurysm, of adenomatous, syphilitic,
or other neoplasms of the mediastinum, pleuro-pericardial fibrosis,
and so forth, must not be overlooked ; in syphilitic cases aneurysm
and mediastinal gumma will not be forgotten : but this is not the
place to enter into so large a digression. We must make sure
that angina is not associated with a latent aneurysm ; pressure
pain may persist between anginal attacks. In all such cases
the X-rays will be used. I have mentioned already one case
of angina in which dilatation of the aorta was thus definitely
verified ; physical signs had indeed indicated it. The second
case was a remarkable one in this respect, that the first
examination " on a bad day " likewise clearly showed dilatation
of the aorta ; but on a second occasion, when the patient had felt

510 ANGINA PECTORIS partii

much better, the vessel had recovered its normal dimensions. I
remember one case of mediastinal growth, and one of extensive
fibrosis, in both of which angina was at first suspected, but set
aside in part by the ray picture. I have remarked incident-
ally concerning perforations of heart or stomach, pancreatic
haemorrhage, etc., that if for a moment they might be taken
for anginous attacks, the collapse, and in many of them vomiting,
would soon remove them from this category.

Some authors approximate Stokes- Adams disease to angina
pectoris, but by confusion rather than by comparison. I have
no recollection of a case of my own partaking in any considerable
degree of both diseases, though of course the double event is
not unlikely, especially in syphilis, influenza, or rheumatic fever ;
and the a.-c. interval may for a while be prolonged. In the
syncopic variety attacks of epigastric anxiety, pallor, and suspen-
sion of respiration might at first suggest epigastric angina, or
angina sine dolore ; but the effects of atropine, the venous pulse,
and so forth, should soon clear up any doubt. I will conclude this
somewhat critical but, I trust, not censorious section, by taking
to myself a confession of Dr. Goodhart,1 a touch which makes
all physicians kin ; he says, " I sadly and sorrowfully admit it.
I have made mistakes so often that I no longer blush for them."
Few of us perhaps can so well afford this frankness ; none in
a few words could have set us a better ethical example.

The effects of nitrite of amyl, positive or negative, have
been put forward as a diagnostic test. It is not worth much ;
it relieves many spasmodic conditions not angina pectoris.
1 Goodhart, Sir J., Lancet, July 1, 1905.

CHAPTER VIII

PROGNOSIS

Prognosis, even more than diagnosis, is almost wholly
implied in the discussion of symptoms ; yet here again I would
formally declare that the issue of angina pectoris is by no means
always mortal. If the interpretation of its symptoms be such as
I have advocated, we have seen that death in angina pectoris
is an accident, in old persons a frequent accident, yet, even were
this issue invariable, it is a contingency nevertheless. The
proportion of cured cases on my list is large, and includes a few
elderly persons with the disease in its classical form. Dr. James
Mackenzie reports that one of his patients, a man set. 48, with
all the classical symptoms of the disease, recovered. Broadbent 1
described a case in a man set. 50 (apparently syphilitic ?), in
which, but for an aortic murmur, the patient got well, and
returned to business. " Fortunately," as he surmised, " the coron-
aries were not implicated." His diagnosis was of angina never-
theless. One of Fothergill's patients, a typical case, with the
usual breast and arm pains, set. 30 (syphilis ?), recovered com-
pletely, and was in good health twenty years later. Fothergill
gave him cinnabar and Bath waters. Yet among medical
men the conviction that angina must be mortal is so strong
that if it fail to kill it is deprived of its name. I have quoted
Broadbent's remark that the dead house is no place to look
for cures. Desportes, surveying his collection of cases, con-
cluded that a favourable issue might be hoped for in patients
under middle age with sound hearts. We shall warn the patient,
however, or his nearest friend,2 that in angina only too frequently

1 Broadbent, Sir W., Lancet, May 27, 1901.
- As for the patient himself perhaps Ktodos iv KaKoh ayvwala.

511

512 ANGINA PECTOEIS partii

death is sudden, often at the beginning of an attack ; but, if
long deferred, the event is more often by way of ordinary heart
failure. Gairdner, it is true, considered death to be an essential
term in the accurate definition of angina pectoris, yet death
is no more essential to the conception of angina pectoris than
of the plague. Some recent writers on angina, in pardonable
reaction against the counterfeits of the disease, dwell on its
" almost invariable fatal termination." They declare that about
angina pectoris there must be no mistake. It is indeed no
disease to be trifled with, but we must not be compelled by
modern necrologists into too gloomy a prognosis. I have argued
in many paragraphs that in acute cases in young people,
whose coronary circulation may be unimpaired, recovery,
however grievous the seizures, is not the exception, but rather
the rule ; and even in old men, with degenerate arteries,
recovery is not to be despaired of. The older writers, less
enthralled by the dicta of the modern post-mortem room,
less chastened perhaps by its discipline, recorded not a
few recoveries, crude and tentative as their treatment neces-
sarily was. As under chloroform : one patient, whose chances
seem slender, escapes, while another, whose cardiac condition
proves post - mortem to have been fair enough, succumbs.
Desportes' pronator teres patient, although a bulky, gouty, sedent-
ary clock-maker, suffering from typical attacks, completely re-
covered on the maintenance of a moxa in his thigh for 18 months.
Heberden and Fothergill each relates a case of cure in patients set.
30 and 35 respectively, i.e. in young adults. I have upon my
notes the following extract from an author of the eighteenth
century, whose name I have unfortunately mislaid, " experientia
tamen morbum immedicabilem vocare non licet, quum plures
angina pectoris laborantes perfectae sanitati restituti sint." A
case of cure is also credited to Abercrombie,1 in a girl set. 13,
but on reference to his report I cannot read the diagnosis
as sufficiently definite ; she had cardiac symptoms. Jurine
collected no little evidence of recoveries, " even in old chronic
cases," and uses them as an argument against the coronary hypo-
thesis. Laennec speaks confidently of recoveries, even in severe
cases.2 Afriend of my own, well stricken in years, and whose vessels
1 Abercrombie, Trans, Med. Chir, Soc. 2 Laennec, loc. cit., p. 350.

sec. ii PKOGNOSIS 513

are probably as far advanced in senescence (he is not a patient
of mine), suffered severely for two or three years from angina,
both major and minor. At one period he could not walk fifty
yards, however cautiously, without bringing on stenocardia.
Happily under treatment the disease abated, and now for several
years he has been restored to his eminent public functions, and
is able without anxiety to address large meetings, and continually
to answer no inconsiderable demands upon his strength of body
and mind. Of late however he tells me that on severer efforts,
which cannot always be avoided, some substernal tightness is
prone to return. In other parts of this essay I have mentioned
similar cases under my own care. Sir Lauder Brunton said,
at the Belfast Meeting, that " cases (of angina) — even very
severe ones — might apparently recover entirely, and remain well
for years." This seems to upset the notion of cardiac degenera-
tion ; but such, by the way, is not his hypothesis.

With Dr. Lloyd Jones I saw Mr. P., set. 53. Typical sternal and
brachial pain radiating to lower jaw. Continually stopped by it
while walking, " when he turns pale." No dyspnea. Grey com-
plexion, and looks older than his years. Urine normal. Is sure he
has had no syphilis, and there is no sign of it. Very moderate in
alcohol and tobacco ; and no great worries in home or business.
Blood pressure, full systolic, 150. Slight systolic murmur at base,
and clacking second sound. Accessible arteries a little thick. This
patient — of whom I have often heard since from Dr. Jones — in time
got well, so far at any rate as to consider his health good, to walk
to business, and to do all his work.

A clear case of recovery under Dr. Bramwell has been alluded
to already. Also in my own notes I find the following instance of
recovery of a patient under the care of Dr. Atkinson of Saffron
Walden :

Male, aet. 59, nervous, and of a neurotic family. Dr. Atkinson
was called to him urgently on his first attack, which was typical
and severe. There was neither then nor afterwards any sign of dis-
eased heart or kidney ; and so far as the finger could tell, no per-
sisting rise of blood pressure. The arteries of the limbs were a little
too palpable and visible. Sir William Broadbent, who also saw the
patient, agreed with our diagnosis. He became unable to walk up
any ascent, and had almost to give up the horse exercise to which
he was accustomed. After a course of treatment lasting some time,
in which Dr. Atkinson found 5-grain doses of iodide of potassium

514 ANGINA PECTOKIS partii

to be effectual, he gradually recovered ; and twelve years later
Dr. Atkinson wrote in answer to my enquiry, " He is now very well
if he would only think so."

This note touches a point of importance. In several other
instances I have seen how the foreboding of angina, or the agony
of it, had so unstrung the nerves of the patient that he did not
dare trust to his regained freedom ; tests of immunity are
dreaded, and every uneasy or incidental sensation dwelt upon.
Such is the shadow of the wing of the black hawk !

Some years ago, with Dr. Prince of Buntingford, I saw an old
squire (vide p. 250) who from the age of 88 to 92 was subject
to typical angina. He recovered under nitrites, of which drugs
he became gradually independent. He died, set. 95, of
" bronchitis," but never had any sign or symptom of " heart
failure." Again, Mr. Walker, formerly of Lowestoft, will
remember a case of angina in a middle-aged man, who was
suffering also from aortic insufficiency. (Syphilis denied, but
there was a long alcoholic history.) The anginal attacks were
very severe and very frequent. The alcoholic indulgence was
stopped, and when I saw him again, a year later, the angina had
ceased. Mr. Walker wrote to me much later (July 17, 1911)
that the patient had continued to be quite free so far as the
angina was concerned.

My colleague Dr. Humphry also will remember a case of
typical angina (p. 163) which we saw together, a case in which
the attacks were many, severe and unmistakable, but recovery
was complete, and now for many years permanent.

The following case also offers a good instance :

Female, past the change of life, sent to me on June 7, 1906, by
Dr. Forrest of Terrington. He was called to her eighteen months
ago for angina. Soon afterwards the symptoms amounted to
the " status anginosus," the paroxysms being almost continuous.
Amyl gave little relief, and caused nausea. She was brought round
under injections of morphine, followed by nitroglycerine, used
very frequently, which, with strict precautions of life and diet, com-
passed a substantial amendment. But in February some social
pressure had thrown her back, though not to the gravest state. Yet
even now she is continually subject to attacks. The pain starts
at midsternum, and radiates to the left shoulder and arm ; the
arm may become " numb " ; sometimes the pain may drive into

sec. ii PEOGNOSIS 515

both arms. The attack is attended with a sense of " fearful faintness."
Attacks not rarely occur during sleep ; she wakes with a " dream
of fainting which is worse than the pain, though this is bad enough."
Without my suggestion she spoke of the deathlike sensation. She
was a woman of high spirit and courage, moved much in society,
and had lived well, not denying herself a few glasses of wine with
her meals. She had driven out a good deal, but taken little bodily
exercise. The systolic pressure was 180. Dr. F. reported the pulse
as usually about 60. Generally the pulse showed little disturbance,
but in her worst phases the heart became irregular and almost
showed signs of failure. This however was temporary. There
was definite dulness at the manubrium, and a little to the right
of it. To press the finger even lightly into the episternal notch
causes instantly acute pain, something after the kind of the attacks.
Pressure, freely tested, anywhere else discovers no hyperesthesia.
The arteries not tortuous, or notably thick. A systolic murmur at
base. Second aortic loud and rather tympanitic. Urine always
normal (Forrest).

I did not see this lady again till March 1914, when she called
about another ailment. For some time after her last visit she had
suffered a good deal from the angina, but with perseverance it was
subdued. " Now for some considerable time has been wholly free
from it." She did not seem to care to talk much about it, and
evidently feared lest it should return sometime. However she was
sure that she was then, and had been, wholly free, and was going
about as she pleased. The murmur at the base still persisted ; and
the arteries showed some thickening. The manubrial dull area
was unchanged. But now she could bear manipulation in the jugular
fossa without the slightest discomfort. There seemed to be no
history of any infection before the onset of the angina.

Dr. Mackenzie also speaks of " complete cessation of pain and
permanent recovery." Mr. Brook of Lincoln narrated to me two
cases of complete recovery from " true " angina pectoris, and one
of these was in a gentleman of 70 years of age. This patient
survived, in health, for ten years more, and then died suddenly
of " heart failure." Samberger, on his large experience (loc.
cit.), denies that recovery is a rare exception ; a hopeless
prognosis, he says, is justified only in cases with cardiac
disease. After treatment many of his 73 patients recovered so
far as to return to some work ; a few were completely cured.
Morgan (loc. cit.) reports a number of cases of complete recovery.
Unfortunately too often in angina the heart is submitted, not, as

516 ANGINA PECTOEIS part n

under chloroform, to one or two trials, but to a long and search-
ing series of them ; thus the chances of slipping from under
the inhibition are reduced.

But too often these hopes, even confident hopes, are dashed
by the recurrence of the disease after no inconsiderable periods of
cessation. I have more than one record of this unlucky reitera-
tion, in some cases after a patient, even for two or three years
or more, had regarded himself as a free man again, and had
returned to active life ; yet even then there is room for hope.
Dreyer 1 published a case in which for seven years after the
chancre there were no symptoms. Then appeared a long course
of them, especially ulcerative lesions of the skin and tongue and
iritis. During this period angina pectoris set in, was arrested
by specific treatment, and twice reappeared with the same good
therapeutical effect. After the third series of attacks the Wa.R.
became for the first time negative and the angina wholly dis-
appeared. How long, however, syphilitic infection may hang
about, for many a year and even into old age, is well illustrated
by a case sent to me by Dr. Mathewson of Bromley.

Male, set. 60. Thirty years ago rupia. Evidently an orderly
and intelligent person. He placed himself systematically under
specific treatment for five years. No reinfection. Eleven years ago
(see p. 175) became subject to angina, first attack on cycling up a hill ;
although subject to it ever since, has kept it at bay. In typical
attacks the pain used to be substernal, passing to left upper
pectoral muscle and down inner arm ; severe at left wrist ; thorax
compressed. Full attacks are now rare, but is subject to occasional
angina minor. Aortic direct murmur, no regurgitation. Angor
not mentioned.

In many cases a subacute phase of the aortic lesion lights
up again as if to impress upon us the duty of every precau-
tion against persistent hyperpiesis, hard work, and other causes
of vascular strain ; or old adhesions, under some tension, are
tender. I read lately of a case in which, after a period of angina
pectoris in early adult life, the patient, who in middle life had
enjoyed good health and full power of work, was in late life
attacked again by the disease, and fell a victim to it. In such
cases one may postulate a succession of two independent
1 Dreyer, Med. Klinik, May 4, 1913, quoted Epit, B.M.J.

sec. ii PKOGNOSIS 517

attacks of aortic lesion, the earlier one at any rate probably
infective ; although the first attack may in some degree have
prepared the ground for the second. It is unreasonable to
argue, as it was argued in a recent medical journal, that in
such cases the disease had persisted throughout, and had merely
fallen into abeyance, so that a bad prognosis ought never to
have been remitted. Such occasional coincidences pertain to a
minority of cases, and may be independent. Furthermore, we
should be careful as clinical observers to ascertain, in such
a recurrence of cardioarterial disease, that the death was a
death by angina. About ten years ago, in consultation with the
late Mr. Hyde Hills of Cambridge, I saw a gentleman of middle
age, who was attacked by angina pectoris of some severity. In
the course of a year or two he got well and returned to his
ordinary occupations. Four or five years later he fell ill of heart
disease and died ; but, as we learnt on careful enquiry, not with
the symptoms of angina pectoris, but with those of ordinary
cardiac failure, due in all probability to coronary occlusion and
associated myocardial degeneration ; no uncommon sequel. As
Dr. Graham Steell has said (loc. cit.), the angina may subside while
symptoms and signs of myocardial failure run their ordinary
course to death. Our colleague Lucas Champonniere, whose death
we are lamenting, had suffered, it appears, from angina pectoris
" some years before," but " by strict precautions " had been
long free from it. One who at a certain stage of cardiovascular
disease has suffered from angina pectoris may at a later stage
die suddenly of heart disease ; but, unless there were definite
clinical evidences of a return of the angina, it would always
be precipitate, and often erroneous, to attribute the death, as
so commonly in such cases it is attributed, to this malady.
Angina, although frequently associated with the various kinds
of heart failure to which old people are but too prone to
succumb, creates no immunity against them ; and in earlier life
an infection may set up not angina only but also a cardiac lesion
to end fatally ; as in the undergraduate of Selwyn, referred to,
p. 274, whom I saw with Dr. Christian Simpson. From his acute
rheumatic angina, terrible as this was, he recovered completely ;
but ten years later he died suddenly of the aortic valvular lesion
originally associated with it. It may be taken as a maxim that

518 ANGINA PECTOEIS part ii

cases originating in an infection offer a more hopeful prognosis.
In these cases especially, prognosis depends upon early diagnosis
and prompt and skilful treatment (see case, p. 529). Syphilitic
angina often issues in relative recovery, in disappearance, that is,
of the angina ; though always with permanent injury to the
vessel itself, and only too often with permanent destruction
of the aortic valve. But how, while the local lesions progress,
by corrosion of sensory areas or alteration of stresses, anginal
attacks may cease is illustrated by a case of Curschmann's
(loc. cit.), in which long continued attacks of angina wholly
vanished (" vollstandig wieder verschwanden "), but brady-
cardia set in. After death, at the autopsy, bulging of the
ascending arch was found, with disease of the coronary arteries
and fibrous degeneration of the myocardium, involving, no
doubt, the auriculo-ventricular tracts.

I have said in the foregoing pages that I regard angina
with more hope than do many of my colleagues ; that agonizing,
appalling, as it is, its mortality partakes of the nature of an
accident, the accident of an inhibition of a heart often already
frail or undermined ; and that even a healthy heart may, rarely,
succumb under the inhibition of an intensely irritated afferent
nerve : many such cases are on record. I have mentioned
one, of a lady, not more than 30 years of age, and otherwise
healthy, who died under such inhibition in the agony of a
gall-stone. A decaying heart, one which under comfortable
circumstances might carry on life for years, is far more liable
to be upset by an inhibition so intense as an attack of anginal
pain may compass ; so that, as Latham said of this malady, " A
man may often with stricter propriety be said to be ill of his
symptoms than to be ill of his disease ; and, what is more, to die
of his symptoms than to die of his disease." The vagus nerve
does not lose its inhibitory powers pari passu with deterioration
of the cardiac muscle ; a degenerated heart perhaps makes a
stronger appeal for protection at all hazards, even to be nursed
into death ; it seems to be inhibited, not less but more readily.
In denser " heart block " the vagus effect cannot, it is true, pass
so actively from the auricle to the ventricle ; but in partial block
its influence is still manifest enough to become fatal ; it is felt
until dissociation is complete.

sec. ii PKOGNOSIS 519

Here recurs the opinion that there is no close relation
between the peril of death and the severity of the seizure.
A slight seizure may prove fatal without warning either to
patient or physician ; as Sir William Osier graphically writes,
" a stony stare, a slight change in facial expression, two or three
gasps, and all is over." In three of this author's cases death
occurred in the first attack — attacks assailing, no doubt, hearts
already degenerate.

Of the several symptoms, I am disposed to think the degree
of " angor " to be the most ominous. Angina minor, if without
angor, may hang about for many a year without cutting the
thread of life ; and may ultimately disappear.

In some cases the disease remains stationary, or variable,
for many years. Osier (Lumleian Lectures) cites 10 cases ex-
tending each over ten years ; Norman Moore (loc. cit.) quotes
one of this duration, and alludes to others. Forchheimer relates
that not a few of his angina patients survived for eight or ten
years ; one survived for seventeen years.1 John Hunter's attacks
lasted over twenty years, increasing in frequency, and latterly
recurring almost daily. Mr. Edmund Owen has pointed out that
Hunter's angina was probably due to the experimental inoculation
of syphilis when he was about forty years of age. A well-known
man of business in Cambridge was subject to typical angina
for eighteen years ; ultimately he died in an attack. A lady
whom I used to see from time to time in Yorkshire must have
suffered for nearly as long a period. In June 1885, with Dr.
Hebblethwaite of Cheltenham, then of Hare wood, I saw G. Y.,
stud-groom. He had typical and very severe angina pectoris.
There were then no physical signs of cardio-arterial disease.
On August 4, 1911, in answer to my enquiries his son kindly
wrote to me to say his father died on October 10, 1905, aged
78 ; the death certificate being " Hemiplegia and senile decay."
He had remained subject to the angina, " if hurried in any
way," to the end of his life, though he did not die of it. Before
our consultation the attacks had been a terrible fight, but
the nitroglycerine then ordered (1885) had " never failed since
to give instant, or almost instant, relief. He was never tired

1 Forchheimer, Illinois Med. Journ., May 1910 (epitome in Arch, des mal.
du cceur, Feb. 1911).

520 ANGINA PECTOKIS part n

of blessing the day he began to use it." So again Dr. Hinde
of Harrogate has reminded me of a gentleman whom I saw with
him at Stockton for typical angina pectoris, and who lived in
spite of it for twenty years longer, and then, at the age of 90,
died of a hemiplegia. The angina, though it never vanished
entirely, had much abated. If these stationary cases are some-
what exceptional, their number is nevertheless considerable ;
and if in the individual we cannot reckon upon these degrees
of tolerance, the knowledge of the possibility may mitigate the
severity of the physician's sentence.

Finally, can we by physical examination obtain any signs
wherewith to guide our prognosis ? Few, if any ; by the ortho-
diascope, or more simply by percussion, we may discover a dilata-
tion of the ascending aorta, perhaps therewith a basic systolic
murmur, and a clacking second sound ; but these and such signs
are too frequent in old people to give us any special message
concerning angina pectoris. Degrees of blood pressure are incon-
stant. Signs of cardiac failure— cardiac dyspnea, pulmonary
crepitations — would of course alarm us in respect of life, but not
especially concerning the angina.

CHAPTER IX

TREATMENT

A physician can have no greater reward than the know-
ledge that he has been the means of bringing relief in a
cruel disease, especially when this relief prevails over an
agonizing symptom. As in the older writers we turn
over the chapters on the treatment of angina, and note the
multiplicity, and on the whole the futility, of their vehement,
often overvehement, endeavours to assuage the torture which
defied their remedies, it is then that we realise the debt
which we owe to Lauder Brunton for the discovery, in 1867, of
the nitrites in the treatment of angina. Not one of us but has
had volumes of thanks for our small share in handing on to
some of the most tormented of mankind this ineffable charm.
If the nitrites seem to be soothing rather than curative, yet
we shall admit that by their use we are enabled to compass
something more than a truce ; while calming the transports
of the sufferer and the grief of his friends, we liberate the
functions which make for recovery ; thus we gain not time
and courage only but some therapeutical efficacy also, and
advance, often far, on the way to more substantial amendment.
With the subsidence of the causes, the peril to life may pass
away. Although in our text-books the section on the treatment
of angina pectoris generally begins with the maxim that we
must hold up a failing heart, I have tried to show that this
maxim needs radical qualification. As Dr. Hertz says, tension
is the only cause of true visceral pain. Usually, indeed, on
the same page we are inconsistently warned not to administer
the heart tonics of the digitalis class, but rather " by nitrites
and the like to abate the energy of the heart."

521

522 ANGINA PECTORIS pakt n

But what is needed first, even in the angina of young
persons, and more and more as age increases, is to protect the
heart against inhibitive shock ; and this is best attained by the
more or less continuous use of atropine. Even in heart block,
unless extreme, atropine retains some influence ; and in case of
pneumogastric irritation, as for instance by an encroaching
adenitis, by atropine a pulse-rate of 30-40 may in 15 minutes be
nearly doubled (Dehio and others). Vaquez reports that in a case
of bradycardia " due to vagus irritation from an appendicitis,"
atropine at once removed the inhibition. Gerhardt, in a case of
syncopic bradycardia due to irritation of the left vagus involved
in a cancer of the tongue, found these attacks cut short by
atropine.1 Danielopolu,2 judging by his experiments on slow
pulse in jaundice and the like, tells us that our doses are often
too small really to suspend the vagus. When the " tone "
of the vagus is intense the dose of atropine should be
2 mg. (adult).3 In a case of jaundice, by injecting 2 mg. he
accelerated the pulse from 48 to 100 in the course of three-
quarters of an hour. Moreover, if Eppinger and Hess are right,
atropine, although it is said on the whole to raise blood pressure
somewhat, perhaps by check of the vagus, dilates the peripheral
and perhaps the coronary vessels.4 To every sufferer then
from frequent attacks, I administer atropine systematically,
increasing the dose gradually as the system may be acquiring
immunity ; and besides its specific protective, the drug has also
some sedative virtue.5 It is said that atropine is of less effect
in old persons ; I doubt this, because in certain heart-block
cases its effects are apparent, and in experiments upon myself
I find it active enough. Professor Waller, as an antidote to
vagus arrest under chloroform, recommended bromide of ethyl.
There is no harm in giving lactate of calcium regularly on the
chance that calcium ions, as opposed to potassium, may check
inhibition (but see p. 526). When the attacks are infrequent

1 Gerhardt, Deutsche Arch. f. klin. Med. Bd. cvi., 1912.

2 Danielopolu, Soc. de Biol., 5 juin, 1908.

3 See Hecht u. Nobel (of von Pirquet's laboratory, Vienna), Zeitschr. f. exp.
Med. Bd. i. He. 1 u. 2, 1913.

4 Eppinger u. Hess, Zeitschr. f. exp. Path. u. Ther. vol. v. p. 3.

B It is said that the methyl-bromid of atropine is a useful form of the drug ;
I have not yet tried it.

sec. ii TEEATMENT 523

the application of the remedy is less convenient. Conversely, it
is indiscreet during an attack to apply smelling-salts or other
peripheral irritants whereby the heart might be more exposed
to cumulative reflex inhibition.

If, as frequently happens, the angina is associated with
gout, we must counteract this part of the case, whether by spa
treatment or, at home, by appropriate regimen and medicines,
including colchicum, or by both methods ; much will depend
on the conditions of particular cases.1 If the arterial pressures
are abnormally high, and in all they are higher than the
morbid susceptibility of the suffering parts can tolerate, so
in every case means must be taken to moderate pressures.
Baths and technical exercises therefore are ordinarily out of
the question ; unless in a quiescent interval, when they should
be instituted with the utmost caution. I can understand that,
instituted with such precautions, the Swedish methods may,
in certain phases of certain cases, have some efficacy.

I am better aware of the usefulness of the high frequency
current ; under this method I have seen some cases of
the lesser stenocardia (a. minor), with high blood pressure,
if not permanently cured, yet substantially relieved, even
for years ; for to this means high pressure without angina
is amenable (See p. 110). A patient under the care of Dr.
A. Roberts of Harrogate and myself for high pressure with
angina minor, thus received over a period of six years continuous
benefits. In this case the course, which included, it is true,
mild sulphur baths and waters, needed some three or four
repetitions ; but the effects of the later courses were more
enduring. Ultimately however angina reappeared in more
typical form and defeated all remedies. For angina major I
have not made a full trial of it. A good deal has been written
at home and abroad concerning the virtues of the high
frequency current in angina, but the evidence is very con-
flicting. Dr. Humphris, evidently from no little experience, has
spoken favourably of the method, but chiefly as a moderator
of high pressures.2

1 See Ebstein, Gicht, p. 257.

2 Humphris, F. H., Section of Balneology, etc., of Roy. Soc. Med., session
in April 1913. See also Arteriosclerosis (p. 112).

VOL. II 2 L

524 ANGINA PECTOEIS partii

Rest. — When the malady first appears decisively, and still more
during periods when the attacks are frequent, the patient should
be advised to keep his bed for a while, and injections of morphine
and atropine may become imperative ; but if the attacks are
slight and the recurrences infrequent, it is difficult to urge
counsels of perfection ; moreover, such a confinement might
entail countervailing disadvantages. To put a very old
person to bed for some weeks may mean his never getting up
again ; and even the elderly are often depressed by it ; the
appetite and digestion fall off, crepitations appear in the
lungs, the muscles deteriorate, and prostatic troubles increase.
I am content to say : Never bring on the pain ; every renewal of it
keeps up the intolerance. If for this end absolute stillness in
bed be required, then bed for a while it must be, with a corre-
sponding reduction of food. Thus, if at first the attacks be not
abolished, they will be mitigated, and usually taper off. The
subsequent imprisonment must be determined by the sagacity
of the physician, guided by the sensations of an intelligent
patient. Pawinski (he. cit.) insists likewise on rest ; in mild
cases, . he says, the confinement need not be irksome ; but in
severer cases " absolute rest for weeks, even for a year, may be
imperative " — imperative, that is, if the patient think it worth
while. A man of middle age may submit to conditions which
an old man may not think worth while. For two severe cases
I prescribed recumbency for long periods in the fresh air, after
the manner of the sanatorium, and with no little success. It
is for this reason, if for no others, that Pawinski demurs, as I
have done, to the use of baths ; either forbidding them entirely, or
using them rarely and cautiously at neutral temperatures (p. 103);
advice which Fiessinger x has recently emphasised. Landouzy
and Heitz however at Koyat do not hesitate to use the C02
baths, even in angina if with high blood pressures, to reduce "peri-
pheral pressure " (? resistance) ; they declare that at the end
of the " cure " radioscopy, front and oblique, may exhibit
a recovery of the diameter of the aorta by one-fifth or one-
fourth. They find the risks negligible. In ten years, with
200 anginal patients they have had only one sudden death
during the treatment. They are able to obtain a " vaso-
1 Fiessinger, Sem. mid., 30 nov., 1910.

sec. ii TEEATMENT 525

dilatation tres douce " which eases all off so that things go
smoothly. Heitz advises these baths in the angina of chronic
aortic disease and warns against them in coronary angina,
a fanciful distinction. Tripier (loc. cit.) urges the anginous to
avoid all effort, " et garder un repos absolu a la chambre —
avec alimentation legere, et point de tabac." The return
to life should be very gradual. Shorter rests, as of four or
six weeks in bed, while, as generally admitted, they reduce
blood pressures, and give time for the lesion to gain some repair,
may be cloying to the body or disheartening to the mind ;
much depends on the patient's temperament, elderly persons
bear such confinement better than the young. The practical
rule is that whether in bed, shelter, or reclining-chair, the
attacks are, if possible, to be prevented, for each attack rises
again and again from effect to cause. The principle and practice
of rest in angina are then much the same as in aneurysm,
and in such junctures a serene habit of mind is a blessed
aid. The patient will instinctively find out the position of
greatest ease. In some, even severe, cases I have observed
that the patient found a little relief in raising the arms above the
head. Peter Joseph Frank taught x that throughout the course
of angina the left arm especially should be kept at rest.

Diet. — A certain anginous patient exclaimed, " I should soon
be all right if I could live without eating." The sympathy in
angina between the attacks and the functions of the stomach
have been discussed already (p. 343). We hear from enthusiasts
that recoveries from angina pectoris have been compassed by a
dietary so careful and ingenious as to " reduce coronary arterio-
sclerosis " ; such cases, illustrated by X-ray photographs, would
be full of interest. However, by exclusion of purins, and by
moderation of high feeding, much may be done to abate
angina ; especially in the minor form so often dependent on
high pressures. Our forefathers relied greatly upon the same
discreet and abstinent diet as we should now prescribe. They
also insisted that the diet must be such as to keep down as much
as possible the flatulence from which these patients suffer ; that
the carbohydrates, especially bulky farinaceous and green foods,
should be reduced, and liquids at meals restricted. The meals
1 Frank, P. J., Traite de path, interne, vol. iv. p. 460 (1857).

526 ANGINA PECTOKIS part ii

should be spare and frequent. Parry reduced both food and
wine, gave gentle laxatives, wisely economised the bodily
warmth, and preached equanimity. Fothergill was bolder ; he
" cured " a case by vegetarian diet and gentle horse exercise.
In all cases full meals and late meals should be carefully
avoided. In nocturnal angina, as in asthma, a meal after
midday should be of the lightest and simplest ; such as a
little boiled fish with dry toast or biscuit. In obese persons
some cautious means should be taken gradually to reduce the
fat. For flatulent, so-called " gouty " dyspepsia, no remedy
is better than the old-fashioned mixture of soda, rhubarb, ginger,
cardamoms, and gentian. Dr. Verdon, in troublesome " gastric "
cases of angina, recommends the " Salisbury diet." All physi-
cians of experience warn us in angina against a loaded colon,
and recommend mercurials occasionally, and more frequently
podophyllin in frequent small doses (say y1^ gr. thrice daily).
Sir James Barr thinks that in angina the heart has too much
calcium ions, therefore he eliminates lime from the drinking water
and food, and restores the phosphoric acid and acid fruits re-
commended by many physicians of the past, and adopted by
Desportes. He records a case in which on this system much
relief was obtained ; that is, the rate came down from a dozen
attacks a day to one in three or four days ; but he is careful to
add that the patient was also confined to bed. The older
notion was that by these means the " ossification " of the
coronary arteries might be counteracted ; Barr, as Desportes
before him, claims for the method a still larger efficacy.

If lime be injurious, the milk cure advocated by Karell and
others may be inadmissible. The Karell cure (p. 91), which in
angina I have never attempted, consists in a week's rest in bed
on a diet of 1000 cc. of milk daily ; it is recommended in cases
of frequent mild attacks in persons of overloaded stomach and
inflated abdomen. In a case complicated with a foul colon and
" torpid fiver," if resorted to for this short time only, and
together with strict bodily rest, it may be efficacious ; but in the
many cases of puffy, big-bellied persons with flabby hearts, I
should regard it as an unfit, or even a perilous, method.

In one or two cases on my notes, in one patient especially
under the care of Dr. Ralph Wilson of Kew, the lactic acid

sec. ii TREATMENT 527

bacillus method of treatment, addressed, as we are informed, to
toxins in the bowels, was at least coincident with a remark-
able amelioration, perhaps a cure, of a case of severe " steno-
cardia " with high pressures. With the " propter hoc " I will
not meddle. The precautions in respect of the digestion are
to be sedulously imposed and noted, for indeed a windy
stomach, if not a primary cause of angina, may suffice to part
the slender threads of life. At least the patient must rest both
mind and body for an hour before as well as after his meals ;
if convenience permit, in recumbency.

Exercise, then, must be restricted to gentle walking, and on
the level only ; for ascent of the gentlest incline may determine
an attack. The bedroom must be on the ground floor, and it
is better to take the air in a low, easy carriage. The rule as
to exertion is that nothing should be done which might
induce an attack. Every seizure means a peg down in our
progress. Even mental occupation should be restricted to
routine duties, mental excitement being jealously averted ; and,
as an old author writes, " Bacchi denique et Veneris consortium
ceu pestem fugiant aegroti."

It is difficult to see one's way in angina pectoris to the
use of systematic exercises, active or passive. At the outset of
the effort the pressures must rise, if to fall later. When the
attacks are not frequent, trials might with great caution be
attempted in quiet intervals. I have no personal experience of
any such trials, but were I to make the attempt, I should do it
on the Zander method, in which no effort of the will or even of
the attention is required. On account of the irritability of the
vagus (p. 522), as Dr. Walford has said, the neckbands should
be quite loose.

As to drugs, a course of the iodides is the accepted routine,
and, even if the case be not syphilitic, the doses may be carried
cautiously to the extremer quantities. Sir Lauder Brunton
thinks no drug wards off angina pectoris so effectively as full
doses of iodide of potassium, or other preparation of iodine ;
but to appreciate the virtue of these medicines and their doses,
the syphilitic must be distinguished from the non-syphilitic cases.
Dr. Janeway gives the iodide in small doses over a very long period.
For my own part I prefer iodide of sodium in angina, lest a

528 ANGINA PECTOEIS part n

potassium salt should forward inhibition, perhaps a whimsical
fear. The salt should be largely diluted in water or, as at Bath,
in mineral water. Syphilis must be carefully enquired for, and
on any reasonable suspicion specific treatment vigorously in-
stituted. Salvarsan is said by many observers, as by Barie
(loc. cit.) and Weintraud,1 to relieve the angina of syphilitic
aortitis very quickly ; but it must not, in my diffident opinion,
be trusted alone, nor without much precaution. I am told that
the intravenous injection is followed by a drop of arterial
pressure (10-20 mm.) so sharp that it might in case of vagus
lability or closed coronaries be perilous. Of course in these
cases all " ambulant " treatment is to be deprecated. In this
infection I have most experience of mercurial inunction, after
the method of Aix-la-Chapelle, now practised at Harrogate and
elsewhere ; by this method I have seen syphilitic angina
promptly cured, and, generally speaking, without relapse of the
angina. Curschmann has published 2 an interesting case of
syphilitic angina thus relieved :

A woman aged 32 (previously under his care for syphilis). While
again under a relapse, she was suddenly seized with severe angina
pectoris and dyspnea, and she had a painful node upon the manu-
brium and another on the right radius, 2 cm. above the wrist.
Physical signs negative, but the author suspected gumma about
the base of the heart (aortitis ?). She was submitted to 30 inunctions
during 3 months, when she was quite freed both from symptoms and
signs. The nodes also had vanished.

In a few recent cases I have advised patients of this class
to submit to mercurial injections, and in one case of specific
aortitis under continuous observation, with permanent relief to
the angina. Moreover after the course was finished the Wa.B.,
repeated three times, was negative. Aortic insufficiency remained.

In the case under the care of Dr. Walker of Lowestoft (p.
268), specific treatment was very successful.

Male, set. 48, suffering from severe and typical angina pectoris ;
the pain originated under the upper sternum, presented the usual
radiations, and the attacks were very frequent. When I saw him

1 Weintraud, Ther. d. Gegenivart, Okt. 1911.

2 Curschmann, " Arbeiten aus med. Klinik, Leipzig," Pathol, d. Kreislaufs,
1893.

sec. ii TKEATMENT 529

with Dr. Walker, he told me that under his observation a systolic
murmur had appeared first, then a diastolic ; then the heart dilated,
and pressure fell, on which account digitalis had been given for a
short time, and with advantage. I also found a double aortic mur-
mur ; the diastolic murmur — down the left border of the sternum —
very loud. Under active specific treatment, Dr. Walker found the
diastolic murmur first and then both murmurs to diminish ; then
the diastolic wholly disappeared, and the systolic grew less and less.
Meanwhile the attacks of angina, always amenable to the nitrites,
abated, so that the patient could sit up in bed and begin to move
gently about. The heart pulled itself together. In a few weeks
the angina was at an end, though a weary aching about the chest
continued for a long time afterwards (adhesions ?). I saw the patient
again some time later, when he was fairly well ; the heart then was
normal in all respects except a very soft systolic murmur and a
dullish area to be detected at the manubrium and a little to the
right of it. The patient denied syphilis, probably in good faith ;
but there could be no doubt about the nature of the illness (cf. case,
p. 179).

However, salvarsan, if the kidneys be sound, and the heart
not gravely affected, may be better still ; Vaquez and Lantry,1
in 28 cases of syphilitic aortitis, speak highly of its efficacy ; but
whatever course be taken I would insist on promptitude. In
syphilis the iodides are of course more than appropriate ; if the
heavy doses are ill-borne, as only too often they are, Tripier
gives the salt per rectum, dissolved in half a glass of water ;
he gives two clysters of the solution, night and morning.
Every two or three days he increases the doses by 10 or 12 gr.
and continues this course for a month ; then he suspends it
for a fortnight, repeating it thus as often as seems necessary.
Some physicians find the new combinations of iodine (iodopin
and others) better borne by their patients.

As syphilitic aortitis is no infrequent malady, and as perhaps
the majority of instances of angina in patients of or under middle
age are of this nature, Wassermann's test should be used in all
such cases. In cases of this site and nature the percentage of
positive results is very large (see case p. 210). Jacobaeus 2 used

1 Vaquez and Lantry, Soc. Med. des Hop., 7 juin, 1912.

2 Jacobaeus, Deutsche Arch. f. klin. Med. Bd. cii., 1911. See also Stadler :
protocol of discussion of a medical society, reported Deutsche med. Wochenschr.,
14 August, 1913.

530 ANGINA PECTOEIS partii

this test in a large number of cases of chronic cardio-arterial
degeneration ; he excluded aneurysm and obvious gummatous
aortitis, yet found notwithstanding that in a considerable pro-
portion of the cases the response was affirmative. With
improved technique the percentage is rapidly mounting up.
A positive result indicates in suitable cases the immediate and
active administration of antiluetic remedies.

Arsenic is credited, and in my opinion justly, with an alleviat-
ing effect in angina pectoris ; it was used first, I believe, in this
disease by Mr. Edward Alexander, a Halifax surgeon,1 and at
a later date was strongly recommended by Anstie. It is to be
instituted in minute doses with meals, and gradually augmented
even to some 15 or possibly 20 minims daily ; but for short
periods only, not more than a month or six weeks. I have not
used doses so large. The bromides also are helpful, especially when
the nervous centres have been exasperated by incessant pain.
For continuous use the bromide of strontium is said to be
preferable. Of their occasional use, to relieve attacks, I shall speak
presently (p. 535). The nitrites are often administered, not only
as palliatives to ward off or stop attacks, but continuously and
systematically as a means of cure. It seems reasonable that by
persistently abating aortic pressure, and so relieving stress,
the lesion should have the better chance of repair. Sir William
Osier, Ortner, and others with this view recommend doses of
nitrite of sodium, or of Liquor Trinitrini, in increasing quantities
as the case may need, even up to 20 grains or more of sodium
nitrite per diem, or 15-20 m. of the solution ; nay, in urgent
distress, as we shall see, to larger doses still. For this increase
the trinitrine is preferable to the sodium salt. I have no
experience of these heroic doses ; sometimes indeed sodium nitrite
has appeared to me to be not without some toxic quality.

Generally speaking, digitalis and its kind are in mere angina
to be eschewed ; it is not easy to see any reason for the use
of it, and it may raise arterial pressures and intensify vagus
inhibition. We shall not agree then with the writer in
Penzoldt and Sterzing's System (iii. 373), who proposes
digitalis and caffeine, even during attacks ; especially when
we recollect that by mitral regurgitation angina pectoris
1 Alexander, E., Med. Comm., Dec. 3, 1789.

sec. ii TREATMENT 531

is assuaged. Yet, although this be the abstract view of the
matter, it is true notwithstanding that in many cases, either
on error of diagnosis, or deliberately for some special reason,
digitalis and the cooler baths have been cautiously used without
aggravating angina. In particular cases of failing heart the
use of such measures as these must be left to the discretion
of the physician, who will balance as best he can the several
variables and their indications one against another.

Theobromine, in 7-10 gr. doses, is recommended by not a
few writers (e.g. Marchiafava, Ortner, etc.) in the form of
diuretin ; whether for the thoracic or abdominal form it has many
advocates, among whom I reckon myself. Janeway however
has not much faith in it. It is said that when inserted into a
vein in a moderate dose it lowers the blood pressure, apparently
by splanchnic dilatation. Albu (loc. cit.) gives diuretin especially
for the abdominal mode, 5-6 grm. daily for several days at a
time ; at the same time he administers the iodides freely.
Dieulafoy recommends aspirin, in doses of 50 centigrammes every
two hours ; but only of course in urgency, for immediate aid.

When attacks are hanging about a carminative draught may
expel the wind, to the great relief of the patient. In the lack
of more specific remedies the physicians of a hundred years ago
used these drugs abundantly: camphor, assafcetida,cajeput, musk,
castoreum, valerian, oil of anise on sugar, and, best of all, in
Fothergill's opinion, essence of peppermint. Once break the
wind, they would say, and the attack is relieved. The following
case, taken from a recent publication, was cited as " pseudo-
angina pectoris " and attributed to flatulent distension of the
stomach, " as the heart did not appear sufficiently diseased for
there to be true angina ! "

A middle-aged lady with a thick-walled, high-tension pulse had
for some months been subject to " suffocative feelings " in the chest,
coming on generally about an hour after meals. Then pain took the
place of these feelings, and spread to the left arm. The attacks
became more frequent, occurring five or six times a day and once
or twice in the night, and had no relation to exercise. On examining
the heart the apex beat was an inch outside the nipple fine, but was
forcible, and the sounds were good ; the aortic second sound was
accentuated.

532 ANGINA PECTORIS part n

Yet true angina no doubt it was. Dr. Verdon, whose
interpretation of angina pectoris as a gastric affection I have
discussed (p. 406), says that to pass the soft oesophageal tube
may, by discharging the load of the windy stomach, give
prompt and precious aid ; I think this operation should be
attempted only in a patient inured to it, and protected
by a dose of atropine. Flint reported of one of his
cases that to swallow solid food would bring on the paroxysm.
I have quoted Dr. Mackenzie's x advice to warn such
patients against swallowing wind during efforts of eructation ;
and his observations on the influence of swallowing upon
the vagus warn us to enjoin upon the patient to swallow
as little as possible during an attack ; he tells us that
swallowing slows the sinus rhythm, and depresses the con-
ductivity of the a-v fibres, so that their way may be blocked. The
nerve supply of the oesophagus is mainly vagal (Langley). Herz
of Vienna, advises the patient to take a small quantity of water
into the mouth, then to throw the head back as far as possible
in order to stretch the oesophagus, and at the same time to
swallow, when the desired eructation will ensue. This attitude
again, even if tolerable, may have its vagus perils. Mayer and
Pribram showed that to irritate the wall of the stomach slowed
the pulse and raised the blood pressure, effects which divisions
of the vagus prevented. I find hydrocyanic acid a useful remedy
in cases with much gastric disturbance, and Tr. Pruni Vergin.
may conveniently be used for some weeks. Our audacious
ancestors went so far as to give emetics in the attacks, an uncouth
and forbidding, but possibly an efficacious remedy. Whether
the sympathy between heart and stomach is only by mediation
of the vagus, or is in part mechanical, we scarcely know.

It is unnecessary to dwell on the scrutiny of the various
excretory functions, and the avoidance of gouty and other toxic
elements of the diet, some of which may be vasoconstrictive.

More instantly, to prevent the seizures, the means at our
service are first, of course, the nitrites. Atropine I have already
mentioned (p. 522). The virtue of these agents is supposed to
lie in their property of reducing the arterial pressures ; this may

1 Mackenzie on this point refers to Wyllie on Gastric Flatulence, Edin.
Hosp. Reports, vol. iii.

sec. ii TKEATMENT 533

be the explanation, as also of the antimonial draughts which
our forefathers administered to the same end ; nevertheless, it
is not to be forgotten that the nitrites often relieve certain cardiac
perturbations during which the pressures are moderate, perhaps
by an active rather than a passive dilatation promoting the
blood - stream. On the other hand by nitrite of amyl Dr.
Mackenzie x promptly relieved an attack of angina in a man
whose blood pressure was at the onset 190 ; though soon after
the passage of the attack it proved to be 200. In a case, of
which I have some notes, it momentarily reduced a pressure of
200, and the attack was checked, but the pressure soon rebounded
to 230. These substances may possess some sedative or regu-
lative virtue imperfectly known to us. In angina with aortic
regurgitation, in which disease the periphery is usually fully
expanded already,2 the nitrites often give substantial relief
nevertheless. It is often stated, in the confident way in which
people propound unproved opinions, that the nitrites relieve
angina by dilating the coronary arteries. That, unless in poisonous
doses, they have any effect upon supposed constrictions of the
coronary arteries is mere fancy. No one knows that they have
this effect in the body ; on the contrary, large peripheral dilata-
tions elsewhere make it improbable. We have seen that the
activity of these vessels depends directly on cardiac metabolism.
In the jaws of a seizure, nitrite of amyl is often inhaled
from the crushed capsule, and the vapour, if not so certainly
efficacious as nitroglycerine, answers, when it does answer,
more quickly. In some persons it acts unpleasantly, and is
not efficacious ; it may be that in them irritation of the
mucous membrane (fifth and tenth nerves) causes a reflex rise
of blood pressure ; if so, whatsoever reduction of pressure it may
effect may be lost in a rebound ; such persons might try
the drug by the mouth ; although, by the way, we have
noted that in an attack the patient should swallow as little
as possible, lest he intensify inhibition. However, because it is
not wholly free from other irritating ethers (Stokvis, Albert
Abrams, Vaquez),3 amyl nitrite is falling out of favour. The

1 Mackenzie, Brit. Med. Journ., Oct. 20, 1906.

2 See, however, Mackenzie's case, p. 335.
3 Arch, des mal. du cceur, Janvier 1903.

534 ANGINA PECTOKIS partii

objections to chloroform, sometimes recommended in the status
anginosus, I have considered (p. 483), it may imperil the
heart ; in cases of great urgency Sir Kichard Powell prefers
to inject m.j. of the standard nitroglycerine solution, with a
little ether, subcutaneously.

Nitroglycerine by the mouth acts in about ten minutes ;
it is generally efficacious and well tolerated. The tablets are
convenient for the pocket, but the alcoholic solution acts more
quickly and surely. As much as 10 minims of the Liquor
trinitrini (1 per cent solution) may have to be given to an
accustomed patient at the outset of a severe attack. I have
quoted Sir W. Osier's opinion that nitroglycerine is used much
too timidly, and then dropped as ineffectual ; but the un-
accustomed patient is to be warned that the immediate effects
of much smaller doses may be flushing and headache. These
effects are harmless, do not mean pressure on the brain, and
in time of need must be tolerated. To keep the periphery
open, the nitroglycerine may be needed every two or three
hours, when some increasing tolerance of the drug may
have to be reckoned with. Erythrol tetranitrate, which for
instant relief is less effectual, is considered more proper for con-
tinuous use, its pressure-reducing effect being more abiding ; its
scope is restricted by its higher cost, and it is said to be not
without some toxic quality. However Dr. Churton of Leeds, in
1912, mentioned a case of angina pectoris of four years' standing
in a man, aged 51, who had taken erythrol tetranitrate (gr. §)
every six hours for fifteen months with great benefit. Unless
the case be a severe one, and instant prevention imperative,
reduction of pressures during some considerable part of the day
may be sufficient to soothe the aorta, or at any rate to mitigate
the sense of distress. With us all, pressures are fluctuating
widely from hour to hour ; and, as it is found by experiment
that in the rabbit to raise aortic pressure considerably for
short periods only will induce aortic lesions, so conversely it
may be presumed that temporary reductions of pressures may
soothe a damaged vessel. In mixed cases, in cases of angina
with dyspnea and other cardiac symptoms, the nitrites are,
on the whole, of less service, and if they reduce cardiac
energy may even do harm. Alcohol as a vasodilator may be

sec. ii TKEATMENT 535

effectual ; thus it is said that a glass of hot grog at bed-time
may avert nocturnal attacks.

If the attack be prolonged, a hot foot-bath, and hot fomenta-
tions or mustard poultice to the chest, are often comforting ;
Dieulafoy, on the contrary, has found an ice-bag, a means I should
hardly venture to try, to give immediate ease. In past times
the physician busied himself to evoke an attack of gout in a limb,
and to this end used hot foot-baths, mustard, and the like ;
curious instances of relief by such methods are recorded in the
older books. " Champagne and a tight boot " is, I am told,
the modern form of the prescription.

A soporific named " Somnoform " is said to suspend the
peripheral cardio-inhibitory fibres, and, if this be so, in severe
and protracted seizures it may be both palliative and
protective. Ethyl bromide is credited with the same dis-
criminating virtue, and may be tried as a prophylactic. From
chloral I shrink in these cases as I do from chloroform. In
one case I saw the severe pain assuaged by rather liberal doses
of antipyrine, but this drug again is one I should myself
regard with some mistrust. I have said that in case of
frequent worrying attacks, in which the nervous system is
quivering under pain and insomnia, ammonium bromide in
20-grain doses may be prescribed with advantage. In one such
case Dr. Mackenzie succeeded in blocking the pain by stupefying
doses of bromide of ammonium.

Max Herz says that oxygen inhalations, administered for
a short time two or three times a day, ward off stenocardia,
improve the general condition, and even mitigate attacks.
Some German physicians speak well of Finsen's light bath.
Certain outrageous methods, such for instance as scalding the
chest, front and back, with effusions of water boiled at the
bedside, the application of large blisters, and so forth, testify,
I hope, rather to the fierceness of the disease than to the
barbarity of the medical warrior.

In severe and prolonged attacks, or in the "status anginosus,"
if the state of lung and kidney permit, hypodermic injection of
morphin, or of morphin with atropin, is the most efficient
means we have. It is said that in dragging (p. 483) operations
morphia is a completer block than atropine. Heberden and

536 ANGINA PECTOEIS part n

his successors used opium in some form or other, such as the
aromatic tinctura thebaica, or laudanum. Latham used to
give laudanum (10-30 m.); von Dusch relied on opium, castoreum
and camphor ; and many authors of experience have attributed
to opium (or morphine) not only palliative, but also more
permanent service. In modern practice of course morphine by
subcutaneous injection (usually and rightly with atropine) is our
way of using the opiate, and in an attack of any severity it is
worse than useless to palter with the doses ; a quarter of a grain
should be given at once and, if required, a sixth more and more,
at intervals of a quarter of an hour. Pain so exceeding carries
off much morphine. Michaelis1 truly says that " in many attacks
we cannot get through without injection of morphine." He adds,
" I have never seen death due to it, but the best results all
round." When in very severe and pertinacious assaults the
nitrites fail to be of service, no very infrequent difficulty, then
morphine is our only, or our chief, resource. Morphine pulls the
heart together, strengthens the beat and opens the peripheral
circulation. It does also priceless service by the psychic peace
which it induces. Ortner 2 prefers to morphine a form of opiate
called pantopon ; this preparation I find, in Merck's Catalogues
for 1908-9, is an artificial combination of the alkaloids of opium.
It is said to act more rapidly, efficaciously, and pleasantly than
morphine ; and rather improves than spoils the stomach and
appetite. 1 cc. of a 2 per cent solution is injected under the
skin ; or by the mouth -^-|-ths gr. may be given, in pill or
powder. Frankel economises the morphine by intermediate
subcutaneous injections of heroin hydrochloride, half a syringe
of a 1 per cent solution = 0*005 gramme (^^o^n °^ a gram)-
It is said to retain its virtue without increase of dose.

The many stories of cure by issues in this as in many other
diseases are remarkable. Desportes' clockmaker, to whom I have
alluded (p. 512), though a heavy, sedentary, gouty man, com-
pletely recovered on the insertion of a moxa in his thigh, which
was kept open for eighteen months or more. I may mention also
the case of Dr. MacBride of Dublin (a.d. 1776) and of Dr. Darwin,
cited by Dr. Knott, in which complete cures were wrought by

1 Michaelis, Ther. d. Gegenwart, 1909, p. 567.
2 Ortner, Jahreskurse, Feb. 1911.

sec. ii TREATMENT 537

issues, containing one or two peas, on the inside of the thigh.
Such testimony cannot be utterly ignored.

Venesection, by Heberden and Robert Hamilton, was put
aside as useless. Whytt and Percival however did not discard
it " for proper subjects " ; still, even if by reduction of high
pressure it had proved to be as serviceable a remedy as might
be expected, it was generally agreed that, whatever the instant
relief, to anaemiate a patient favoured the recurrence of attacks.
Therefore I have never used the remedy in angina, tempted
at times as I have been. Leeches, or a wet -cupping on
the front of the chest, a favourite old remedy, may be worth
trying in an obstinate case. But " cures " in angina are apt to
be deceitful. Liberal venesection is said to be effectual in
pulmonary oedema. Drugs, such as strychnine, which exalt
the central irritabilty, will as a rule be avoided.

It would seem strange to leave a disease of or about the heart
without more than my former allusion to Digitalis. But the
part of digitalis in the treatment of angina pectoris can
never be large, and is rather dark and perilous.1 Digitalis
stimulates the vagus centre, at any rate at first ; any use of
it must therefore be preceded by atropine Those who believe
that angina pectoris implies a degenerate myocardium should
think twice before using a drug which in such states has a
double edge. If it should make for increase of arterial pres-
sure, and for a widespread constriction of the arterioles, it might
aggravate the evil ; but these qualities of it are now again in
doubt. In my view that angina pectoris is usually due to a
sore aorta, why use a drug which has no special value
in disease of this vessel, and which by vagus and sym-
pathetic influences might multiply its perils ? Notwithstand-
ing, there are conditions under which, if used with caution and
vigilance, digitalis may do service. Assuredly while the patient
is beset by anginal attacks we cannot use it ; it can be used
only when the disease is mild or quiescent, when, if not for the
angina itself, it may be needed for some concurrent cardiac disease,
such as in old people is not infrequently associated with it, and
constitutes its peril. We may then consider certain observations

1 A good review of this question will be found by Sir Lauder Brunton, Brit.
Med. Journ., Nov. 15, 1910.

538 ANGINA PECTOEIS part n

and experiments, from the time of Traube and Niemeyer to this
day, proving that under certain conditions, even of high pressure,
digitalis has seemed even to reduce arterial tension. Or again
by spurring the heart to make an extra push in a critical phase
excessive resistance may be overcome, and velocity promoted.
For my part I cannot suppose such a mode of relief to be
often desirable ; so sharp a call might awaken the angina, and
thrust the patient into an attack. Mr. Verdon has seen digitalis
used in several cases of angina, and thought that by its use the
attacks were aggravated.1 I have tried it in a few cases of
angina with faltering heart and also in syphilitic cases, wherein
one might reckon more or less on a sound heart, but it seemed to
do more harm than good. However, in the important article
of Schmidt, in Pfluger's Archives (vol. cxxv.), we are told, in
contradiction of Gottlieb and Magnus and current legend, that
digitalis may dilate the splanchnic vascular area ; and Pick,
at the Wiesbaden Medical Congress in 1909, confirmed and
even extended this assertion. By plethysmographic experi-
ments upon the limbs, 0. Miiller found no change in this vascular
bed under digitalis, but as the cardiac output was enlarged,
he agreed with His that there must have been dilatation some-
where ; though one does not see why increased velocity should
not make at any rate some part of the relief, a relief which we
often see from the drug in granular kidney. A good many
experiments indicate that with a constant arterial diameter the
blood race may be accelerated ; on the other hand, if under high
pressures the left ventricle is driving at the utmost capacity,
and after a while strain effects become evident, how are we to
get more out of the heart, unless perhaps for a transient spurt ?
Thus it would seem that the relief must be peripheral, and we ask
ourselves again if the views of Hasebroek, and Griitzner (Vol. I.
p. 51), on a peristaltic activity in the muscular arteries, can
be true ? Some observers have assumed a livelier metabolism
in the various organs as the means of acceleration, but we have
no knowledge of any such influence on nutrition by digitalis.

Finally, in case of apparent death in or after an attack, the
first duty is to inject intravenously (for an adult) 2 mg. of
atropine. Meanwhile as I have often suggested, artificial
1 Verdon, H. W., Lancet, July 13, 1912.

sec. ii TEEATMENT 539

respiration should be practised assiduously. If the atropine and
ansemia of the bulb should abate the mastery of the vagus,
the once inhibited heart might be coaxed to beat again. Dr.
Morison tried the method once, in vain ; but his was an
unpromising case, one in which indeed cerebral haemorrhage
may have been present.1 In cases of far gone cardiac decay,
of course little can be expected ; yet Broadbent (loc. cit.)
quotes an extreme case, in which on artificial respiration the
pulse rallied, and the patient, partially restored, endeavoured
to speak : the rally, however, was but transient. Sir Lauder
Brunton in one of such cases kept the heart going for an hour,
but the patient failed to get hold on life.2 Dr. Curtin (in, a
letter to me on seeing this recommendation) wrote that
independently he had tried artificial respiration in a case of
great jeopardy. " About fifteen minutes after the seizure
began the pulse became very unsteady, dropping about one
beat in four. The result surprised me ; my attempts restored
the pulse, and normal rhythm was with some pains restored."
Sir Kichard Powell, on the same principle, recommends wafting
of oxygen from a funnel over the face of the exanimate patient.
This might be used with artificial respiration.

Upon the strict physiological lif e, open secretions, and psychic
tranquility, so needful in these cases, I need not dwell at greater
length ; nor upon those measures, general and special, which are
appropriate to any cardiac disease with which the angina may
be associated. For some reflections on the adaptation of these
general rules to individual peculiarities I would refer the reader
to Sir William Osier's treatise on Angina Pectoris.

In conclusion, I find it necessary to repeat that success
in treating angina pectoris must be based on a correct
analysis of each case. So long as the minds of young
practitioners, and not of these only, are unsettled by the writings
of eminent authors, who into this class have thrown pell-mell
all sorts of neurotic or toxic, as well as some cardiac, disorders,
cases which resemble angina only in that they are attended
with motley distresses and various pains in the thorax, we
cannot hope for consistent therapeutics. (Moreover, the

1 Morison, Cardiac Pain, p. 28.

2 Brunton, Sir L., Lancet, Feb. 23, 1912.

VOL. II 2 M

540 ANGINA PECTORIS paet n

physician, for his further discouragement, is assured that a
differential diagnosis of such maladies is, or in certain
cases may be, very difficult ; this difficulty I have tried to
appraise. Anginous patients seek many opinions, and, as I
have given some attention to the subject, my experience of the
disease has been fairly large ; yet I do not hesitate to repeat,
with a view to treatment, that if the observer will clear his
mind of all the confusing disputes about " anginiform pains,"
" vasomotor anginas," " pseudo-anginas," " true anginas," and
the rest of it, he will find no more difficulty of differential
diagnosis than there must be in some few of the obscurer in-
stances of any disease whatsoever. Such difficulty as may
occasionally arise will be with those cases in which the
symptoms are so incipient, or so masked, or so imperfectly
observed, that for a while the data are insufficient ; yet even
of these a little patience and common sense, and the accurate
and patient use of modern methods of diagnosis, will enable us
to form no idle opinion ; then the proper treatment will
present itself.

P.S. — At the last moment a paper on Angina Pectoris by
Vaquez has appeared in the Arch, des mal. du cceur, mars-avril
1915, in which the author goes a long way towards the pathology
of the disease advocated in these pages. Some interesting facts
in support are recorded. He would have done better still had he
not clung to a fanciful distinction between the angina of effort
and that of rest ; between, that is, attacks produced by effort
and those which come on without effort — as at night (see p. 254).
Morgagni's case, with necropsy (p. 328), is almost enough to
testify decisively to the contrary. Vaquez pleads still for a
cardiac causation at any rate for the attacks of rest — or, as he
names it, of " decubitus." The cases he has in view are of
course those — not a few — complicated with heart disease. But
the same patient is often subject to attacks coming on now in
the one, and now in the other, of these modes of onset. To
other points of Vaquez's argument I have in the previous pages
given full consideration.

INDEX

Abdominal anginal pectoris, ii. 304-
312, 500-504; and atheroma of
mesenteries, ii. 310, 504

Abdominal crises, i. 446

Abdominal pain in arteriosclerosis, i.
445-447

Abdominal symptoms in arterio-
sclerosis, i. 444-452

Abram's reflex, ii. 44

Adrenal arteries, arteriosclerosis of,
i. 227

Adrenalin, destroyed by liver and
muscles, i. 266 ; effects of, on
arteries, i. 220, 228, 232 ; effects of,
on media, i. 478 ; effects of, vary in
different arteries, i. 232

Adrenals, blood pressure and, i. 226 ;
and high pressure in kidney disease,
i. 369

Adventitia, functions of, i. 197 ; in
infectious aortitis, ii. 422 ; lesions of,
i. 467 ; lesions of, in syphilis, i. 469,
479 ; lesions of, in syphilis of aorta,
i. 468, 469, ii. 183, 422 ; in rupture of
aorta, ii. 464 ; spirochseta in, i. 479,
ii. 183

Afferents, cardio-arterial, ii. 411

Albuminuria, and high pressure with-
out Bright's disease, i. 311 ; dia-
gnosis of Bright's disease and, i. 311,
316, 319; in elderly without
Bright's disease, i. 316, 347

Alcohol, ally of other poisons, i. 249 ;
arteriosclerosis and, i. 246 ; influ-
ence of, on blood pressure, i. 246

Altitudes, dyspnea of high, i. 402

Ambard's uric constant, i. 322

Amines, i. 270

Amino-acids, i. 270-272

Aneurysm of aorta, ii. 205 ff. ; acute
rheumatism and, i. 479, ii. 155
anginal pains in, ii. 421, 433
angina pectoris and, ii. 431 ff.
angina pectoris not infrequent in, ii
499 ; atheroma an effect of, ii. 205

atheroma rarely causes, ii. 168,
205 ; begins with gummous lesions
in media, i. 479 ; children and, ii.
154, 155 ; occasionally non-syphi-
litic, i. 479 ; pain in shoulder in,
ii. 421 ; periarteritis nodosa and,
i. 480 ; posterior, and spinal pains,
ii. 499 ; pressure pains of, ii. 311,
509 ; rupture of, ii. 206 ; small
about root, and angina pectoris, ii.
205, 433 ; syphilitic generally, i.
479 ; toxic, i. 479

Angina, minor, "Stenocardia," ii.
494 ff. ; high pressure and, ii. 287 ;
importance of recognising, ii. 287 ;
pain substernal, ii. 289 ; prognosis
in, ii. 519 ; rheumatism and, ii. 274 ;
syphilis and, ii. 262 ; tobacco
angina and, h. 507 ; in women not
uncommon, ii. 288

Angina, mock, ii. 221 ff. ; angina
pectoris contrasted with, ii. 231,
234 ; arm pain and numbness in,
ii. 495 ; breathing in, ii. 231 ;
diagnosis of, ii. 507-508 ; does not
pass into angina pectoris, ii. 239-
240 ; heart in, ii. 235 ; heart, pain
in, ii. 231 ; hypersesthesia local in,
ii. 285 ; nitrites often relieve, ii.
495; palpitation in, ii. 232, 235;
pain, seat of, in, ii. 285 ; pain,
submammary, in, ii. 225, 231, 495 ;
pulse in, ii. 232 ; restlessness and
agitation in, ii. 231 ; tender spots
in, ii. 235 ; vasomotor disturbances
in, ii. 227, 508 ; visceral lesions often
cause of, ii. 227

Angina pectoris, ii. 211 ff. ; abdominal,
ii. 304, 306, 308, 311, 500, 503-504 ;
age incidence of, ii. 249-250 ;
aneurysm and, ii. 431 ff., 499 ;
angor animi and, ii. 319-323 ;
aorta, signs of, in, ii. 345, 346; aortic
disease and, ii. 409, 410, 416, 430,
436 ff . ; aortic injury and, ii. 430 ;

541

542

INDEX

aortic tenderness in notch, ii. 346 ;
aortitis and, ii. 422 ; arteriosclerosis
may be absent in, ii. 345 ; auricular
fibrillation in, ii. 387 ; blood
pressure and, ii. 255-256, 333, 357 ;
causes of, ii. 249 ff. ; children and,
ii. 152-155, 249 ; chloroform and,
ii. 483, 535 ; coronary disease and,
ii. 352 ff. ; coronary occlusion and,
ii. 265 ; coronary thrombosis, ii.
449; death in, ii. 466, 486-488;
dextral radiation in, ii. 300, 304 ;
digitalis and, ii. 530, 537 ; dread and,
see Angor animi; dyspnea and, ii.
312, 319; epigastric, see Abdominal ;
extra-systoles in, ii. 471 ; gout and, ii.
257, 260 ; gouty attacks and, ii. 258 ;
heart, action of vagus on, and, ii. 466 ;
heart may be normal in, ii. 345, 497,
499 ; heart, physical signs in, ii.
345 ; hyj>erpiesia and, ii. 240-242,
265 ; malignant endocarditis and,
ii. 276 ; megrim and, ii. 401, 402 ;
men and, ii. 251 ; mitral disease
and, ii. 387-389, 442-448; mock
angina does not pass into, ii. 239 ;
myocardial degeneration and, ii.
389 ; name of a disease, ii. 212 ff. ;
pain, cause of, in, ii. 416, 449 ; pain
from other causes and, ii. 449 ;
pain on walking uphill in, ii. 498 ;
pain, radiation of, in, ii. 291 ;
pericarditis and, ii. 202, 454 ff. ;
phthisis and, ii. 268 ; pulse in, ii.
329 ff. ; respiration in, ii. 312 ;
rheumatism and, ii. 274; rheuma-
tism in children and, ii. 154 ; sine
dolore, ii. 323-327, 492 ; subclavian
artery and, ii. 346 ; symptoms of,
ii. 279 ff. ; syphilis and, ii. 239,
260 ff. ; termination of, ii. 317 ; vagus
hypersensitive in, ii. 475; vaso-
constriction rare in, ii. 401 ; vaso-
motor phenomena and, ii. 236, 238,
340
Angina pectoris, causation of, ii.
249 ff. ; age and, ii. 249 ; arterial
disease similar causation, ii. 202 ;
atheromatous processes in aorta and,
ii. 239, 260; bodily labour and,
ii. 252 ; coronary disease and, ii.
352 ff. ; gout and, ii. 257-260 ;
heredity, ii. 251 ; hypothesis of
author, ii. 416 ; infectious poisons,
ii. 260 ; influenza, ii. 163, 239, 260,
268, 272; malaria and, ii. 273;
malignant endocarditis, ii. 276 ;
mental and emotional, ii. 256 ;
periaortitis, ii. 424 ; pericarditis,
ii. 454 ff., 465 ; rheumatism, ii.

239, 274 ; rheumatism in children,
ii. 154 ; sex, ii. 251 ; station of life
and, ii. 250 ; syphilis most frequent,
ii. 239, 260 ; in young, ii. 239

Angina pectoris, diagnosis of, ii.
491 ; from aneurysm, ii. 499, 509 ;
cardiac dyspnea, ii. 504 ; coffee
poisoning, ii. 507 ; coronary throm-
bosis, ii. 502 ; gastric crisis, ii. 503 ;
intercostal herpes, ii. 507 ; medi-
astinal tumours, ii. 509 ; mock
angina, ii. 507-508 ; neuralgia, ii.
507 ; pain from extra-systoles, ii.
500 ; pain from walking uphill,
ii. 498 ; paroxysmal dyspnea, ii.
504 ; Stokes-Adams disease, ii.
510 ; tobacco poisoning, ii. 507 ;
ursemic dyspnea, ii. 504 ; vaso-
motor cases, ii. 508 ; visceral
perforation, ii. 502

Angina pectoris, hypotheses of, ii.
350 ff. ; aortic investment, tension
of, ii. 416, 429 ; cardiac plexus
irritation, ii. 402 ; coronary disease,
ii. 352 ; coronary occlusion, ii. 368 ;
coronary spasm, ii. 356 ; gastric,
ii. 406 ; heart, cramp of, ii. 382 ;
heart, intermittent claudication of,
ii. 397 ; heart, reduction of con-
tractility, ii. 393 ; heart, systolic
effort, ii. 390 ; heart, ventricular
distress, ii. 386 ; mediastinum,
distension of, ii. 400 ; neuralgic,
ii. 402 ; neurotic, ii. 399 ; uric
acid retention, ii. 405 ; vasomotor,
ii. 400

Angina pectoris, prognosis of, ii.
511 ff. ; angina minor, ii. 519 ;
" angor animi " ominous, ii. 519 ;
dependent upon associated con-
ditions, ii. 378-379, 517 ; infectious
causes, ii. 270-271, 518 ; in older
persons, ii. 379, 512 ; slight and
severe attacks, ii. 519 ; syphilitic,
ii. 262, 495, 518 ; in young, ii. 250,
270, 378, 512

Angina pectoris, treatment of, ii.
521 ff. ; Acetyl, acid, salicylic, ii.
521 ; atropine, ii. 522 ; arsenic, ii.
530; bromides, ii. 530, 535;
calcium lactate, ii. 522 ; colchicum
if gouty, ii. 523 ; diet, ii. 525 ff. ;
diuretin, ii. 531 ; erythrol tetra-
nitrate, ii. 534 ; exercise, ii. 527 ;
Pinsen light, ii. 535 ; high frequency
currents (angina, minor), ii. 523 ;
iodides, ii. 528 ; issues, ii. 538 ;
leeches, ii. 537 ; Liquor trinitrini,
ii. 530, 534; mercurials, ii. 526-
528 ; moderate blood pressures, ii.

INDEX

543

523 ; nitrites, ii. 532 ff. ; podo-
phyllin, ii. 526 ; rest, ii. 524 ; sodium
nitrite, ii. 530 ; syphilitic, iodide,
ii. 528 ; syphilitic, mercury, ii. 528 ;
syphilitic, salvarsan, ii. 528-529;
theobromine, ii. 531 ; venesection,
ii. 537
Angina pectoris, paroxysms of, agita-
tion rare in, ii. 328, 507 ; angor
animi in, ii. 319-323 ; arm, oedema
in, ii. 300 ; arm, pain in, and, ii.
291, 497 ; arm, paresthesia of, and,
ii. 298; arm, paresis of, and, ii.
298 ; arterial pressure in, ii. 255,
337-338 ; complexion in, ii. 236,
341-342 ; cessation on fall of
blood pressure in, ii. 256 ; death in,
ii. 466, 488 ; delusions in, ii. 340 ;
determinants, immediate, of, ii. 401,
406 ; dextral radiation of, ii.
300 ; digestion and, ii. 343 ;
dyspnea and, ii. 312, 318 ; effort
often determines, ii. 254 ; erythema
in, ii. 339 ; flatulency in, ii. 343 ;
hallucinations in, ii. 340 ; hand,
pain in, in, ii. 496 ; heart's action in,
ii. 329-334 ; heart's sounds in, ii.
330-332 ; herpes on arm in, ii. 297 ;
horror in, ii. 319-323 ; hyper-
aesthesia in, ii. 508 ; immobility in,
ii. 327 ; movements and, ii. 507 ;
muscles tender, ii. 300 ; painless,
ii. 323-327, 492 ; pain in, ii. 280 ;
pain, cause of, ii. 160, 416 ; pain,
cessation of, ii. 295, 304 ; pain,
degree and nature of, ii. 285, 384,
451 ; pain from coronary block and,
ii. 449, 461 ; pain from rupture of
heart and, ii. 449 ; pain on exertion,
ii. 296 ; pain, paroxysmal, ii. 297 ;
pain, radiation of, ii. 291, 296 ;
pain, seat of, ii. 219, 280, 282, 291 ;
pain, substernal, ii. 282 ; pain,
paresthesia in, ii. 298 ; paresis in,
ii. 298 ; polyuria in, ii. 508 ; pulse in,
ii. 329 ; pulse amplitude in, ii. 337 ;
pulse, changes in, during, ii. 471 ;
pulse, volume and tone, ii. 335 ;
pupils in, ii. 299, 349 ; respiration
in, ii. 312, 319, 385 ; rest and, ii.
254, 328 ; saliva, flow of, in, ii. 339 ;
sighing and, ii. 319 ; in sleep, ii.
254, 328 ; Stokes- Adams disease and,
ii. 510 ; substernal oppression and,
ii. 297 ; swallowing and, ii. 344 ;
sweating in, ii. 338 ; tender points
in, ii. 300 ; thoracic muscles in, ii.
385-386 ; urination profuse after,
ii. 342 ; vertigo in, ii. 340 ; yawning
and unrest in, ii. 340

Angina pectoris, paroxysms, treatment
of — amyl nitrite, ii. 533; am-
monium bromide, ii. 535 ; apparent
death, artificial respiration in, ii.
538 ; apparent death, atropine
intravenously in, ii. 538 ; hot foot
bath, ii. 535 ; morphia, ii. 483,
535 ; mustard poultices, ii. 535 ;
nitroglycerine, ii. 534 ; oxygen inhala-
tions, ii. 535 ; prevention of, ii. 532
ff. ; smelling-salts, avoid, ii. 523

Angina pectoris, severe, " status
anginosus," treatment of — aceto-
morphine hydrochloride, ii. 536 ;
morphia, ii. 535 ; morphia and
atropine, ii. 535-; opium, ii. 536

Anginal pain, generated in heart, ii.
462 ; in mitral disease, ii. 443, 462 ;
in mitral stenosis, ii. 445 ; in
rupture of aorta, ii. 463

Angiomalakia, i. 488

Angor animi in angina pectoris, ii.
319-323

Animal extracts and hypotension, i.
264

Aiimals, changes in arteries of, i. 4,
214-216

Anterior tibial artery, early sclerosed,
i. 461

Aorta, abdominal, arteriosclerosis of,
i. 446, 457

Aorta, adrenals and, i. 220 ff. ; affected
always in angina pectoris, ii. 422 ;
aged and, i. 20, 39, 518 ; aneurysm
of, ii. 205 ; aneurysm of, in children,
ii. 154 ; angina pectoris and, ii.
409, 416, 422, 436 ff. ; arteriosclerosis
of, i. 154 ff., 374, 455, ii. 206 ; areas of
pain in, ii. 297 ; arteriosclerosis of,
in young, i. 176 ; atheroma of, ii.
151, 206 ; atheroma of vasa
vasorum of, i. 464 ff. ; ascending,
chronic aortitis of, ii. 190 ; ascend-
ing, elongation of , ii. 199; ascending,
tension of, and angina pectoris,
ii. 2S7 ; blood pressure and, i. 190,
ii. 191 ; calcification of, in children,
ii. 153 ; cardiac hypertrophy, effect
of, on, ii. 191 ; compression of, i.
223 ; congenital deformities of, ii.
208 ; congenital dilatation of, ii.
210 ; connective tissue, increase in,
i. 518; dense adhesions about, and
angina pectoris, ii. 437 ; depressor
nerve and, ii. 468, 477 ; diameter of
normal, ii. 197 ; dilatation of, i.
189, ii. 197, 346 ; distensibility of,
i. 257 ; elasticity of, in elderly, ii.
144 ; gout, i. 277, ii. 258 ; hyper-
trophy of, ii. 349 ; hypoplasia of,

544

INDEX

ii. 209 ; increased irritability of
inflamed, ii. 482, 484 ; infective
disease and, i. 290, 477, ii. 146, 148-
188 ; innervation of, ii. 297, 467 ;
investments of, ii. 414-416 ; invest-
ments of, and anginal pain, ii. 416 ;
lengthening of, ii. 71, 199, 395;
lengthening of, and apex impulse,
ii. 71, 199, 395 ; medial coat, effect
of adrenalin, i. 223 ; medial coat,
effect of compression, i. 223 ;
medial coat, effect on, of nicotine,
i. 223 ; nerve end-organs in, i. 468,
ii. 291, 414, 418; obliterative
arteritis of, i. 306 ; Pacini bodies in,
ii. 414, 418; pain, sources of, in, ii.
303 ; palpation of, in jugular notch,
ii. 199; perforation, acute, ii. 206-
207 ; pericarditis and, ii. 458 ;
resiliency of, i. 39 ; ring lesions of,
painful, ii. 436 ; root of, and
angina pectoris, ii. 436 ; rupture
of, ii. 206, 463 ; sensitive area of,
ii. 415-416 ; size of normal, ii. 197 ;
stenosis of, ii. 208 ; suprasigmoid
area of, see below ; syphilis of, see
Syphilitic aortitis ; tenderness of,
in angina pectoris, ii. 199, 346 ;
tension of, and pain, ii. 410 ; tuber-
culosis of, ii. 166

Aorta, Hodgson- Welch, i. 189, 479,
ii. 167-168, 177-179, 186, 188;
blood pressure in, ii. 180 ; heart
in, ii. 180 ; pulse amplitude in, ii.
180

Aorta, suprasigmoid area of, angina
pectoris and, ii. 436, 438, 487 ; and
changes of blood pressure, ii. 290 ;
depressor nerve and, ii. 468 ;
distension of, and blood pressure,
ii. 468 ; irritability of, ii. 482, 484 ;
pain, seat of, ii. 192, 290 ; sensitive-
ness of, ii. 410 ; " sensitive tam-
bour," ii. 423 ; site of aortitis, ii.
175

Aortic disease and radiography, ii. 70,
203

Aortic murmurs in atheroma, ii.
268 ; in syphilis, ii. 268

Aortic regurgitation, blood pressure
in limbs in, i. 36 ; hyperesthesia
in, ii. 300

Aortic second sound, audibility of, i.
388

Aortic valves and atheroma, ii. 151 ;
and syphilis, ii. 268

Aortic valvulitis, ii. 151, 436

Aortitis, ii. 143 ff. ; abdominal, ii.
209 ; acute, ii. 148 ; angina pectoris
and, ii. 422 ff. ; blood pressure and,

ii. 145 ; causes of, ii. 148 ; chronic,
ii. 190 ; dilatation in, ii. 346 ;
diphtheria and, ii. 164 ; endo-
carditis and, ii. 459 ; erysipelas and,
ii. 162 ; examination for, important,
ii. 146, 437 ; examination for,
microscope needed, ii. 149 ; experi-
mental, ii. 189 ; febrile phases in, ii.
153, 339 ; gonorrhceal, ii. 166 ; e;out
and, i. 277, ii. 189, 258 ; infection,
acute, and, i. 285, 477, ii. 147, 14S ff.,
260 ; influenza and, ii. 163, 268 ; lead
and, ii. 188 ; malaria and, ii. 165 ;
malignant endocarditis and, ii. 160 ;
measles and, ii. 149 ; microbes,
specific, in, ii. 260 ; mild and
transient often, ii. 148 ; muscular
stress and, ii. 188 ; pain in, ii.
192-193 ; perforating, ii. 273 ;
pericardial friction in, ii. 202 ; peri-
carditis and, ii. 160, 459-460 ; peri-
carditis, basic, and, ii. 202, 331 ;
pneumonia and, ii. 149, 165 ;
presternal oppression in, ii. 193 ;
rheumatic, ii. 150, 274; rheumatic,
aneurysm and, ii. 154 ; rheumatic,
angina pectoris and, ii. 154 ;
scarlatinal, ii. 149 ; small-pox and,
ii. 149 ; suppurative, ii. 162 ;
symptoms of, ii. 192, 424, see
Syphilitic aortitis ; tenderness in,
ii. 199 ; tuberculosis and, ii. 166 ;
typhoid and, ii. 162 ; ulcerative,
ii. 161 ; vasa vasorum and, i. 285
Aortitis, syphilitic, i. 478, ii. 145, 167
ff. ; adventitia in, i. 468, ii. 183, 187.
423 ; age and, ii. 173 ; alcohol and,
ii. 175 ; aneurysm and, ii. 168 ;
anatomy of, ii. 145-146, 170, 186 ;
angina pectoris and, ii. 436 ; aortic
dilatation in, ii. 197, 346 ; aortic
regurgitation in, ii. 176, 180 ;
aortic valves in, ii. 175, 186 ; apex
mobility in, ii. 199 ; area of dul-
ness in, ii. 197-198 ; arteriosclerosis
and, ii. 266 ; atheroma and, ii. 167,
173, 183-187, 190, 206; auscul-
tatory, signs of, ii. 200 ; bruit de
tabourka, ii. 200 ; chronic generally,
ii. 167 ; congenital cases of, ii. 173 ;
coronary orifices and, ii. 175, 178 ;
diagnosis of, ii. 187, 197 ; dulness
" en casque," ii. 198 ; dyspnea in, ii.
197; fever in, ii. 192 ; frequency of,
ii. 167, 171 ; general fatigue in, ii.
195 ; general paralysis in, ii. 175,
181 ; gumma in, ii. 184 ; histology
of, ii. 170, 182 ; Hodgson's dilata-
tion and, ii. 168, 186 ; hypertrophy
of heart and, ii. 200 ; inflammatory,

INDEX

545

ii. 140, 182; interval since infection,
ii. 174, 188, 230 ; intima in, ii. 185;
latency of, ii. 174 ; media in, i.
478, ii. 184 ; mercury in, ii. 188 ;
occupation and, ii. 175 ; pain in,
ii. 192-194; peripheral arteries
and, ii. 193 ; presternal oppression
in, ii. 192 ; presternal oppression
on exertion, ii. 264 ; prognosis in,
ii. 176-177 ; pulse in, ii. 196 ; pulse
amplitude in, ii. 180 ; regurgitant
murmur in, ii. 201 ; regurgitation in,
ii. 176-177; repair by fibrosis, ii. 185;
salvarsan in, ii. 188, 205 ; second
sound in, ii. 200; sex and, ii. 172;
signs of, ii. 197 ; site of, ii. 175 ;
spirochseta in, ii. 183; symptoms of,
ii. 191 ; symptoms of pressure in, ii.
196 ; subclavian sign of Gerhardt, ii.
199 ; tabes and, ii. 175, 181 ; tertiary
lesion, ii. 188 ; treatment of, ii. 188,
204, 208 ; vasa vasorum and, ii. 182 ;
ventricular hypertrophy in, ii. 178 ;
Wassermann reaction and, ii. 175,
192 ; X-rays and, ii. 175, 195, 203

Arm, herpes of, in angina pectoris, ii.
299 ; oedema of, in angina pectoris,
ii. 300 ; pain in, in angina pectoris,
ii. 291, 496 ; paresthesia of, in
angina pectoris, ii. 298 ; paresis of,
in angina pectoris, ii. 298

Arsenic in hyperpiesia, ii. 133

Arterial coats, i. 462

Arterial decay, rate of, i. 400

Arterial disease, adrenalin and, i. 223 ;
ancients" conception of, i. 3 ; attri-
buted to neuritis, i. 303 ; attributed
to nervous influences, i. 306 ;
barium chloride and, i. 231 ; com-
pression of aorta and, i. 223 ;
diphtheria and, i. 289 ; experi-
mental, of medial type, i. 224 ;
history of knowledge of, i. 3-13 ;
in ancient Egyptians, i. 5, 180, 237 ;
in animals, i. 4, 214-216 ; infections
and, 281 ; injections of bacterial
emulsions and, i. 283, 286 ; in-
fluenza and, i. 291, ii. 273 ; nicotine
and, i. 223 ; rheumatism and, i. 288 ;
squill and, i. 223 ; tubercle and,
i. 292 ; typhoid and, i. 283-288

Arterial epithelium, a lipoid mem-
brane, i. 38, 430

Arterial hypertrophy of Johnson, i.
311, 470; correlation with cardiac,
i. 475 ; product of intermittent
stress, i. 496 ff.

Arterial plethora or hyperpiesia, i. 10

Arterial pressure, see Blood pressure

" Arterial tension," i. 11

Arterial thrombosis, pain in, ii. 409
Arterial tone, i. 50, 193 ; and lateral

pressure, i. 199, 459
Arterial wall and blood pressure
measurements,!. 72-84; and pressure
gauge, i. 72; and wave velocity, i.
33 ff.
Arteries, arteriosclerosis of, order of

liability to, i. 332, 456, 461
Arteries, Addison's disease and, i. 222
Arteries differ in different regions of
body, i. 82 ; external relations of,
i. 198 ; in hyperpiesia, i. 384 ; in-
ward disease of, i. 70 ; investments
of, ii. 414 ; lateral pressure in, i. 11,
199, 459; longitudinal stretching of,
i. 11 ; loss of elasticity of, i. 458 ;
of children, arteriosclerosis and
calcification of, i. 174-176 ; of limbs,
calcification of, i. 499, 506 ; of
limbs in labourers, i. 193, 205 ; of
women smaller, i. 474 ; pain in,
ii. 408 ; pressure gauge experi-
ments on excised, i. 77-81 ; syphilis
of, i. 478 ; tortuosity and elonga-
tion of, i. 459 ; tortuosity in
relation to pressure, i. 461 ; tibial
and varicose veins, i. 199, 201 ;
typhoid and, ii. 162
Arterio-capillary cushions, i. 38
Arterioles, fall of pressure in, i. 36 ;

nutrition of, i. 463
Arteriosclerosis, see also Decrescent
and Toxic ; age and, i. 167 ; alco-
holic cirrhosis and, i. 248 ; alcohol-
ism and, i. 246 ; animals and, i. 4,
214 ; aorta and, i. 154, 374, 455, ii.
206 ; aorta, abdominal, and, i. 446 ;
arteries, abdominal, and, i. 444 ; ar-
teries, cerebral, see Cerebral arteries ;
arteries, coronary, see Coronary
arteries; arteries, gastric, and, i.
446 ; arteries, inward, and, i. 70 ;
arteries, mesenteric, of, i. 188, 332,
349, 461, ii. 310 ; arteries most fre-
quently affected, i. 332 ; arteries,
pancreatic, i. 331 , 349, 449 ; arteries,
radial, see Radial arteries ; arteries,
retina], i. 433-436 ; arteries, splenic,
i. 331, 332, 349 ; arteries, sub-
clavian, i. 395 ; arteriosclerotic kid-
ney and, i. 372 ; atheroma distinct
from, or not, i. 508 ff. ; atrophies,
local, in, i. 447 ; beer-drinkers and,
i. 211 ; blood pressure and, i. 154 ff.,
161, 182 ff., 344, ii. 3 ; brain workers
and, i. 213 ; cachexia and, i. 307 ;
calcareous water and, i. 182 ; cal-
cification with, i. 499 ; cancer and,
i. 303 ; children and, i. 174 ; chronic

546

INDEX

rheumatism and, i. 277, 289 ; classi-
fication of, i. 160 ; climate and, i.
182 ; definition of, i. 510 ; diagnosis
of, ii. 59 ; emphysema and, i. 406 ;
electro-cardiogram and, ii. 71 ; gout
and, i. 273 ; great muscular develop-
ment and, i. 212 ; hallucinations
and, ii. 340 ; heart hypertrophy
and, i. 155-158, 189 ; heart, morbid
anatomy of, in, i. 158, ii. 6 ; Hert-
zell's test for, i. 163 ; Huchard's
views of, ii. 1 ; insane frequency in,
i. 9, 12, 351, 426 ; kidneys and, i.
309, 324, 329, 370 ; kidney, granular,
is it an essential part of, i. 334 ;
latent, of von Bosch, i. 11, 379 ; of
labourers, i. 205 ; of large arteries
and blood pressure, i. 31 ; of liver
arteries, i. 450 ; local manifestations
of, i. 375 ; manometry and, i. 80 ;
manual labour and, i. 205 ; me-
chanical causes of, i. 182 ; miners
and, i. 210 ; nerve lesions and, i.
304 ; neuritis and, i. 303 ; not a
disease, i. 13, 154 ; obesity and, i.
252 ; origin of name, i. 6 ; oscilla-
tions of pressure and, i. 193 ; portal
system and, i. 450 ; pregnancy and,
i. 307 ; prognosis of, ii. 71 ff. ; pul-
monary, i. 202 ; race and, i. 180 ;
senile, see Arteriosclerosis, decres-
cent; sex and, i. 179; of splanch-
nic areas, i. 156, 188 ; symptoms
of, i. 374 ; thoracic, i. 156 ; tobacco,
i. 211 ; toxic, see Arteriosclerosis,
toxic ; Wassermann reaction in, i.
292 ; vascular spasms and, i. 161 ;
vasomotor response diminished in,
i. 162; vasa vasorum and, i. 285;
ii. 147, 464-465 ; vertigo in, ii. 340;
in young, i. 171, 174, 175, 280
Arteriosclerosis, causation of, i. 154 ff. ;
adrenalin and, i. 220 ; adrenals,
irritation of, and, i. 225, 369 ; age
in regard to, i. 167 ; alcohol, i. 246,
247 ; aldehydes, i. 213 ; amines and,
i. 270 ; aortic compression, i. 223 ;
autogenetic toxins, i. 261 ; bacterial
emulsion injections and, i. 283 ;
bacterial toxins and, i. 212 ; barium
chloride and, i. 231 ; beer-drinking
and, i. 211 ; calcareous waters and,
i. 182 ; cancer and, i. 303 ; choles-
terin and, i. 212 ; diabetes and, i.
279 ; diet and, i. 234 ; diphtheria
and, i. 289 ; emotion and, i. 236 ;
extracts from intestinal contents,
i. 262 ; gout and, i. 273 ; hereditary
transmission and, i. 164 ; high blood
pressure and, i. 161, 182, 196 ; high

blood pressure and friction and, i.
192 ; infections and, i. 177, 281 ;
influenza, i. 291 ; lactic acid and,
i. 212 ; lead, i. 278 ; meat, excessive,
and, i. 239, 241, 243 ; mechanical
causes, i. 182, 193 ; neuritis, i. 303 ;
overfeeding, i. 240 ; pituitary
disease and, i. 229 ; pressor sub-
stances from urine and, i. 267 ;
pressure, large oscillations of, i. 193 ;
pulse rate and, i. 204 ; rheumatism,
i. 288 ; salt in excess, i. 231 ; stresses,
tensile and shearing, and, i. 513 ;
syphilis and, i. 292 ; thyroid gland
and, i. 230 ; tobacco and, i. 250 ;
toxic causes, i. 232 ; tuberculosis,
i. 292; typhoid and, i. 284; tyra-
mine, i. 268 ; urates and, i. 274 ;
vasoconstriction, extensive, and, i.
216, 219 ; worry and, i. 238

Arteriosclerosis, decrescent, abdominal
disorders in, i. 444 ; age incidence,
i. 170 ; blood pressure in, i. 10, 166,
186, 427, 431 ; brachial artery in,
i. 398 ; cerebral atrophy in, i. 436 ;
cerebral palsies of, i. 426 ; diet not
a cause of, i. 238 ; diagnosis of, ii.
69 ; emphysema in, i. 56, 406 ;
enfeeblement of legs in, i. 430 ;
general condition in, i. 426 ; haenia-
temesis in, i. 448 ; heart in, i. 155,
158, 393, 426, ii. 6, 16; hemi-
plegia, cause of, in, i. 428 ; hot
climates, frequency in, i. 181 ;
heredity and, i. 164-167 ; hyper -
piesia, episodal attacks of, in, i.
156, 396, 427, 452, ii. 65, 72;
hyperpiesia with, i. 401, ii. 60 ;
incidence, variable, ii. 77 ; kidney
in, i. 339, 355, 371-373 ; knee-jerks
in, i. 442 ; limbs shrunken in, i.
426 ; mental changes in, i. 436, 438,
442 ; mitral valve and, i. 393 ; name,
origin of, i. 17; nocturnal restlessness
in, i. 443 ; ophthalmic signs in, i.
432 ; organs, failing irrigation of, in,
i. 426 ; paraesthesias in, i. 420, 444;
poor, frequency in, i. 180 ; pro-
gnosis of, i. 170, 431, ii. 72,77,137-
140 ; pulse in, i. 398 ; senile
convulsions and, i. 410 ; sex and,
i. 179 ; skin, withered, in, i. 426, ii. 3 ;
sleep, disorders of, in, i. 442 ; symp-
toms of, i. 425 ff. ; thyroid gland
and, i. 230 ; transient paresis in,
i. 429 ; urine in, i. 452 ; vertigo,
i. 409

Arteriosclerosis, decrescent, treatment
of, ii. 137 ; concerns morbid changes
originating it, ii. 137 ; iodides of

INDEX

547

little use, ii. 129, 139 ; nutritive
and restorative, ii. 139; ward ofi
attacks of high pressure, ii. 138

Arteriosclerosis, morbid anatomy of, i.
455 ff. ; adventitia lesions of, i. 467 ;
calcification in, i. 499 ; incidence,
partial, i. 434, 456 ; intima, lesions
of, i. 508 ; mainly degenerative, i.
509 ; media, is there a form peculiar
to, i. 4S1 ; media, lesions of, i. 477 ;

• order of lesions, i. 456 ; order of
liability, i. 456, 461 ; patchy, why ?
i. 527 ; pathological phenomena
may be varied, i. 455 ; site of origin
in intima, i. 531 ; syphilitic arterial
disease, resemblance to, i. 480 ;
Thomas's views of, i. 486 ff. ; vasa
vasorum and, i. 464 ff.

Arteriosclerosis, toxic, i. 10, 232 ff.
blood pressure in, ii. 59, 139
causes of, i. 232 ; diabetes and, i
279; diphtheria and, i. 17 7,282,289
infections and, i. 177, 281 ; in
fluenzal, i. 282; head and, i. 278
rheumatism and, i. 178, 282 ; scarlet
fever, i. 178, 282 ; syphilis, chief
cause of, i. 170, 202, ii. 59 ; treat-
ment of, ii. 139 ; typhoid, i. 178,
282, 283 ; vasa vasorum, i. 465 ; in
young, i. 172-178

Arteritis, acute, ii. 70 ; obliterans,
i. 297 ; of influenza, ii. 273

Artery, constricted, protected from
strain, i. 218, 459 ; silver wire, in
arteriosclerosis, i. 435 ; structure of
normal, i. 457 ff., 512

Asthma, arteries in, i. 404 ; blood
pressure in, i. 403

Atheroma, i. 508 ff., ii. 167, see Arterio-
sclerosis; aorta, ii. 206 ; cholesterin
in, i. 252; defined, i. 510, 533; early,
i. 467 ; fat in, i. 252 ; streaky,
distribution of, i. 528

Atherosclerosis, i. 16, 508, see Arterio-
sclerosis ; defined, i. 510

Atrophy, local, from arteriosclerosis,
i. 447

Atropine, action on vagus, ii. 472, 483 ;
in angina pectoris, ii. 522, 538 ; in
heart block, ii. 522 ; in vagus
irritation, ii. 522 ; protects heart
against inhibition shock, ii. 522

Auricle, fibrosis of, ii. 13

Auscultatory method of ascertaining
blood pressure, i. 94

Autogenetic toxins, i. 261 ; existence
of, hypothetical, i. 261

Barium chloride and blood pressure,
i. 231

Baths, effect of, on viscosity, i. 147

Blood density and blood pressure, i.
114, 144

Blood mass, i. 44 ; and blood pressure,
i. 44 ff., 218

Blood not a homogeneous fluid, i. 125

Blood pressure, adrenals and, i. 226,
i. 369 ; alcohol and, i. 246 ; angina
pectoris and, ii. 255 ff., 333 ff., 357 ;
in arterioles, i. 54 ; arteriosclerosis
and, i. 154 ff., 161, 182, 192, ii. 3,
344 ; arteriosclerosis of particular
areas, i. 189, 349 ; atmospheric
pressure and, i. 22, 181 ; asthma
and, i. 403 ; attitude during obser-
vation of, i. 72 ; barium chloride
and, i. 231 ; blood mass and, i. 44 ff.,
218 ; blood density and, i. 114, 144 ;
calcification of arteries and, i. 499 ;
capillary obliteration and, i. 45,
219; capillaries and, i. 54; cerebral,
i. 427 ; coal miners and, i. 210; child-
hood,!. 19, 25, 93, 168; constipation
and, i. 266 ; constriction of renal
area and, i. 351; Cheyne- Stokes
respiration and, i. 407 ; destruction
of renal epithelium and, i. 352; in
diabetes, i. 279 ; during anginal
paroxysm, ii. 337 ; during day, i.
21 ; during sleep, i. 21 ; early studies
of, i. 4-8, 19 ; effect of posture on,
i. 22 ff. ; epilepsy and, i. 411 ; estima-
tion of, by finger, i. 64 ; estimation
of, by instruments, i. 84 ; exertion
and, i. 26 ; extirpation of kidneys
and, i. 353 ; extracts of kidney
cortex and, i. 358

Blood pressure, fall of, from sudden
coronary occlusion, ii. 370 ; in
febrile infections, i. 43 ; of cardiac
origin, i. 42

Blood pressure gauge, and arterial
wall, i. 72-84 ; and contraction of
artery, i. 79-82 ; and sclerosis of
artery, i. 78-81

Blood pressure, gout and, i. 275

Blood pressure, gradients, fall of, in
arterioles, capillaries, and veins, i.
26 ; velocity and, i. 26

Blood pressure, granular kidney and,
i. 338, 343, 34S ; glomerular lesions
and, i. 353 ; Graves' disease and, ii.
63 ; headaches and, ii. 129 ; heart
and, i. 40 ff., ii. 4-8, 16 ; hot climates
and, i. 181 ; hour of observation and,
i. 72 ; in elderly, i. 19, 21 ; in in-
fancy, i. 19; influence of emotion
on, i. 68-71 ; influence of fiver on, i.
266 ; influence of stimulation of
nerve on, i. 22, 368 ; in later life, i.

548

INDEX

19, 21 ; in lead poisoning, i. 275; in
limbs in aortic regurgitation, i. 36 ;
mania and, i. 437 ; in man, i. 19 ;
meals, influence of , on, i. 22; mean,i.
93; measurement of, i. 61; mechani-
cal means of estimating, i. 57, 61 ;
mental effort and, i. 238 ; neur-
asthenia and, ii. 61 ; obesity and,
i. 252 ; ovarian extract and, i. 230 ;
pregnancy and, i. 307 ; in peri-
pheral areas of constriction, i. 30;
pupil, size of, and, i. 437 ; in pul-
monary o?dema, i. 402 ; pulse rate
and, i. 24, 43, 399 ; raised by
" stuffing," i. 245 ; relaxed arteries
and,i. 29; records, in limbs, i. 75; red
blood cells and, i. 256 ; in sclerotic
kidney, i. 338 ; sodium chloride and,
i. 231 ; in syphilitic arterial disease,
i. 156, 302, ii. 129 ; temperature,
changes of, and, i. 22, 181 ; tobacco
and, i. 250 ; tortuosity of arteries
and, i. 461 ; total and unit, i. 68 ;
in veins, i. 54 ; viscosity and, i.
118, 127, 143 ; Von Bosch's work
on, i. 19 ; xanthine bodies and, i.
274

Blood pressure, diastolic, i. 20, 86 ff. ;
in children, i. 93 ; estimation of,
difficult, i. 86, 89, 93 ; estimation by
auscultatory method, i. 95 ; high,
harmful, i. 196 ; high, and cerebral
apoplexy, i. 427 ; importance of, i.
86 ff., 89 ; in man, i. 93 ; in middle
life, i. 90 ; relation to systolic, i.
91 ; tobacco raises, i. 251

Blood pressure, high, angina and, ii.
255, 357 ; aorta and, i. 190, ii. 191 ;
aortitis and, ii. 145 ; arteriosclerosis
and, i. 182 ; arteriosclerosis, ab-
dominal, and, i. 188 ; blood density
and, i. 114 ; Bright's disease and, i.
342 ; cerebral haemorrhage and,
i. 164-166, 412 ff. ; cerebral, and
sense of well-being, ii. 85 ; dicrotism
and, i. 398; digitalis, use of, in, ii.
134 ; due to cerebral haemorrhage,
i. 423 ; episodal, in elderly, i. 156,
396, 427, 452, ii. 65 ; epistaxis in,
i. 423 ; extensive vasoconstriction
and, i. 216 ; extra-svstole and, i.
390 ; gallop rhythm in, i. 391 ;
heart and, ii. 4-8, 16 ; high-feeding
and, i. 239 ; meat and, i. 241, 243 ;
melancholia and, i. 437 ; meningeal
haemorrhage and, i. 423 ; miliary
aneurysm and, i. 429 ; nephritis,
acute, and, i. 342 ; neurotic, ii. 60 ;
paroxysmal dyspnea of, i. 402 ;
paroxysmal vomiting, i. 451 ; sleep,

disorders of, and, i. 443; splanch-
nic contraction and, i. 217 ; strain
of, continuoush7, ii. 255; transient
paretic attacks and, i. 412 ff. ; with-
out kidney disease, i. 311-313, 343,
347, ii. 191

Blood pressure recorders, i. 84 ;
Gartner's, i. 98 ; Herz, i. 97 ; Hill
and Barnard's, i. 85 ; Oliver's, i. 85,
97; Pachon's,i. 88,91; Riva-Rocci,
i. 85, 91 ; Uskoff's, i. 87

Blood pressure, systobc, in arterio-
sclerosis, i. 92 ; in elderly, i. 20 ;
influence of psychical factors on,
i. 71 ; instrumental fallacies in,
i. 89 ; in man, i. 93 ; prognosis of,
in arteriosclerosis, ii. 75 ; relation
to diastolic, i. 91

Blood stream velocity in aorta, i. 30 ;
in arterioles, i. 30

Blood, uratic content of, i. 322

Blood, viscosity of, i. 104 ff. ; of laked,
i. 128

Brachial artery, arteriosclerosis of, i.
398,457; in hyperpiesia, i. 398; used
for pressure records, i. 82

Brachial plexus, injury of, may cause
fall of blood pressure, ii. 482

Bright's disease, see Kidney disease ;
diagnosis of, i. 316 ; effect of, on
heart and vessels, i. 190 ; high
blood pressure and, i. 342 ff. ; hyper-
piesia and, i. 344 ; prealbuminuric
stage of, i. 9, 11, 196,334

Bruit de tabourka in aortitis, ii. 200,
268

Bundle of Kent, in diphtheria, ii. 52 ;
fatty change in, ii. 47, 52 ; patho-
logical relations of, andmyocardium,
ii. 52 ; syphilis and, ii. 51

Calcification, i. 499 ff. ; age incidence,
i. 500 ; areas of, soft during life
" not set," i. 506-507 ; associated
more with decrescent variety, i. 507 ;
associated with moderate pressures,
i. 499 ; chemistry of, i. 501 ff. ;
concerns intima as well as media,
i. 503, 507 ; iron, traces of, in, i.
508 ; microscopic and chemical
detection, i. 500 ; not necessarily
mischievous, i. 505 ; passive, not
active change, i. 504 ; possibility
of bacterial decomposition, i. 501

Calcium content and coagulation, i.
Ill

Calcium salts and viscosity, i. 126,
133 ; in hyperpiesia, ii. 131

Capillaries, fall of pressure in, i. 26

Capillary disease, i. 463

INDEX

549

Capillary dynamics, i. 54

Capillary fields, obliteration of, i. 45

Capillary pressure, i. 54 ; Lombard's
method of estimating, i. 54

Carbon dioxide and viscosity, i. 129,
131

Cardiac aneurysm, ii. 368

Cardiac callosities, ii. 14, 20, 49 ;
clinical signs of, ii. 22, 49

Cardiac function and vagus stimula-
tion, ii. 473

Cardiac nerves, relation of, to cardiac
function, ii. 53-54

Cardiac plexus and angina pectoris,
ii. 402 ; disease of, painless, ii. 405 ;
function, motor, ii. 405

Cardiac reserve, ii. 28 ; and hyper-
trophy, ii. 32 ; trainable, ii. 57

Cardio-arterial afferents, ii. 411

Cardio -arterial sympathies, ii. 467

Cardiograph, Marey's, i. 57

Cardiosclerosis, ii. 1 ; common use
of term, ii. 1, 4 ; has no definite
conception, ii. 7, 24

Cerebral apoplexies, hsemorrhagic and
obstructive, i. 407

Cerebral arteries, contractile capacity
low, i. 218 ; in brain workers, i.
213 ; miliary aneurysm of, i. 429 ;
rich in elastic fibres, i. 514 ; walls
of, thin, i. 514

Cerebral arteries, arteriosclerosis of,
basal suffer early, i. 198 ; early
affected, i. 344 ; frequently syphi-
litic, i. 292 ; in young, i. 178

Cerebral blood pressure, i. 427

Cerebral hemorrhage, blood pressure
and, i. 164, 412, 427 ; cause of tran-
sient parietic attacks, i. 415, 422 ;
causes of, i. 411 ; causes rise of
blood pressure, i. 423 ; frecpaency in
night, i. 424 ; greatest danger in
high blood pressure, i. 411 ; heart
and, i. 426 ; hereditary tendency to,
i. 164, 412 ; in cerebral syphilis, i.
432; in hyperpiesia, i. 166, 412;
kidney disease and, i. 166; rare in
decrescent arteriosclerosis, i. 166,
426-427

Cerebral palsies of decrescent arterio-
sclerosis, i. 426 ; transient, see Tran-
sient paretic attacks

Cerebral seizures in arteriosclerosis, i.
407

Cheyne-Stokes respiration, blood pres-
sure in, i. 407

Cheyne-Stokes respiration in hyper-
piesia, i. 407

Children, angina pectoris in, ii. 152,
155, 249 : hyperpiesia in, i. 172, ii. 84

Chloroform, effect of, on vagus, ii.

483-484, 534
Cholesteraernia, i. 254, 506
Cholesterin in arterial walls, i. 252
Choline, lowers blood pressure, i. 266
Claudication of heart and angina

pectoris, ii. 397
Coagulability and viscosity, i. 110
Coagulation and calcium content, i.

Ill
Coagulometer, i. 110
Coats, arterial, i. 462 ff.
Cobra venom, action of, i. 268
Coffee, cardiac irregularity and, ii.
500, 507 ; substernal oppression
and, ii. 500, 507
Colic and abdominal arteriosclerosis,

i. 447
Colubrine poisons, i. 268
Compensation, misuse of word by
Thoma, i. 487 ; sense in which
word may be used, i. 497
Complexion in anginal paroxysm, ii.

341
Connective tissue, distribution of, in
arteries, i. 515 ; elastic contrasted
with, i. 514 ; increases with age,
i. 518 ; increases with stresses, i.
515 ; properties of, i. 514 ; signifi-
cance of increase, i. 516
Constipation, blood pressure in, i. 266
Coronary arteries, action of adrenalin
on, i. 222, ii. 359 ; aneurysm of, ii.
464 ; arteriosclerosis of, greater in
decrescent than in hyperpiesia, ii.
338 ; arteriosclerosis of, in kidney
disease, i. 331 ; arteriosclerosis of,
in young, i. 178 ; block of, and
pain, ii. 369; block of, symptoms
of, ii. 450, 453, 461, 465; con-
tractile capacity low, i. 218 ; disease
of, ii. 352 ff. ; disease of, and
causation of angina pectoris, ii.
352 ff. ; disease of, effect of, on
myocardium, ii. 17, 21-23, 267,
360, 462 ; disease of, generally
unattended by angina pectoris, ii.
265, 353 ; embolism of, ii. 369, 373 ;
enlarge with work of heart, ii. 8 ;
heart and, ii. 21, 179, 360 ; hyper-
trophy of heart and, ii. 22 ; not
end arteries, ii. 362 ; occlusion of,
and death in angina pectoris, ii.
265 ; occlusion of, as a cause of
angina pectoris, ii. 352 ; occlusion
of, effect of sudden, ii. 370-371 ;
occlusion of, effect of, on myocar-
dium, ii. 21, 179, 360 ff. ; spasm of,
as a cause of angina pectoris, ii. 356 ;
thrombosis of, as a cause of pain, ii.

550

INDEX

368 ; thrombosis of, may simu-
late abdominal angina, ii. 502 ;
thrombosis of, may simulate vis-
ceral perforation, ii. 502 ; throm-
bosis of, myocardium in, ii. 462 ;
thrombosis of, symptoms of, ii.
450, 452 ; vasomotor governance
of, ii. 358-359

Coronary circulation and fibrosis, ii.
21

Coronary orifices, syphilitic disease of,
ii. 178 ff.

Coronary flow, regulation of, ii. 359

Corpuscles and viscosity, i. 126-129,
131

Cyanosis and viscosity, i. 129

" Dead fingers," in elderly, i. 164

Death, by inhibition in angina pectoris,
ii. 466; from "peripheral heart"
failure, ii. 45, 55 ; in pleural opera-
tions, ii. 479 ; from severe pain, ii.
484-485

Decadent processes, appearance in
patches, i. 527

Decrescent arteriosclerosis, see Arterio-
sclerosis, decrescent

Decrescent, origin of term, i. 17

Delusions in arteriosclerosis, ii. 340

Depressor nerve, heart and, ii. 467 ff. ;
sensory nerve of aorta, ii. 468, 477

Dermatographic phenomena in
elderly, i. 164

" Dextral " angina pectoris, ii. 300-
304 ; and lesion of right heart,
ii. 301

Diabetes, blood pressure low in, i. 279 ;
in children with thick arteries, i.
280, 450

Diaphoretics in hyperpiesia, ii. 103

Diastolic blood pressure, see Blood
Pressure, diastolic

Diet, arteriosclerosis and, i. 239
Chittendens and others, i. 241
flesh, and intestinal bacteria, i. 263
hyperpiesia and, ii. 84, 87 ; viscosity
and, i. 117

Dietary, purin-free, ii. 89

Digitalis in angina pectoris, ii. 537 ;
in hyperpiesia, ii. 134 ff.

Dilatation of heart, see Heart, dilata-
tion of

Diphtheria, aortitis from, ii. 164 ;
arterial disease from, i. 282, 289 ;
bundle of Kent in, ii. 52 ; heart
failure in, ii. 45 ; muscle fibres in,
ii. 4S ; nephritis from, i. 365

Disease, angina pectoris a, ii. 212 ;
arteriosclerosis not a, i. 13, 154 ;
meaning of term, i. 14, ii. 215

Dorsalis pedis artery, arteriosclerosis
of, i. 399

Dyspnea, i. 401 ff., ii. 312 ff. ; angina
pectoris and, ii. 312-319 ; kinds of,
i. 402 ; no essential symptom of
angina, ii. 312, 317 ; of high
altitudes, i. 404 ; of high blood
pressure, i. 402-406 ; of high intra-
ventricular pressure, i. 404 ; of
high intraventricular pressure and
angina pectoris, i. 404 ; toxic, i.
406; uraemic, and angina pectoris,
ii. 504

Dyspnea, paroxysmal, i. 402 ff. ; an
acid intoxication, i. 402, 405 ;
central, i. 405 ; distinguished from
angina pectoris, ii. 504 ; pulmonary
oedema in, i. 403

Dystrophic sclerosis, ii. 17

Egvptians, ancient, arteriosclerosis

in, i. 5, 180, 237
Ehret's phenomenon, i. 94
Elastic tissue, calcification of, i. 516,

520 ; changes in disease, i. 522 ;

changes under stretching, i. 520 ;

contrasted with connected tissue, i.

514 ; distribution of, in arteries,

i. 515 ; effect of stress upon, i. 515 ;

heart in the, ii. 11 ; in infectious

diseases, i. 522; physical qualities

of, i. 516 ; properties of, ii. 514 ;

relation to connective tissue, i. 517 ;

reparative phenomena in, i. 523 ;

rupture of, and arteriosclerosis, i.

515
Elasticity, definition of, i. 457
Elderly, episodic phases of high

pressure in the, i. 156, 396, 427, 452,

ii. 65
Electric treatment in hyperpiesis, ii.

109
Electrocardiograph and myocardial

value, ii. 41
Elongation of artery, i. 459
Embolism of mesenteric arteries and

intestinal pain, i. 447, 449
Emotion, influence of, on blood

pressure records, i. 68-71
Emphysema in arteriosclerosis, i.

406
Endarteritis obliterans in the kidney,

i. 330
Endothelium, vascular, a lipoid mem-
brane, i. 38, 430 ; immunity from

disease, i. 466
Epigastric angina pectoris, ii. 304
Episodic hyperpiesia in the elderly, i.

156,396,427,452, ii. 65; treatment

of, ii. 100, 125

INDEX

551

Episternal notch, palpation of aorta
in, i. 394, ii. 199

Epistaxis in hyperpiesia, i. 442, ii. 68

Ergot oxin, i. 267

Erysipelas and aortitis, ii. 162

Exercise, and blood pressure, ii. 99 ;
in hyperpiesia, ii. 96 ; value of, ii.
96 ; violent, deprecated in middle-
aged, ii. 99 ; viscosity and, i. 119

Extra-systoles in angina pectoris, ii.
471 ; and oppressive pains, ii. 500 ;
of high blood pressure, i. 390

Erythremia and blood pressure, i. 256

Erythrocytosis and viscosity of blood,
i. 126

Face in paroxysm of angina pectoris,
ii. 341

Fat people, two kinds of, i. 252

" Fatty degeneration " of heart, ii. 47

Femoral artery, wave in, i. 77

Fever in acute aortitis, ii. 339 ; in rheu-
matic aortitis, ii. 339

Fibrosis and cardiac function, ii. 15,
17, 18

Fibrous tissue, in ageing hearts, ii. 10;
in auricles, ii. 9, 13; in children's
hearts, ii. 10 ; function of, ii. 10, 13 ;
in ventricles, ii. 9

Finger, advantage of, over sphygmo-
meter, i. 66 ; as pressure gauge, i.
61-68

Friction, at the sides of vessels, i. 37 ;
in capillaries, i. 56 ; internal, i. 123 ;
within blood itself, i. 37

Fruit in hyperpiesia, ii. 93

Gallop rhythm in high blood pressure,
i. 391

Gastric arteries, arteriosclerosis, i.
446, 448, 449

Geisbach's disease, i. 256, 260 ; and
hyperpiesia, i. 260

Gelatiniform patches, atheroma or
syphilis ? i. 466

Glomerular lesions, and blood pressure,
i. 353 ; and hypertrophy of ven-
tricle, i. 356

Glomeruli in arteriosclerotic kidney,
i. 355 ; in granular kidney, i. 355

Glycosuria, and arteriosclerosis of
pancreas, i. 280 ; and arterio-
sclerosis in elderly, i. 280

Gonorrhceal aortitis, ii. 166

Gout, and angina pectoris, ii. 257-260;
and aortic disease, i. 277, ii. 189,
258 ; and arteriosclerosis, i. 273 ;
blood pressure in, i. 275

Gouty seizures and anginiform seizures,
ii. 259

Graves' disease, blood pressure in,

ii. 63
Guaiacum in hyperpiesia, ii. 132

Hsematemesis from gastric arterio-
sclerosis, i. 448

Hsemorrhage, cerebral, see Cerebral
haemorrhage

Hallucinations in angina pectoris, ii.
340 ; in arteriosclerosis, ii. 340

Headache, arteriosclerosis and, i. 408 ;
renal disease and, i. 409 ; syphilitic,
i. 408

Heart, action of, during anginal
paroxysm, ii. 329-334 ; alcoholic, ii.
67 ; apex of, mobility of, ii. 71,
199, 395 ; blood pressure and, i.
40 ff., ii. 4-8, 16; chemistry of
degenerated, ii. 5 ; chemistry of
hypertrophied, ii. 5 ; children's,
fibrous tissue in, ii. 10 ; consump-
tion of oxygen in, ii. 8 ; cramp of,
and angina pectoris, ii. 382 ; decres-
cent arteriosclerosis and, i. 555, 158,
393, 426, ii. 6, 16; dilatation of, ii.
9, 14, 32 ; dilatation of, and anginal
pain, ii. 386, 396, 440 ; disease and
pain, ii. 395, 396, 420 ; distress, pain
in, ii. 440, 495, 496 ; distress, pain
in, nature and site of, ii. 440, 442 ;
enfeebled, influence of vagus on, ii.
473 ft'., 484 ; enlargement during
exertion, i. 397 ; estimation of size
of, i. 396, 397 ; fibrosis of, see
Myocardial fibrosis ; fibrous tissue
in elderly, ii. 10, 11 ; gouty, and
angina pectoris, ii. 258; gouty, and
aortic disease, ii. 258 ; granular
kidney and, i. 338, 343, ii. 8 ; hyper-
piesia and, i. 158, 382, ii. 4, 7, 8, 16 ;
infections and, ii. 29, 45 ; infectious
nephritis and, i. 366 ; inhibited by
pleural irritation, ii. 478, 480 ; in-
hibited by vagus injury, ii. 483 ;
in trained persons, ii. 4 ; invest-
ments of, ii. 414 ; is there an angina
of, ii. 439, 462, 465 ; " knot," ii.
415 ; morbid anatomy of, in
arteriosclerosis, ii. 6 ff. ; pain,
anginal, generated in, ii. 463 ; pain
in functional disease, ii. 496 ; pain
in valvular disease, ii. 496 ; palpita-
tion of, in mock angina, ii. 232, 235 ;
parenchymatous nephritis and, i.
343 ; " peripheral," ii. 45, 55 ;
peripheral resistance and, i. 46 ;
reserve of, trainable, ii. 57 ; rupture
of, ii. 463 ; sounds, accentuation of
second, i. 389 ; sounds of, during
anginal paroxysm, ii. 331 ; " swing-

552

INDEX

ing," i. 395 ; vasomotor connections
of, ii. 467, 477 ; "weak," of women,
ii. 55 ; work, measurement of, i. 98

Heart failure, ii. 25 ff . ; acute infections
and, ii. 45; alteration of pulse rate
in, ii. 37 ; cardiac nerve and, ii. 53 ;
depends upon many coefficients, ii.
33 ; diagnosis of, ii. 31-46, 58 ;
diphtheria and, ii. 45, 48 ; fibrosis
and, ii. 18 ; peripheral heart and, ii.
55 ; pulse and, ii. 36 ; pulsus alter -
nans and, ii. 37, 335 ; rheumatism
and, ii. 48 ; scarlet fever and, ii. 45 ;
signs of, ii. 32-39 ; symptoms of, ii.
31, 36-40 ; valvular disease and, ii.
31 ; vasomotor system and, ii. 55

Heart, hypertrophy of, absent in
syphilitic arterial disease, i. 156 ;
arteriosclerosis and, i. 155- 15S, 189 ;
destruction of renal epithelium and,
i. 352 ; detection of, i. 395 ; fibrosis
and, ii. 14, 18 ; heart reserve and,
ii. 32 ; myocardium in, ii. 12 ; not
a disease, ii. 7, 8, 32 ; structure of,
ii. 8, 9

Hepatic arteries, arteriosclerosis of, i.
450

Hereditary influences and arterio-
sclerosis, i. 164-167

Hertzell's test for arteriosclerosis, i. 163

High pressure dyspnea, i. 402

Huchard's presclerosis, i. 11, 183, 343,
ii. 2

Huchard's views on arteriosclerosis, ii.
1 ff.

Hypersesthesia in aortic regurgitation,
ii. 300

Hyperpiesia, i. 10, 17, 37S ff. ; ab-
dominal symptoms in, i. 444 ; ad-
vanced stage of, i. 382 ; age inci-
dence, i. 167, 169; angina pectoris
and, ii. 240-242, 265; aorta and, i. 394;
arteries, brachial, i. 398 ; arteries,
calcification of, i. 401; arteries,
subclavian, i. 395 ; blood pressure,
decline of, in, i. 394 ; brachial artery
in, i. 398 ; Bright's disease not
identical with, i. 344 ; bronchitis in,
i. 407 ; cerebral haemorrhage in, i.
164-166, 411-412; Cheyne-Stokes
respiration in, i. 407 ; children and, i.
171 ff. ; cough in, i. 407 ; decrescent
with, i. 401, "ii. 60; defined, i. 10, 17,
313, 345; despondency in, i. 382,
436; diagnosis of, ii. 59, seelater; diet
and, i. 180, 238 ; drowsiness and,
i. 443 ; dyspnea, i. 382, 401, ii. 71 ;
early stages of, ii. 72 ; episodic
attacks in elderly, i. 156, 296, 427,
452, ii. 72 ; epistaxis in, i. 442, ii.

68; etiology unknown, i. 313;
extrasystoles in, i. 390; functional
cardiac attacks and, ii. 67 ; gallop
rhythm in, i. 391 ; gastric dis-
tension in, i. 397 ; haemoptysis and,
i. 407 ; haemorrhages, cerebral, i.
164-166, 411-412 ; haemorrhages,
meningeal, i. 423 ; haemorrhages,
retinal, i. 423 ; haemorrhages, skin,
i. 423 ; haemorrhages, uterine, i. 452 ;
haemorrhoids, i. 452 ; headache and,
i. 408 ; head, fulness of, and, i. 409 ;
heart in, i. 158, 382-384, ii. 4, 7, 8, 16;
hereditary influences and, i. 164 ff. ;
kidneys and, i. 344, 371, ii. 67 ;
knee-jerks in, i. 442 ; melancholia
in, i. 437 ; mental symptoms in, i.
436 ; menopause and, i. 452 ;
migraine and, i. 40S ; ophthalmic
signs, i. 432 ; paretic transient
attacks in, i. 413 ff. ; paroxysmal
dyspnea and, i. 402 ff. ; plethora
vera and, i. 255 ; pneumonia and,
i. 425 ; polycythsemia rubra and,
i. 256 ; pressor substances and, i.
270-272 ; prognosis, i. 170, 320, ii.
71 - 79, 81 - 82, 140 ; pulmonary
oedema in, i. 402-403, ii. 76 ; pulse
in, i. 384, 397 ff.; pulsus alternans in,
i. 401 ; respiration in, i. 382, 384 ;
retinal haemorrhages, i. 423; sex
and, i. 179; sleep, disorders of, and,
i. 442 ; urine in, i. 384, 452, ii. 77

Hyperpiesia, diagnosis of, from, ii. 59
ff. ; alcoholic heart, ii. 67 ; cerebral
syphilis, ii. 63 ; dyspnea of high
pressure, ii. 64 ; dyspnea, hysterical,
ii. 64 ; general paralysis of the
insane, ii. 63 ; heart embarrass-
ments, ii. 65 ; hypochondriasis, ii.
64 ; neurasthenia, ii. 61 ; tabes, ii.
63

Hyperpiesia, treatment of, ii. 81 ;
alcohol banned, ii. 88 ; anti-
syphilitic, ii. 129-130 ; arsenic, ii.
133 ; baths, spa, ii. 103 ; baths,
light, ii. 109 ; calcium salts, ii. 131 ;
cardiac distress, morphia or heroin,
ii. 134 ; climate, ii. 102 ; determina-
tion of stage of malady, ii. 81 ;
diaphoretics in, ii. 103 ; diet of
primary importance, ii. 84, 86, 87 ;
digitalis and, ii. 134 ; discipline of
patient, ii. 83 ; diuretin, ii. 132 ;
electric, ii. 109; exercises, natural
better than artificial, ii. 96 ; food,
reduce intake of, ii. 87 ; fruit, ii.
93 ; guaiacum, ii. 132 ; heart to be
relieved of stress, ii. 86 ; intestinal
antiseptics, ii. 93 ; iodides, ii. 126?

INDEX

553

129 ; iodopin, ii. 128 ; Karell cure
and, ii. 91 ; lumbar puncture and,
ii. 119; massage in, ii. 100; meat
and, ii. 89 ; mercury in, ii. 1 25 ;
milk diet in, ii. 91 ; morphia, ii.
129 ; nitrites, ii. 121 ; oxygen
inhalations in, ii. 133 ; podophyllin,
ii. 125 ; purin-free diet, ii. 88-89 ;
radium emanation waters, ii. 108 ;
regulated hill - climbing, ii. 97 ;
rest and, ii. 100 ; salines, ii. 125 ;
salt-free diet, ii. 93 ; salvarsan, ii.
129 ; sodium salicylate, ii. 132 ;
sodium silicate, ii. 130 ; sparteine,
ii. 124 ; stovaine, ii. 124 ; strych-
nine, ii. 129, 134 ; thyroid extract
in, ii. 125, 134; tobacco, tea, coffee,
ii. 89, 93 ; vasodilators in, ii. 120 ;
vegetarian diet in, ii. 92; venesec-
tion in, ii. 75, 114; vibrotherapy, ii.
114 ; waters, drinking of, ii. 107 ;
whey, ii. 130

Hypertonus, i. 17

Hypochondria, ii. 64

Hypoplasia of aorta, ii. 209

Hypotheses, of angina pectoris, ii. 350
ff. ; Huchard's, of arteriosclerosis, i.
343, ii. 1 ; Mahomed's, re Blight's
disease, i. 9

Indolethylamine, action on vaso-
motor centres, i. 267

Indoxyl group and high blood pres-
sure, i. 270

Infarct, pulmonary, i. 403

Infections, acute, effect of, on heart,
ii. 29, 45

Inf ec t ious diseases, and art eriosclerosis,
see Toxic arteriosclerosis ; and
kidneys, i. 365 ff. : changes in
arteries due to, i. 281

Infectious lesions of aorta, i. 290, ii. 146,
148-188 ; and area of aortic dulness,
ii. 346 ; and vasa vasorum, ii. 147 ;
pain frequently absent in, ii. 193

Influenza, angina pectoris in, ii. 163,
239,260,268, 272; arteritis of, ii. 273 ;
changes of arteries due to, i. 282,
291, ii. 273

Influenza, aortitis in, ii. 163, 268 ;
prognosis favourable in, ii. 164

Innervation of aorta, ii. 297

Insane; arteriosclerosis in, i. 351 ;
infrecpaency of intracerebral haemor-
rhage in, i. 165

Instruments for estimating blood
pressure, i. 57-98

Intercostal pain in angina pectoris,
ii. 296 ; in mock angina, ii. 226

Intermittent claudications, i. 413 ff.
ii. 397

Intestinal antiseptics in hyperpiesia,
ii. 93

Intima, blood-vessel proper, i. 197 ;
cause of disease in, i. 513, 524, 531 ;
decades of life and, i. 526 ; defined,
i. 513 ; diseases of, i. 50S ; nutri-
tion of, i. 464, 466 ; seat of disease
in, i. 513, 531 ; seat par excellence
of arterial disease, i. 474 ; in
syphilitic aortitis, ii. 185

Intimal connective hypoplasia, i. 197

Investments of heart and arteries,
ii. 414 ; and anginal pain, ii. 416

Involutionary arteriosclerosis, see Ar-
teriosclerosis, decrescent

Iodide of potassium, effect of, upon
arterial circulation, i. 144-145 ; in
hyperpiesia, ii. 124 ; in viscosity,
i. 145

lodothyrin, depressor action of, i. 268

Jugular notch, palpation of aorta in,
i. 394, ii. 199

Kidney, affections of arteries in, i.
329, 331, 332; endarteritis ob-
literans in, i. 330; medial hyper-
trophy, i. 330, 471 ; no arterial
disease peculiar to kidney, i. 330

Kidney, amyloid disease of, and blood
pressure, i. 342, 349 ; and heart,
i. 349

Kidney and arteriosclerosis, i. 309-
372 ; modern opinions of, i. 315 ;
morbid anatomy, i. 324 ; nervous
factors and, i. 368

Kidney, arteriosclerotic, i. 335, 339,
355, 371, 373 ; age incidence, i. 340 ;
arterial changes in, i. 339 ; blood
pressure in, i. 338 ; contrasted with
granular, i. 334, 339, 372; and
general arteriosclerosis, i. 377 ;
glomeruli in, i. 335, 355 ; heart not
enlarged in, i. 338 ; interstitial and
tubular changes in, i. 335 ; mean
age at death, i. 320

Kidney and bacillus coli, infection of
urinary tract, i. 366

Kidney, cardiac, i. 348 ; contracted
white, i. 320, 348 ; cortex, extract
of, and blood pressure, i. 358

Kidney, decrescent, see Kidney, ar-
teriosclerotic

Kidney disease, and adrenals, i. 368 ;
aorta and arteries in, i. 190 ; blood
pressure in, i. 342 ff., 349, 350;
cerebral haemorrhage in, i. 411, 436 ;
diagnosis of. i. 316 ; epistaxis in,

554

INDEX

i. 442 ; headache in, i. 408 ; heart
in, i. 190 ; high pressure in, i. 342
ff., 350 ; myocardial arterioles in,
i. 331 ; paroxysmal dyspnea in, i.
402 ; pulmonary oedema in, i. 403 ;
pulsus alternans in, i. 401 ; systemic
arteriosclerosis and, i. 332 ; tyramine
and, i. 26S

Kidney, extirpation of, and blood
pressure, i. 353

Kidney, granular, adrenals and, i.
369 ; age incidence, i. 170, 340 ;
arterial changes in, i. 339, 344, 351 ;
blood pressure in, i. 338, 343, 348 ;
contrasted with arteriosclerotic
kidney, i. 334, 339, 372; due to
some poison, i. 363 ; glomeruli in,
i. 355 ; heart hypertrophied in, i.
338, 343, 348; hypothetical toxin
in, i. 341 ; interstitial hyperplasia
in, i. 339 ; mean age at death, i.
320 ; oedema in, i. 343 ; relation
to general arteriosclerosis, i. 334;
slow irritative process, i. 335 ;
ventricle in, i. 343

Kidney, infectious disease and, i. 365 ;
glomeruli, lesions of, and high blood
pressure, i. 353 ; lead poisoning and,
i. 341 ; parenchyma lesions and
high blood pressure, i. 352; scarla-
tinal, i. 366; senile, see Kidney,
arteriosclerotic ; shrunken, i. 328,
329, 338 ; stuff as pressor, i. 357 ;
syphilitic, i. 367, ii. 266

Kidney values, method of appreciat-
ing, i. 320

Lability, the synonym for resiliency,

i. 458
Labourers' arteriosclerosis, i. 193,

205, 509 ; limbs and lactic acid,

i. 213
Laking of blood, effect of adding

haemoglobin, i. 129 ; raises mole-
cular friction, i. 129 ; relation to

viscosity, i. 128
Latent arteriosclerosis of von Basch,

i. 11
Lateral pressure in arteries, i. 11
Lead poisoning, arteriosclerosis in,

i. 278 ; high blood pressure in, i.

278 ; kidney in, i. 341
Legs, enfeeblement of, in old persons,

i. 430 ; arteriosclerosis of arteries

of, i. 431
Leucocytosis and viscosity of blood,

i. 126
Limbs, blood pressure records in, i.

75-78 ; paraesthesia of, due to

arteriosclerosis, i. 442

Lipoid membrane in arteries, i. 38,

ii. 430
Liver, alcoholic cirrhosis of, and

arteriosclerosis, i. 248, 450 ; blood

pressure in, i. 248, 266
Livierato's reflex, ii. 44
Lombard's method of estimating

capillary pressure, i. 54
Longitudinal stretching of arteries,

i. 11
Ludwig's kymograph, i. 58
Lumbar puncture in hyperpiesia, ii.

119 ; in chronic kidney disease,

ii. 119

Mahomed's, Dr., prealbuminuric stage
of Bright's disease, i. 9, 11, 311

Malaria and aortitis, ii. 165

Malignant endocarditis, and angina
pectoris, ii. 276 ; and aortitis, ii. 160

Mania, blood pressure in, i. 437

Manometry, effect on, of changes in
arterial wall, i. 72-84

Manual labour, arteriosclerosis and,
i. 205

Marey's cardiograph, i. 57 ; plethys-
mography i. 7 ; sphygmograph, i. 57

Massage in arteriosclerosis, ii. 100

Measles and aortitis, ii. 149

Meat, arteriosclerosis and, i. 241 ;
high blood pressure and, i. 241,
243, 261

Mechanical causes of arteriosclerosis,
i. 182

Mechanical laws in physiology, validity
of, i. 48

Mechanical stress, and the cardio-
arterial system, i. 193

Media, adrenalin and, i. 233, 478 ;
functions of, i. 197, 477 ; " gum-
mous lesions " of, i. 299, 479 ;
hypertrophy of, i. 470 ff. ; hyper-
trophy of, in high pressure, i. 472 ff . ;
hypertrophy of, intermittent lateral
pressure and, i. 476 ; hypertrophy
of (Johnson), i. 12, 311, 330, 470;
infectious diseases and, i. 288 ff.,
477 ff. ; is there a primary arterio-
sclerosis of, i. 481 ; lesions of, i.
477 ff. ; primary degeneration of
(Monckeberg's sclerosis), i. 197, 482 ;
syphilis, gravest infection of, i. 478 ;
syphilis of, i. 299-302, 478, 480,
ii. 184; thickening of, i. 470 ; ways
disease of, may arise, i. 506

Melancholia, blood pressure in, i. 437 ;
hyperpiesia and, i. 437-438

Mental stress, aortic disease and, ii.
239 ; granular kidney and, ii. 239 ;
heart disease and, ii. 239 ; hyper-

INDEX

555

piesia and, ii. 240 ; vasomotor
instability and, ii. 239
Mental symptoms in arteriosclerosis, i.

436
Mercury, episodal high pressure and,
ii. 240 ; hyperpiesia and, ii. 84,
125, 129 ; syphilitic aortitis and,
ii. 188 ; toxic arteriosclerosis and,
ii. 139
Mesenteric arteries, arteriosclerosis of,
i. 449, 461, ii. 332; abdominal
pain and, ii. 310, 504 ; fine vessels
generally intact, i. 188 ; granular
kidney and, i. 349
Mesenteric arteries, thrombosis of,

i. 447, 449
Migraine, granular kidney and, i.

408 ; hyperpiesia and, i. 408
Miliary aneurysms in high pressure,

i. 429
Miliary ruptures, i. 421
Milk diet in hyperpiesia, i. 91
Mitral disease, and angina, ii. 433 ff. ;

pain in, ii. 440
Mitral regurgitation, a palliative of

anginal pain, ii. 442
Mitral stenosis, angina pectoris and,
ii. 445 ; palsy of left recurrent
nerve in, ii. 448; syphilis and, ii. 172
Monckeberg's sclerosis, i. 197, 482 ff.
Morphia in hyperpiesia, ii. 134
Muscular effort, effect of, on arteries,

i. 205
Myocardial insufficiency, apex impulse
and, ii. 32, 34, 35 ; auscultation
and, ii. 34 ; blood pressure and, ii.
44 ; diagnosis of, ii. 29, 49 ; dilata-
tion and, ii. 32-34 ; dyspnea and,
ii. 31 ; electrocardiograph, ii. 41-
43 ; extra-systoles and, ii. 40 ;
fibrillation and, ii. 44 ; heart
sounds and, ii. 34 ; morbid anatomy
of, ii. 46 ; nervous influences and,
ii. 54; pulse and, ii. 31, 36-40;
signs of, 32 ; sphygmomanometer,
ii. 41 ; sudden death and, ii. 31 ;
symptoms of, ii. 31 ff., 36 ; symp-
toms of, may be absent, ii. 31, 39,
45, 46 ; syncope and, ii. 31, 36 ;
vertigo and, ii. 36
Myocardial values, ii. 25, see also

Myocardial insufficiency
Myocarditis, chronic, ii. 48 ; rheu-
matic, ii. 48
Myocardium, acute infection and, ii.
46 ; angina pectoris and, ii. 365 ;
arterioles of, unaffected in renal
disease, i. 331 ; in children, ii. 10 ;
coronary occlusion and, ii. 179,
267, 360 ; fatty degeneration of,

VOL. II

ii. 47 ; in hypertrophied heart, ii.
12, 16, 32 ; sclerosis of valves and,
ii. 24 ; Tawara's bundle and, ii.
50 ff. ; veins of Thebesius and, ii.
23
Myofibrosis, in auricles, ii. 9, 13 ;
coronaries and, ii. 21, 24, 49 ; of
Dehio, ii. 9 ; diffuse and, ii. 10,
15-17; dystrophic, ii. 17-19;
effect of, ii. 10, 13, 18; heart
failure and, ii. 18 ; interstitial, ii.
12, 13, 17-19 ; nature of, ii. 11, 17 ;
non-inflammatory, ii. 11 ; patchy,
ii. 10, 49 ; site of, ii. 50 ; substitu-
tive, ii. 13, 17-19

Nauheini methods in hyperpiesia,

ii. 102, 105
Nephritis, acute parenchymatous,

blood pressure in, i. 342 ; chronic

interstitial, see Kidney, granular ;

chronic parenchymatous, i. 342-

343 ; infective, i. 365-367 ; syphi-
litic, i. 367, ii. 266
Nerve-end organs in aorta, i. 468, ii.

291, 414, 418
Nerve, left recurrent laryngeal, palsy

of, in aortic disease, ii. 448; in mitral

stenosis, ii. 448
Nervous influence and arterial disease,

i. 303-307
Neuralgia, intercostal paroxysmal,

ii. 498 ; and angina pectoris, ii.

498
Neurasthenia, blood pressure in, ii. 61 ;

hyperpiesia and, ii. 61 ; mobility of

heart in, ii. 199
Nicotine, action of, on vasomotor

centres, i. 267
Nitrites, action of, i. 409, ii. 532-533
Nucleo-protein, effect of, on blood,

i. 125

Obesity, blood pressure in, i. 252 ;

hyperpiesia and, i. 252
(Edenia, of lungs, see Pulmonary

oedema ; in granular kidney, i. 343
(Esophagus, distension of, a cause of

substernal pain, ii. 501
Ophthalmic signs in arteriosclerosis,

i. 436
Oscillations, extreme, a cause of

arteriosclerosis, i. 193
Ovarian extract and blood pressure,

i. 230
Oxidation activities, i. 51
Oxygen, a reducer of viscosity, i. 120,

129 ; inhalation in hyperpiesia,

ii. 133

2 N

556

INDEX

Pacinian bodies in aorta, ii. 414, 418 ;

in phrenic nerve, ii. 418
Pain, abdominal, in angina pectoris,
ii. 304 ; in abdominal aneurysm,
ii. 503 ; in angina pectoris, ii. 416 ;
aortic sources of, ii. 303 ; in
aortitis, ii. 192 ; in arms in angina
pectoris, ii. 496-497 ; arterial, ii.
408 ; in atheroma of aorta, ii. 193 ;
in cardiac dilatation, ii. 386, 396,
440 ; in cardiac disease, ii. 296,
386, 395, 496 ; cause of, in angina
pectoris, ii. 416, 419 ; in coronary
thrombosis, ii. 368, 450, 452;
dextral, in angina pectoris, ii. 300 £f . ;
in disease of suprasigmoid area of
aorta, ii. 192, 194, 290 ; epigastric, in
angina pectoris, ii. 304, 305, 311 ;
in extra-systoles, ii. 500 ; in func-
tional heart disorders, ii. 496 ; in
gastric crisis, ii. 503 ; in heart
distress, ii. 440 ; in heart rupture,
ii. 449 ; intercostal, in mock
angina, ii. 226 ; in mitral disease,
ii. 440 ; paroxysmal, and pressure
pain, ii. 431 ; in pericarditis, ii.
454 ; referred, ii. 421 ; in rheu-
matic aortitis, ii. 1 93 ; segmental,
and internal organs, ii. 421 ; in
shoulder, in aneurysm, ii. 421 ; site
of cardiac, ii. 496 ; stretching of
investments, ii. 311, 420 ; in
syphilitic aortitis, ii. 193 ; tension
cause of visceral, ii. 414, 521 ; in
valvular disease, ii. 496 ; visceral,
tension cause of, ii. 414, 521
Palpitation in mock angina, ii. 232
Pancreatic artery, arteriosclerosis of,

i. 331, 349, 449
Paretic attacks, see Transient paretic

attacks
Paroxysmal dyspnea, see Dyspnea
Paroxysmal tachycardia, i. 43
Paroxysmal vomiting in high pressure,

i. 451
Pelvic arteries, arteriosclerosis, i. 462
Periaortitis, a cause of angina pectoris,
ii. 424 ; and left recurrent nerve
paralysis, ii. 448
Periarteritis nodosa, i. 469, 480
Pericardial friction and aortitis, ii.

202
Pericarditis, angina and, ii. 454 ff.,
457, 465 ; aortitis and, ii. 160, 202-
203, 458-460 ; pain in, ii. 454-457 ;
posterior basic, ii. 203, 331
Peripheral constriction, extension in-
wards, i. 398
** Peripheral heart," ii. 45, 55
" Peripheral heart " failure, ii. 45, 55

Peripheral resistance and the heart,
i. 46

Phonendoscope, i. 94

Physics, cardio-arterial, i. 19 ff.

Pituitary body, atherosclerosis and,
i. 229 ; cardiac hyperplasia and.
i. 229

Plebosclerosis, i. 18

Plethora, alcohol and tobacco in,
ii. 88 ; curable, ii. 86 ; treatment
of, ii. 87 ; vera, i. 255 ; vera, pulse
in, i. 64

Plethoric families, frequency of apo-
plexy, i. 165

Pleura, irritation of, causing cardio-
inhibition, ii. 478, 480 ; inflamed,
effect of irritating, ii. 479

Pleural operations, death from, ii. 479

Plumbism, aortitis and, ii. 188

Pneumococcal aortitis, ii. 165

Poiseuille's law, i. 28, 48, 109, 123

Polycythemia, rubra, i. 255-257, 260 ;
hypertonica, i. 257

Portal system, arteriosclerosis of, i. 450

Portal vein, arteriosclerosis of, i. 204,
450; syphilis of, i. 180

Posture and pulse rate, i. 23-25

Prealbuminuric stage, i. 9, 311

Pregnancy and blood pressure, i. 307

Presclerosis, see Huchard's Pre-
sclerosis

Pressor substances, i. 262 ff. ; amines,
i. 267, 270 ; amino-acids of protein,
i. 272 ; ergot-like body of Dixon
and Harvey, i. 267, 272, 363 ; in
faeces, i. 264, 267 ; in urine, i. 267,
363 ; in urine in pituitary disease,
i. 271 ; " kidney stuff," i. 357

" Pseudo angina," ii. 221, 233, see
Mock angina

Pulmonary arteriosclerosis, i. 202, 513

Pulmonary artery, angina pectoris
and, ii. 416 ; syphilis of, ii. 186

Pulmonary infarct, i. 402; signs of,
i. 403

Pulmonary oedema, and dyspnea, i.
402-403 ; and high pressure, i. 403 ;
in hyperpiesia, i. 403 ; signs of, i.
403

Pulse amplitude, in anginal paroxysm,
ii. 329, 471 ; in aortitis, ii. 196 ;
in hyperpiesia, i. 383-384 ; in later
life, i. 20, 92 ; in myocardial value
and, ii. 36 ; in sagging of aorta, i. 20

'"Pulse pressure," i. 91

Pulse rate, and blood pressure, i. 24,
43, 399 ; changes of, and heart
failure, ii. 37 ; and change of
posture, i. 23-25, 399

Pulse, retardation due to pain, ii.

INDEX

557

471 ; tone in angina pectoris, ii.
335 ; touch of, i. 400 ; volume of,
in angina pectoris, ii. 335 ; wave
propagation, i. 35

Pulsus alternans, i. 392, ii. 471-472;
in angina pectoris, ii. 334, 471 ; in
chronic kidney disease, i. 401 ; in
failing heart, i. 401, ii. 334 ; in high
blood pressure, i. 390, ii. 473 ; in
hyperpiesia, i. 401 ; in myocardial
decay, ii. 37 ; vagus and, ii. 472

Pupils, alteration of, in angina pectoris,
ii. 299

Purin-free diet, ii. 89

Purins in hyperpiesia, ii. 88

Radial artery, arteriosclerosis of, and
blood pressure, i. 398 ; and of
aorta, i. 189 ; and of other arteries,
i. 398 ; and of visceral arteries,
i. 189

Radiography, and aortic dilatation,
ii. 70. 203 ; and aortic disease, ii. 70

Rantenberg's experiments on the
kidney, i. 360

Records, instrumental, fallacies of
many, i. 58 ; influence of emotion
on, i. 68

Referred pain, ii. 421

Reflexes in arteriosclerosis, i. 442

Reflexes, blood pressure and, i. 442 ;
inflamed tissues and, ii. 482

Regime in hyperpiesia, ii. 83

Renal infections, i. 363

Renal values, methods of appreciating,
i. 320 ; methylene blue and other
tests of, i. 321 ; Rowntree's
phthalein test, i. 323

Resiliency, i. 38 ; of aorta, i. 39 ;
arterial, inversely as age, i. 167 ;
deferred, i. 457 ; distinguished
from elasticity, i. 457

Resistance, factors of, i. 26 ; peri-
pheral, and the heart, i. 46

Respiration inhibited by crushing
vagus, ii. 483

Retinal artery, arteriosclerosis of,
i. 433 ff. ; spasm of, i. 416

Rheumatic aortitis, ii. 150, 274 ;
aneurysm in children and, ii. 154-
155 ; extension from pericarditis,
ii. 150; histology of, ii. 158;
malignant endocarditis and, ii. 156 ;
micro-organisms in, ii. 260 ; often
painless, ii. 152, 274; often un-
discovered, ii. 151 ; prognosis, ii.
150, 151 ; symptoms of, ii. 157

Rheumatic arteritis of coronaries, ii.
274 ; of peripheral arteries, i. 159

Rheumatic fever, and arteriosclerosis,

i. 288 ; as a cause of angina pec-
toris, ii. 152-159, 239, 249, 260

Rheumatic valvulitis, extension of,
ii. 151, 431

Rheumatism, chronic, and arterio-
sclerosis, i. 289

Salicylates in hyperpiesia, ii. 132
Salisbury diet in hyperpiesia, ii. 89
Salvarsan in angina pectoris, ii. 528-

529 ; in syphilitic aortitis, ii. 188
Sanatoriums and hyperpiesia, ii. 103
Scarlatinal aortitis, ii. 149
Scarlatinal nephritis, i. 365-367
" Schwiele," ii. 14 ff.
Schott exercises in arteriosclerosis,

ii. 101
Secretin and blood pressure, i. 229
Senile arteriosclerosis, see Arterio-
sclerosis, decrescent
Senile epilepsy and arteriosclerosis,

i. 410
Sensory end-organs in aorta wall, ii.

291, 414-418 ; in mesentery, ii. 421
Serum, vasoconstrictor substance in,

i. 268-269
Shearing stresses, cause of exudation

between intima and media, i. 497
Shock as a cause of death in angina

pectoris, ii. 488-489
Sleep, disorders of, in arteriosclerosis,

i. 442
Small-pox and aortitis, ii. 148
Sodium chloride, and blood pressure,

i. 231 ; in hyperpiesia, ii. 93; and

oedema, ii. 93
Sodium silicate in hyperpiesia, ii. 130
Spa treatment in hyperpiesia, ii. 103
Specific gravity of blood, and arterio-
sclerosis, i. 122 ; and blood pressure,

i. 122 ; and viscosity, i. 121-122
Sphygmograph, limitations of, i. 57-

61 ; Marey's, i. 7, 57 ; unsuitable

for recording blood pressure, i. 57
Sphygmometers, i. 44, 57 f., 84 f. ;

advantages of finger over, i. 66 ;

and myocardial values, ii. 41 ; and

variable conditions of arterial wall,

i. 72 ; of von Bosch, i. 7, 57, 84 ;

others, i. 84 f.
Spiral arrangement of cardioarterial

fibres, i. 42
Splanchnic arteriosclerosis and blood

pressure, i. 156
Splenic artery, arteriosclerosis of, i.

331, 332, 349
Status anginosus, ii. 334, 453
Stenocardia, aortitis and, ii. 195 ;

syphilis and, ii. 262, 264 ; tobacco

and, ii. 245

558

INDEX

Stokes-Adams disease and angina,
ii. 510

Stomach, angina pectoris and, ii. 342,
344; distension of, in hvperpiesia,
i. 397

Stopcock action (Johnson), i. 473

Strain, affects intima first, i. 517

Stream activity, i. 28 ; and damage
to long arteries, i. 29

Stress, and development of connective
tissue, i. 515; effect of, on arterial
walla, i. 193, 497, 513

Subclavian arteries, signs of, in arterio-
sclerosis, i. 395

Subclavian sign of Gerhardt, ii. 199

Submammary ache of heart stress,
ii. 284; of mock angina, ii. 226, 231,
495 ; in tobacco angina, ii. 247.

Substernal oppression, intimation of
hyperpiesia, ii. 287 ; precursor of
angina pectoris, ii. 287 ; precursor
of death, ii. 287 ; sign of aortitis,
ii. 287 ; tobacco and, ii. 507

Sweating in angina pectoris, ii. 338

Swedish exercises in hyperpiesia, ii. 102

Syncope from failure of peripheral
heart, ii. 45, 55

Syphilis, cerebral, haemorrhage in, i.
432 ; headache in, i. 408

Syphilis, chief cause of toxic arterio-
sclerosis,.!. 170; most frequent cause
of angina pectoris, ii. 239, 260

Syphilitic aortitis, see Aortitis, syphi-
litic, ii. 145; acuter stages inflam-
matory, ii. 146 ; anginal pain in, ii.
263 ; differs from syphilis of smaller
arteries, i. 296 ; more frequent than
of heart, ii. 167, 171

Syphilitic arterial disease, of ad-
ventitia in, i. 297, 469 ; aorta first
attacked, i. 462 ; blood pressure in,
i. 156, 302, ii. 129 ; of media, i.
299, 478 ; of smaller arteries, i.
292 ff., 296, 478 ; without cardiac
hypertrophy, i. 156 ; without high
blood pressure, i. 156

Syphilitic cerebral arteriosclerosis,
frequency of, i. 292 ; occlusion in,
i. 432 ; vertigo in, i. 409

Syphilitic disease of aorta and heart
together rare, ii. 180

Syphilitic disease of smaller arteries,
i. 292 ff., 296, 478; arrested by
early treatment, i. 297 ; attacks all
the tissues, i. 294 ; diffuse and focal
form, i. 296 ; is lesion single or
various, i. 294, 296 ; resemblance
to arteriosclerosis, i. 301, 480 ;
sub-inflammatory, i. 297 ; time of
appearance, i. 293

Syphilitic kidney, i. 367, ii. 266

Tea and coffee in hyperpiesia, ii. 88,

93
Temporal artery, arteriosclerosis of,

i. 398
Tension, cause of visceral pain, ii. 414,

521
Thoma's views on arteriosclerosis, i.

486-495
Thrombo-angitis, i. 305
Thrombosis of mesenteric arteries and

abdominal pains, i. 446, 449
Thvroid deficiency and senile arterio-
sclerosis, i. 230
Thvroid extract in hvperpiesia, ii.

125, 134
Tinnitus and arteriosclerosis, i. 410
Tobacco and arteriosclerosis, i. 250 ;

and blood pressure, i. 250, 251 ;

and cardiac irregularity, ii. 500 ;

and hyperpiesia, ii. 88
Tobacco angina, ii. 244 ; submaxillary

ache in, ii. 247 ; symptoms of, ii.

244
Tobacco poisoning, substernal oppres-
sion in, ii. 507
Tone, arterial in angina pectoris, ii.

335, 338; protects artery, i. 193,

459
Torpor in arteriosclerosis, i. 442
Tortuosity, and elongation of arteries,

i. 459 ; in relation to pressure, i.

461
Toxi-alimentary hypothesis, i. 269
Toxic arteriosclerosis, see Arterio-
sclerosis, toxic
Transient paretic attacks, i. 412 ff. ;

due to small haemorrhages, i. 415,

420 ; in decrescent arteriosclerosis,

i. 429 ; in hyperpiesia, i. 413, 415 ;

not due to arterial spasm, i. 416 ;

not due to local cedema, i. 418 ;

prognosis of, i. 422 ; premonitions

of mortal apoplexy, i. 422
Tryptophane, i. 270
Tuberculosis and angina pectoris, ii.

268 ; and aortitis, ii. 162 ; and

arterial disease, i. 292
Tvphoid and aortitis, ii. 162 ; and

'arterial disease, i. 283-284, 285, 287 ;

and peripheral arterial disease, ii.

162
Tyramine, i. 268

Unrest in angina pectoris, ii. 340
Uric acid and arteriosclerosis, i. 274
Uric acid estimation, Folin and
Marshall's method, i. 322 ; Hop-
kins and Worner's, i. 322

INDEX

559

Urine in decrescent arteriosclerosis,
i. 452 ; in hyperpiesia, i. 452

Vago- sympathetic group of fibres,
ii. 467

Vago-vasal disorders, ii. 221, 225,
228-229, see Mock angina

Vagus, action of atropine on, ii. 472,
483 ; of ethyl chloride on, ii. 483 ;
of morphine on, ii. 483

Vagus, effect of crushing, ii. 483 ;
hypersensitive in angina pectoris,
ii. 475 ; influence of, on enfeebled
heart, ii. 473-476, 484 ; neuritis of,
and angina pectoris, ii. 402

Valsalva, sinuses of, nerve supply to,
ii. 415

Valves, sclerosis of, ii. 23

Vaquez' disease, see Plethora vera

Vasa vasorum, and arteriosclerosis, i.
285, 464-467, ii. 147 ; atheroma of
aorta and, i. 465

Vascular crisis of Nothnagel, i. 161

Vascular spasm, arteriosclerosis and, i.
161

Vasoconstricting substances, i. 267-
268

Vasoconstriction, exceptional in an-
gina pectoris, ii. 401-402 ; in
large areas, i. 216 ; protection to
arteries, i. 400 ; in tabes, ii. 402

Vasodilators, action of, ii. 123 ; in
hyperpiesia, ii. 120

Vasomotor connections of heart, ii.
467, 477

Vasomotor disturbances in angina
pectoris, ii. 238, 340 ; from nerve
irritation, ii. 234-236 ; in mock an-
gina, ii. 227-228, 230, 508

Vasomotor hypothesis of angina pec-
toris, ii. 400

Vasomotor mechanism, fatigue of, i. 52

Vasomotor system, i. 49

Vegetarianism in hyperpiesia, ii. 92

Veins, fall of blood pressure in, i. 26 ;
sclerosis of, i. 534 ; of Thebesius,
ii. 23 ; varicose, and tibial artery,
i. 199, 201

Velocity, and pressure gradients, i. 26 ;
of blood stream, i. 30

Venesection in high blood pressure,
ii. 114; in hyperpiesia, ii. 114;

periodical value of, ii. 116-117 ;
viscosity and, i. 147

Ventricle, fibrillation of, ii. 44

Vertigo in angina pectoris, ii. 340 ;
in arteriosclerosis, ii. 340

Vertigo, aural, i. 409 ; minute vascular
lesions and, i. 409 ; neurasthenia
and, i. 409 ; syphilitic cerebral
arteriosclerosis and, i. 409

" Virtual tension," i. 41

Visceral pain tension, cause of, ii. 414,
521

Viscometers, i. 108, 111-112

Viscosity of blood, i. 104 ff. ; acidosis
and, i. 130 ; age and, i. 115 ; blood
pressure and, i. 118, 127, 142 ;
calcium salts and, i. 126, 133 ;
coagulability and, i. 110; defined,
i. 105, 123 ; diet and, i. 117 ; in
disease, i. 14S ; estimation of, i.
135, 141 ; exercise and, i. 119 ;
factor in frictional resistance, i.
106, 123: in fevers, i. 150; heart
work and, i. 127, 142 ; increased
by excess of C02, i. 129, 131 ;
iodide and, i. 145 ; normal formula,
i. 132 ; not specific gravity, i. 121 ;
in pregnancy, i. 116 ; reduced by
oxygen, i. 120, 129 ; reduced by
saline intravenous injections, i. 128 ;
sexes and, i. 115

Viscosity of plasma, i. 126 ; of
serum and blood pressure, i. 125

Vomiting, paroxysmal, and high blood
pressure, i. 451

Waters, drinking of, in hvperpiesia, ii.

107 ff.
Wave velocity and arterial wall, i.

33 ff.
Whey, useful for uratic deposits, ii.

130
Women and angina minor and major,

ii. 288

Xanthine bodies, and blood pressure,
i. 274, 364 ; and kidney epithelium,
i. 364

X-rays and aortic disease, ii. 70

Yawning in angina pectoris, ii. 340

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