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Full text of "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 




MACMILLAN AND CO., Limited 

LONDON • BOMBAY • CALCUTTA 
MELBOURNE 

THE MACMILLAN COMPANY 

NEW YORK • BOSTON • CHICAGO 
DALLAS • SAN FRANCISCO 

THE MACMILLAN CO. OF CANADA, Ltd. 

TORONTO 



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 VALUES 1 

" 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. 

Huchard 1 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 i 1 " 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 — dishing 1 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 be r too 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, C0 2 , or ; 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 C0 2 , 

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 
Schiitgen 1 find that air and oxygen bubble-baths are less irritant 
than those with C0 2 , 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, C0 2 baths 
or 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 French 1 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 Riie 6 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. Kraus 7 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. Curschmann 4 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. Edgren 3 
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. Allen 2 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 muc ous 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 Bordet 1 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. 
Osier 6 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 PECTORIS 1 
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's 3 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 Osier 1 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. Poynton 4 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 Baumes 5 
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. Albu 3 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. 22 e 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." 
Edgren 3 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. Mackenzie 3 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 Osier 2 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 
seizure 3 (under vagus influence?). In another curious case 4 
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. 4 See 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 C0 2 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. 2 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 CO L ,, 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 Neusser 1 
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). Cohnheim 1 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 the