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 NOTES UPON CARDIAC HYPERTROPHY. 
 
 BY \ 
 
 .1. G^ADAMf. :ir.A., M.D., 
 
 ProfesEor of Pathology, MoQili University, Montreal, and Pathologist to the Royal 
 
 Victoria Hospital. 
 
 {Reprinted from the Montreal Medical Journal, May, 1895.) 
 
> ., ,'.,.• r 
 
 •'t> 
 
 NOTES UPON CARDIAC HYPERTROPHY. 
 
 J. G. AuAMi, M.A., M.D., 
 
 Professor of Pathology in McGill University, Mflntreul, and Pathologist to the Royal 
 
 Victoria Hospital. 
 
 I shall, I think, best satisfy you, and at the same time 
 myself, if what I contribute to this evening's discussion 
 takes the form of a series of notes upon the experimental 
 pathology and the anatomy of cardiac hypertrophy, rather 
 than that of an academic survey of the subject from the 
 clinical standpoint. Frequently, it is true, I must of neces- 
 sity illustrate what I have to say by reference to clinical 
 history, hut, on the whole, I shall leave the clinical aspects 
 to be dealt with by those more capable. 
 
 In the first place, if we study the causes of hypertrophied 
 heart, whether of hypertrophy of one or both sides, we see 
 this that reading the clinical history of these cases the 
 assigned causes of hypertrophy may be summed up under 
 the heading of increased work This one heading may be 
 subdivided into three, increased work due to resistance 
 from within, increased work due to resistance from without, 
 increased work due to nervous stimulation and augmentor 
 action. I shall not discuss this last subdivision, because 
 frankly we are ignorant how far the hypertrophy that 
 occurs in exophthalmic goitre and allied conditions is due 
 to heightened blood pressure, and how far it is secondary 
 to excitation of the accelerators or ausfmentors. 
 
 Of the increased resistance from within, or increased 
 tension, the main causes are, heightened pressure in the 
 arterial blood stream, and secondly, obstruction to the 
 onward passage of blood within the heart itself, by stenotic 
 diseases of one or other orifice. Of resistance from with- 
 out, the one great cause is pericardial adhesion. To-night 
 we have, as far as possible, to leave out the subject of 
 valvular disturbance, and I shall neglect nervous disturb- 
 
ances. There is still the large field of hypertrophy due 
 to increased arterial pressure, and the pericardial adhesion. 
 In all these cases, the individual fibres of the heart muscles 
 of the aft'ected regions have to contract under increased 
 difficulty, they have to carry or contract against a greater 
 load, and as a result of this, just as is the case with the 
 skeletal muscles, with the muscles in the blacksmith's arm, 
 and the muscles of [the body in the all-round athlete, in- 
 creased work brings about increased growth — brings about, 
 that is to say, hypertrophy of the muscle. 
 
 • Into the subject of the nature of this increased growth I 
 shall enter in a few minutes' time, at present I wish to 
 carry a word further this parallel between the behaviour 
 of the cardiac and skeletal muscles, under circumstances in 
 which the load is increased. If you take a skeletal muscle, 
 for example, the gastrocnemius of the frog, so dear to the 
 physiologist, and observe its contraction with gradually in- 
 creasing loads, there are two points especially to be made 
 out. In the first place the greatest amount of work is not 
 performed with the smallest load, but there is a certain 
 medium load with which the distance through which the 
 load is pulled multiplied by the weight of the load gives 
 the biggest result. This product of weight moved and the 
 distance through which it is moved is the work done by 
 the muscle. The most work, therefore, is done with a 
 medium load. The second point is that with increasing 
 weights fastened or brought to bear upon the muscle, that 
 muscle in its resting state becomes more and more elongated, 
 and with regularly increasing weights attached the shorten- 
 ing attained by the contracted nmscle constantly diminishes. 
 Or, to put the matter in a slightly different light, and to 
 combine these two statements of fact, although with a cer- 
 tain medium load the greatest amount of work is done, 
 nevertheless with that medium load the muscle in contract- 
 ing does not attain to the same amount of shortening as it 
 does with a lesser load. 
 
 Let me now apply these observations to what is found 
 in the ventiicular muscles of mammals. Experimentally 
 
the amount of work performed by the ventricles of the 
 mammalian heart can be increased by ligaturing the aorta 
 with a sliploop ligature, and drawing this ligature more 
 or less tight, according to need. [This in an animal that 
 has been narcotised and curarised and subjected to artificial 
 respiration, the heart l)eing exposed by making a window 
 in the ribs.] In such a case as this, as shown by Professor 
 Roy and me,* the behaviour of the cardiac muscle can be 
 observed and recorded by an apparatus, of which I give a 
 rough diagram. (See Fig. 1.) The ends of this apparatus 
 are attached to the surface, say of the left ventricle, by fine 
 threads, and ncnv it is possible to observe upon the record- 
 ing rlrum the extent of contraction of the portion of muscle 
 between the two points under different pressures within 
 the heart. Narrow the aorta by drawing the ligature 
 tight and the pressure is increased. Under these condi- 
 tions it is found that the ventricular muscle reacts exactly 
 along the same lines as does the gastrocnemius of the frog. 
 
 Similar results are obtainable if, instead of increasing the 
 pressure in the arterial system by narrowing the aorta, we 
 increase the work of the heart by increasing the amount 
 of blood passing through it, either temporarily, by pressure 
 upon the abdomen, vyhereby a large quantity of blood is 
 expelled from the abdominal viscera, or by injecting into 
 venous circulation some few hundred cubic c . timetres of 
 defibrinated blood. The results in all these . . .es are the 
 same. By the instrument just described it is easy to see 
 that the heart is more filled in diastole, so that the two 
 ends of the levers are pushed further apart, and that in 
 systole the ends do not approximate so nearly as in the 
 condition when there is less resistance or less blood pouring 
 through the organ. 
 
 It is seen from these observations that with increased 
 pressure within the ventricle the wall expands in diastole. 
 There is dilatation of the heart. But with the increased 
 loid to contract against the fibres do not shorten to the 
 
 •JIuirt beat anil iuI.sl' wave. /Voc<tttoner, February, 1894, p. 81. 
 
 ir . 
 
6 
 
 same extent ; that is to aay, with increased work of the 
 heart there is, necessarily, accompanying tlie dilatation in 
 diastole, a dilation in systole. All the blood is not ex- 
 pelled in systole. There is of necessity reaidunl Mood, as 
 Roy and I termed it, in the ventricular chambers. 
 There is a general belief that the healthy heart, even 
 
 Fig. ].— Myocardiocrraph for mammalian heart shown semi-diagrammatioally. The 
 light vertical rod a, which for convenience of space is shown shortened in the 
 figure, is slung from the pivots which are represented in section as seen from 
 above B. This arrangement allows the rod u to swing freely, the centre of rotation 
 being the small hole at b (in B) The lower end. c, of this rod is fixed to the sur- 
 face of the heart-wall as seen in the figure. To obtain tracings of the heart- wall, 
 the small hook d is inserted in the visceral pericardium at a convenient distance 
 from the end of the rod a. To this hook ia attached a strong silken thread, «, which 
 after passing round the light grooved pulley f is conveyed upwards through the 
 small bole b to the lever g, beiof kept taut by the fine rubber thread h. 
 
under conditions of increased work, contracts completely, 
 so that the chamber ia emptied at the end of systole. From 
 what I have said it will be seen that this is not the case. 
 One can go further and prove for one's self that even under 
 (H'dinary conditions the mammalian heart does not com- 
 pletely expel all the blood within the ventricles. By 
 taking a dog that has been curarised and subjected to arti- 
 ficial respiration, opening the chest wall, making an in- 
 cision at the very apex of the left ventricle, so as just not 
 to completely enter the cavity, then it is easy to push the 
 little finger into the cavity through the thin apex without 
 the loss of a drop of blood. The heart action is not re- 
 cognisably disturbed by this procedure, and it can be felt 
 that while the walls of the ventricle in the lower two-thirds 
 up to the apices of the papillary muscles, close completely 
 round the finger, there is a clear space in the upper third 
 which is not and cannot be emptied of blood. 
 
 Although it may seem at first sight to have no direct 
 bearing upon the subject of this evening's discussion, 
 nevertheless it is worth while to make a few remarks upon 
 this subject, inasmuch as it ia so intimately associated with 
 conditions of hypertrophy without valvular disease. It is 
 quite possible that where there is increased work to be per- 
 formed by the heart, there is some economy of the action 
 of the organ when there exists a certain Amount of residual 
 blood, in and dilatation of the ventricles. Taking the ven- 
 tricular chamber as a sphere,* there is this to be noted 
 concerning the relationship between the circumference of 
 the sphere and its contents, namely, that as a sphere ex- 
 pands its cubic contents increase out of all proportion, I 
 was going to say, to increase in circumference, or more 
 truly, the ratio between increase in cubic contents and in- 
 crease in circumference is by no means an arithmetic ratio. 
 
 If the circumferences be taken as abscissae, and the cor- 
 responding volumes as the ordinates, the curve of succesive 
 
 * I'liP^phere *» the nearest geometrieal figure that can be employed here for pui- 
 
 poscs of illustration. 
 
values is what is known to mathematicians as a cubical 
 paraltola. From this it follows that a dej^ree of shortening of 
 
 Fig, % • 
 
 I 
 
 ^ 
 
 Curve reiiTesentinK the relationship between the circumference of a sphere and ist 
 volume, with successive unit increments of oircumferenoet 
 Ordinates — volume in cubic inches. 
 ' AbBoisxc = circumferenoe in inches, 
 
I 
 
 V 
 
 
 the fibres of the heart wall sufficient, let us say, to reduce the 
 circumference of the ventricle onc^ inch, will cause a greater 
 (liuiiiuition in volume (a greater output) the more dilated 
 the ventricle is at the beginning of its contraction. For 
 example, a diminution of the circumference hy one inch of 
 a sphere whose circumference is ten inches causes a diminu- 
 tion of th(! volume or an output, in the case of the heart, 
 efpiul i6 Jf.5 cuhic inches, while a diminution by one inch 
 in the circumference of a sphere //ye inches round causes a 
 diminution or an output of only 1.027 cubic inches, although 
 in the first case the circumference was reduced only by 
 (me-t(^nth, while in the other case it was reduced by (me- 
 fifth. That is to say, if we have a dilated heart the fibres 
 will need to contract a very small amount, in order to 
 expel a given amount of blood, compared with the amount 
 they would have to contract in the normal undilated heart. 
 
 There are other factors to be taken into account, it is 
 true, and Roy and I went a little into this sulyect in our 
 paper published in the Philosophical Transactions* All 
 that I wish to do here is to point out that it is possible that 
 in a hard-working heart a certain amount of dilatation) 
 with presence of residual blood, by diminishing the extent 
 which each fibre is called upon to contract, may really be 
 an economy 'to the organ as a whole. 
 
 It follows from these observations that hypertrophy is 
 never primary, dilatation always precedes hypertrophy. 
 This was recognized as most probable by Hilton Fagge ; 
 few other writers have laid stress upon the point. If, how- 
 ever, the heart muscle is well nouri.shed, where this dilata- 
 tion is due to increased work, by Paget's law hypertrophy 
 ensues, and the numerical hypertrophy or hyperplasia of 
 the ventricular muscle fibre will have the effect of lessen- 
 ing the load of each individual fibre. Consequently, with 
 a lessened load, each fibre will contract more completely 
 and the dilatation will tend to disappear. Where this is 
 the case we have what is known as simple hypertrophy. 
 
 * Phil, Trans, of the Royal Society, London, 1892. 
 
10 
 
 There can be no doubt that in the early stages, where 
 ample reserve force and good compensation are present, 
 this simple hypertrophy exists and may persist for years. 
 But I would add that in the post-mortem room it is more 
 rarely to l)e seen than is generally accepted. If a liyper- 
 trophied heart, say of Bright's disease, without valvular 
 lesion, be examined within a few hours after death, in very 
 many cases we appear to have this simple hypertrophy. 
 If, however, time be given for the rigour and contraction 
 of the muscle to pass off it is found — that at least is my 
 experience — that the cavity of the left ventricle is dis- 
 tinctly larger than the cavity of the normal heart. I 
 would say that only in those cases in which death has 
 occurred from some intercurrent disease, and not from one 
 of the cycle of diseases associated with cardiac hyper- 
 trophy — only when death occurs before the final stage of 
 ' the disease of which cardiac hypertrophy is an integral 
 part — do we obtain evidence of real simple hypertrophy. 
 Eccentric, and not simple, hypertrophy is the rule ; that is 
 to say, hypertrophy associated with definite dilatation of 
 the ventricular cavities. 
 
 As for the concentric hypertrophy, which is said to be 
 observable in non-valvular disease, I feel more and more 
 assured that it is falsely so termed ; there is no such thing 
 . as true concentric hypertrophy, for the condition implies a 
 Jack of economy in the work of the organ, a most un- 
 natural lack ; it implies that the ventrical in contracting 
 expends a large part of its energy, after expelling the 
 blood, in squeezing up the more internal fibres. Only 
 within the last fortnight I obtained a specimen of so-called 
 concentric hypertrophy. The patient, an old woman of 
 eighty, in Dr. Stewart's ward at the Royal Victoria Hos- 
 pital, died from cerebral apoplexy, following upon extreme 
 atheroma of the aorta and the main vessels ; there was, in 
 addition, atheromatous stenosis of the aortic valves, both 
 conditions favouring the development of hypertrophy, with 
 dilatation of the left ventricle, ... ,. : 
 
11 
 
 The old woman had lingered some days in a comatose 
 condition, with presumable lowering of the arterial blood 
 pressure. In addition the tone of ventricular muscle had 
 been in all probability considerably increased by digitalis. 
 At any rate, at the autopsy a very few hours after death 
 the left ventricle was found hypertrophied, and instead of 
 being dilated was so firmly contracted that the only cavity 
 left was immediately around the chordae tendineas. The 
 thickness of the ventricular muscle at the junction of the 
 lower and middle thirds was 20 mm.; that is to say, there 
 was moderate hypertrophy. However, on coming to 
 observe this heart the next day, the concentric hyper- 
 trophy had quite disappeared. With the passing off" of 
 rigidity there was a relatively large cavity left behind. 
 
 Where the left or right ventricle alone is affected the con- 
 dition of the ventricle may be one of either simple or eccen- 
 tric hypertrophy. Where, on the other hand, as Walshe noted 
 more than thirty years ago, there is general hypertrophy 
 of the organ, there hypertrophy is always eccentric. 
 
 A little consideration shows why this must inevitably be 
 the case. So long as there is simple hypertrophy (hyper- 
 trophy without dilatation), so long the mitral valves re- 
 main competent, and there is no regurgitation into the left 
 auricle, no increased work for that organ to do, no hyper- 
 trophy. So soon i*s the left ventricular muscle begins to 
 fail and to be unable to contract properly under its load, 
 dilatation ensues, and with this dilatation expansion or 
 giving way of the muscular ring around the mitral orifice, 
 and with this, relative incompetence of that orifice. It is 
 only when this relative incompetence occurs, or when from 
 other causes the mitral valves fail to perform their duty, 
 that there is any possibility of the other chambers of the 
 heart being called upon to do increased work. Thus it is 
 that general hypertrophy of the heart demands or is asso- 
 ciated with eccentric hypertrophy of the left ventricle. 
 
 Time forbids that I should go more fully into this sub- 
 ject or do more than point out that relative incompetence 
 
12 
 
 of the auriculo-ventricular valves is more frequently found 
 at the post-mortem than it is diagnosed during life. Rela- 
 tive incompetence, therefore, is not necessarily indicated by 
 the presence of a murmur. 
 
 I cannot here enter fully into the histological nature of 
 hypertrophy, although perhaps as a pathologist it might bo 
 expected that I should say some words upon this point. I 
 will only say that while one can, in certain cases of hyper- 
 trophy, make out clearly that the individual fibres have 
 undergone a definite increase in size, it is far more common 
 to note, and of this there can be no doubt, that there has 
 been an actual numerical increase in the fibres. This in- 
 crease appears to be general throughout the ventricular 
 wall and is possibly, nay probably, due not only to a new 
 growth beneath the endocardium especially, but also to a 
 splitting up or division of pre-existing fibres. It must be 
 remembered that the heart muscle fibre is not a single cell, 
 but is a compound, the result of a fusion of several cells 
 into one individual unit. As a consequence of this it is 
 possibly more easy for the fibres to split up into inde- 
 pendent territories without undergoing temporary derange- 
 ment of function than is the case with the cells of those 
 tissues formed of isolated cell units. 
 
 To pass on now to certain aspects of this subject of 
 hypertrophy more immediately in connection wath this 
 evening's discussion, I would point out that of the cases of 
 hypertrophy without valvular lesion, we have to consider 
 in the first place increased resistance through the column 
 of blood. This could be brought about by increased 
 amount of blood to be propelled, or, in the second, by in- 
 creased resistance to passage in the arterial system. Of 
 these two the first may exist as a constitutional condition, 
 but the more one studies the less assured does one become 
 that there is such a condition as general plethora unless 
 these case be regarded as true plethora in which (as in 
 German beer drinkers) there is oft repeated flushing of 
 the circulation with imbibed fluid. Of increased resist- 
 
13 
 
 unce in the arterial stream the reverse would appear 
 to be the case, and with further studies of blood pres- 
 sure in the arteries one begins to see that this plays an 
 extremely important part. The hypertrophy following 
 upon not only gouty conditions and senile artero-sclerosis, 
 but also upon acute rheumatism, chorea and chlorosis may 
 be present with or without lesion of the aortic or mitral 
 valves of sufficient intensity to explain its extent ; so that 
 in all these cases we have to fall back upon increased blood 
 pressure as a cause of hypertrophy. 
 
 Increased blood pressure in itself is capable of setting up 
 a vicious circle of which one segment may be hypertrophy. 
 
 In the first place it leads to an increased nutrition of 
 the walls of the arteries, increased nutrition leads to in- 
 creased connective tissue growth of the walls, the increased 
 fibrous tissue of the walls leads to contraction and in- 
 creased rigidity of those walls, the increased rigidity leads 
 to increased resistance to the passage of the blood current,, 
 the increased resistance required increased propulsive 
 power on the part of the ventricular muscle, that is to say, 
 increased work ; the increased work of the heart leads to 
 overgrowth and hypertrophy, and with this, heightened 
 blood pressure and further increased nutrition of the walls. 
 And now at last the stage is reached, this vicious circle con- 
 tinuing, in which either the walls give way or the heart. 
 
 The longer I study the pathology of the circulation — and 
 during the last eight years I have given more time and 
 thought to this than to any other branch of my subject — 
 the more assured do I feel that increased blood pressure 
 alone (however it be primarily brought about) is sufficient 
 to explain the anatomical changes so constantly seen in 
 arteries, valves and heart walls, without of necessity call- 
 ing in chronic inflammation or specific agency. The changes 
 I refer to are arterio-sclerosis, atheroma, and general fibroid 
 thickening of the valves. Perhaps here again I am diverg- 
 ing from the main subject of this evening's discussion, but 
 I say this as a connecting link with what I have just re- 
 uiarked and with what is about to follow. 
 
14 
 
 While I am far from wishing to indicate that this is to 
 be regarded as the sole cause of atheromatous and arterio- 
 sclerotic changes, I hold that the changes I have mentioned 
 can one and all he explained by the increased pressure 
 within the vessels leading to an increased passage of fluid 
 from the blood into the sub-endothelial layers of the intima, 
 to an increased nutrition, and as a cohsequence to a pro- 
 liferation of connective tissue in this region, which in itself 
 as it contracts cuts off its own supply of nutrition, de- 
 generates, and what is more, leads to degeneration of sur- 
 rounding parts by cutting off their nutrition. The evil 
 effects in arterio-sclerosis, with all its combined lesions, are 
 not necessarily of an inflammatory origin. 
 
 Let us take now the hypertrophied heart. Time per- 
 mits me to refer but briefly to the anatomical changes that 
 may occur in it in the cases before us. 
 
 1. The overgrowth of the arterial walls may be asso- 
 ciated with an increased tendency to the development of 
 fibrous tissue in the immediate neighbourhood of the 
 arteries, and thus a condition of so-called interstitial myo- 
 carditis may be set up ; or 
 
 2. With an increased fibrosis of the arteries the narrow- 
 ing of the channel may lead to incomplete nutrition of the 
 territory supplied by each arterial twig, and as a conse- 
 quence the muscle fibres at the periphery of the territory 
 may be atrophied through lack of nutrition and be replaced 
 by fibrous tissue. This is the so-called dystrophic sclerosis 
 of the French school, and can frequently be seen more espe- 
 cially in the papillary muscles. 
 
 3. With the arterial disturbance there may be actual 
 blocking of the atheromatous arteries, and so infarctous 
 areas may originate, may undergo softening, may cause 
 rupture of the heart or aneurism of the wall, or if the 
 period of softening be successfully tided over, the replace- 
 ment of the necrosed tissue leads to cicatricial development 
 and disturbance of the normal contraction. ' ^ 
 
 All these cases here mentioned inevitably cause interrup- 
 
16 
 
 tion to the proper action of the remaining fibres and lead 
 towards a final failure of the ortran. 
 
 Another set of causes would seem to act alono- rather 
 difl'erent lines, riot so much of disturbances in the coronary 
 arteries as disturbance in the quality of the nutrition, 
 whereby the heart muscle tends to undergo fatty degenera- 
 tion. In the uncomplicated case of hypertrophy, without 
 valvular lesion, however, this fatty degeneration is rare ; 
 more frequent, according to the observations of Renaud, 
 Browicz and Von Recklinghausen, there is a tendency for 
 a sudden rupture of the heart fibres, from segmentation or 
 fragmentation. It would seem as though, from the \ei'y 
 careful observations of the last two, the weakened condi- 
 tion of the muscles permits some slight increase in the 
 work done by the organ to bring about, not a local rupture, 
 but a generalized separation of the fibres. 
 
 Possibly this segmentation may explain the suddenness 
 of many cases of death in those with atrophied and dilated 
 hearts. For my own part I cannot as yet see that it has 
 been proved with absolute satisfaction that the fragmenta- 
 tion of the fibres is agonal or pre-agonal. Nor, looking 
 back, does it seem to me that the most strongly marked 
 cases that I have encountered of this fragmentation have 
 been in cases of sudden death. 
 
 Lastly, to round off* this paper, it is necessary to say a 
 word concerning the hypertrophy that follows pericardial 
 adhesion. Of this I may say that I cannot recall any case 
 seen by me in which the hypertrophy was not markedly 
 eccentric. Most frequently the hypertrophy has disap- 
 peared with, in its place, peculiarly extensive degenerative 
 change.