Chapter XLIII: Part 43

DEFINITION.--An increase in the size of the heart due to an increased thickness, total or partial, of the muscular walls.

VARIETIES.--Two forms may be recognized--simple hypertrophy, in which the cavity or cavities remain of the normal size; and eccentric hypertrophy, in which with increased thickness of the walls there is enlargement of the cavities. Dilated hypertrophy and hypertrophy with dilatation are terms by which the latter form is most frequently described.

By many writers a third variety, concentric hypertrophy, is recognized, in which there is diminution in the size of the cavity with thickening of the walls; but in these cases we have to deal with a post-mortem change--rigor mortis; and if the organ is kept for twenty-four hours or soaked in water, the so-called concentric hypertrophy will usually disappear.

The increased size may affect the entire organ, general hypertrophy; or only one side or one cavity, partial hypertrophy. The latter is the most common. Of the single chambers the left ventricle is most frequently involved, then the right. The auricles are rarely affected alone, but the left is more often than the right.

ETIOLOGY.--Disturbed innervation and increased work are the two principal causes of cardiac hypertrophy. We see hypertrophy from deranged innervation (1) in Basedow's disease (exophthalmic goitre); (2) in long-continued nervous palpitation from any cause, particularly sexual excesses; (3) certain poisons and articles of diet appear to act in this way, as tea, coffee, alcohol, and tobacco.

In all these cases there is simple over-action or increased functional activity, which, if prolonged, certainly produces some degree of hypertrophy. How this condition is brought about is not very clear. We may suppose the increased frequency of contraction to result from stimulation of the accelerator nerves, as seems probably the case in exophthalmic goitre; from irritability of the cardiac ganglia themselves, owing to the influence of such toxic agents as tea, tobacco, etc.; or from defective vagus control. Long-continued neurotic palpitation in reality causes hypertrophy by increasing the work of the heart, for under perverted stimuli the ventricular contractions are doubled in frequency--sometimes in force as well--while maintaining the circulation in normal vessels offering no increased resistance to the blood-flow.

There can be no doubt of the occurrence of actual hypertrophy as a sequence of the irritable heart induced by sexual excesses and tobacco. I had under observation on and off for several years a very emotional and {620} hypochondriacal young man addicted to venery, whose left ventricle became strongly developed and beat outside the nipple-line. His entire thoughts became centred in his heart trouble, and he travelled from one authority to another in this country and Europe seeking advice.[41] The smoker's heart rarely leads to much hypertrophy, but in young lads it may do so, and even induce more serious disease, as indicated by the presence of murmurs and signs of cardiac failure. The abuse of spirits as a cause of hypertrophy is not very clearly established. Alcoholism appears to be a factor in the production of atheroma. I have been struck by the fact that in four typical instances of so-called idiopathic hypertrophy occurring in powerfully-built workers there was a history of intemperance; and it is quite possible that this may have combined with the muscular efforts in inducing the heart disease; at any rate, it would prove an important element in hastening the final breakdown when from any cause hypertrophy had arisen.

[Footnote 41: After three or four years of most unnecessary worry in the expectation of death from heart disease, this patient has quieted into the belief that there is not anything seriously wrong with his heart, and has now rarely any indications of trouble.]

The majority of cases of hypertrophy of the heart are due to mechanical causes leading to increased resistance and increased work on the part of the organ. Under these circumstances, as in other hollow viscera, the muscle develops, gets thicker and firmer, and capable of accomplishing the extra labor thrown upon it. Defects in the valvular mechanism, obstruction, or incompetency, and increased resistance to the blood-flow in the arteries, are the most important causes of hypertrophy. The ultimate factor in all is heightened pressure within the cardiac cavities due to one of two things--increased volume of blood to be moved or difficulty in propelling the normal volume, caused by obstruction to the flow either central or peripheral.

Pericardial adhesions may impede the action of the heart, and either directly cause hypertrophy or induce dilatation and a consequent hypertrophy.

The details regarding the etiology are best considered in a study of hypertrophy as it affects the individual chambers.

Left Ventricle.--This chamber is much more frequently affected than any other, and may be involved alone or as part of a general enlargement of the organ. The more important causes are as follows:

(1) Aortic Stenosis.--To send the normal charge of blood through a narrowed orifice the muscle must contract with increased force, and to accomplish the work the walls increase in thickness. There may be simple hypertrophy without dilatation of the chamber, but in the later stages this inevitably supervenes.

(2) Aortic Regurgitation.--Curling and foreshortening of the aortic cusps permits of a backward flow into the ventricle during its diastole, with the production of dilatation and increased pressure, to overcome which the walls thicken--eccentric hypertrophy. This is one of the most common causes, and leads to enormous enlargement of the heart.

(3) Mitral Insufficiency.--In extreme grades of mitral stenosis the left ventricle is usually small, but when the curtains are curled and the patent auriculo-ventricular orifice large, there may be very great hypertrophy. Free regurgitation is always accompanied by considerable eccentric hypertrophy, due to the distension of the chamber by the extra quantity of blood forced in at each auricular systole.

(4) Pericardial adhesions, particularly when in addition to union of the layers the parietal membrane is firmly united to the pleura or to the sternum, may cause hypertrophy of the left ventricle alone, but more commonly of the whole heart.

(5) Abnormal Conditions of the Aorta.--_(a)_ Atheroma, with or without dilatation of the arch, is a cause of hypertrophy, for the heart has to {621} compensate for the loss of arterial elasticity, an important factor in the onward movement of the blood during the diastole; and, again, there is increased resistance in the wider tube. _(b)_ Great narrowing, as in the congenital coarctation just beyond the ductus arteriosus, which may produce colossal hypertrophy. Pressure upon the large vessels in the thorax by tumors may act in the same way. _(c)_ Aneurism of the aorta is not often accompanied by hypertrophy unless the valves are affected. Theoretically, it might be expected, as a large saccular dilatation would certainly appear to be a cause of increased resistance, but in uncomplicated cases the experience of most observers appears to accord with that of Stokes,[42] who states that we usually find a small heart. Occasionally, however, there is marked hypertrophy even without valvular disease.

[Footnote 42: _Loc. cit._]

(6) Kidney disease, acute and chronic, is very frequently accompanied with hypertrophy of the left ventricle. Indeed, simple hypertrophy is more often met with in chronic Bright's disease than under any other conditions. Increased blood-pressure in the smaller arteries throughout the body is now very generally acknowledged to be the immediate cause. But how this is brought about is a question not yet satisfactorily determined.

We have to deal with two sets of cases. There is the cardiac hypertrophy accompanying acute or subacute nephritis, particularly the scarlatinal. Here there are no chronic arterial changes, and the increased arterial tension appears to be due to contraction of the smaller arteries under the influence of retained excreta, which may act through the vaso-motor centre, as Ludwig observes, or possibly directly upon the unstriped fibres of the tunica media of the arteries. Bright's original explanation still holds good, I think, when he says that the altered quality of the blood "so affects the minute and capillary circulation as to render greater action necessary to send the blood through the distant subdivisions of the vascular system."[43]

[Footnote 43: _Guy's Hospital Reports_, 1836.]

The hypertrophy of the left ventricle in connection with contracted kidneys is more frequent and more marked. Traube suggested[44] that the interference with the local circulation in the kidneys by the obliteration of vessels increased the work of the heart and induced the hypertrophy, but it is much more probable that the change is a widespread one throughout the body. Gull and Sutton hold[45] that in these cases there is a condition of arterio-capillary fibrosis in which the small arteries are thickened and their calibre diminished, leading in time to a more or less widespread sclerosis in various organs, particularly the kidneys. As a result of this fibrosis, the movement of blood in the smaller vessels is much impeded, the arterial tension increased, and the work of the heart greatly augmented. On the other hand, George Johnson[46] maintains that the muscular coat of the arterioles becomes thickened under the influence of retained excreta, and they are in a state of spasm which increases the tension and heightens the blood-pressure in the left ventricle.

[Footnote 44: _Gesammelte Beiträge_, Bd. ii.]

[Footnote 45: _Medico-Chirurgical Transactions_, lv., 1872.]

[Footnote 46: _Ibid._, vol. xxxiii.]

The question can scarcely be considered settled as regards details, but the general fact of increased peripheral resistance is well established, and it is one of the most frequent causes of non-valvular hypertrophy. It may be quite marked in persons without positive evidence of renal disease as indicated by albumen or casts in the urine, but in whom the condition of arterio-capillary fibrosis is evident from the thickened state of the small arteries, the increased tension, and the firm dislocated impulse of the heart.

(7) Prolonged muscular exertion has been much insisted upon as a cause of cardiac hypertrophy by DaCosta, Myers, Albutt, Seitz,[47] and others. {622} Soldiers, blacksmiths, miners, mountaineers, and men whose occupations call for heavy and prolonged exercise occasionally develop hypertrophy of the heart, which it seems reasonable to connect with the over-use of the muscles. DaCosta's irritable heart in young soldiers appears to represent the early stage of this condition. In 38 per cent. of the cases excessive marching was the cause. He was able to confirm the existence of hypertrophy by autopsy. It is not uncommon to meet with cases of pronounced heart disease, with symptoms of failing compensation, dropsy, etc., in large, powerfully-built men who have been engaged in laborious occupations, and who are admitted to hospital with the clinical picture of chronic valvular disease. At the autopsy one is surprised to find an hypertrophied and dilated heart without valve lesion, perhaps no extensive arterial degeneration, and no kidney disease. They are called cases of idiopathic hypertrophy, but I believe that some of them, at any rate, are instances of a condition induced by prolonged muscular effort. I have had an opportunity of studying carefully four such cases, and I have seen autopsies in two other instances. As I mentioned, alcoholism may be also a factor in these cases, as most of them occur in hard drinkers.

[Footnote 47: _Die Ueberanstrengung des Herzens_, Berlin, 1875--a collection of six monographs on the subject.]

How muscular effort acts in inducing hypertrophy has been much discussed. It seems rational to suppose that prolonged action of the heart at a rate more vigorous and rapid than normal would induce enlargement of its muscle, just as constant exercise acts with others; and possibly within limits this does take place. Albutt speaks of the large red left ventricles in the Leeds iron-workers killed by accident or cut off by acute disease. No doubt the thickness of the ventricle is measured by the muscular needs of the system. Muscular contraction affects the heart in two ways: first, the venous flow is accelerated, more blood reaches the right heart, and is sent to the lungs, and more reaches the left ventricle and the systemic arteries. The fuller inspirations also favor flow to the heart. When the exercise is excessive the right heart and the venous system become still more distended, and the outflow from the peripheral arteries proportionately retarded and the tension in them increased--particularly is this the case in efforts requiring straining, as in lifting, etc.; and, secondly, the effect of muscular contraction has been shown by Traube to increase very greatly the pressure in the arteries. Gaskell, however, states[48] that when a muscle contracts its own arterioles dilate; but however that may be, the increased tension during muscular contraction can be determined in the radial by the finger, and still better by the sphygmograph, during steady contraction of the muscles of the arm. In yet a third way the blood-pressure may be increased during violent muscular efforts, particularly when the breath is held. The vaso-motor centre is stimulated by the lack of oxygen, and in consequence the blood-pressure rises in the peripheral arteries. At the end of prolonged contests we sometimes see men get pale or the left ventricle may become so embarrassed that they faint.

[Footnote 48: _Journal of Physiology_, iii.]

(8) That the heart becomes hypertrophied during pregnancy has been specially insisted upon by French writers, Larcher[49] and others. Many doubt the correctness of their deductions, but the weight of evidence seems to point unmistakably to the existence of moderate increase in the thickness of the walls of the left ventricle.[50] Cohnstein[51] connects it with the hydræmic and chlorotic conditions of the blood, so liable to develop during pregnancy.

[Footnote 49: _Archives générales_, 1859.]

[Footnote 50: McDonald, _Heart Disease during Pregnancy_, London, 1878.]

[Footnote 51: _Virchow's Archiv_, lxxvii.]

(9) Hypertrophy of the right heart in disease of the lungs or of the valves is usually followed by more or less hypertrophy of the left ventricle as well, caused by the increased work in consequence of retarded outflow into the venous system.

{623} Right Ventricle.--Hypertrophy of this chamber is most frequently met with in connection with disease of the left side of the heart; next with various chronic affections of the lungs; and lastly with valvular affections of the right side.

(1) Mitral lesions--incompetence or stenosis--are very common causes which act by increasing the resistance in the pulmonary veins and obstructing the free flow of blood in capillaries of the lung. To compensate for this defect the walls of the right ventricle increase in size, and the hypertrophy at first may be unattended with dilatation.

(2) Pulmonary Lesions.--The obliteration of any considerable number of blood-vessels within the lungs by emphysema, cirrhosis, or phthisis (sometimes), occasionally the compression of pleuritic exudation, increases the blood-pressure in the pulmonary artery and rapidly leads to hypertrophy of the right heart. Narrowing of the main branches of the pulmonary artery by the growth of tumors or an aneurism of the aorta occasionally produces the same effect.

(3) Valvular lesions on the right side are rare causes of hypertrophy in the adult, but during foetal life, when endocarditis is more prevalent in the pulmonary and tricuspid valve, stenosis or insufficiency at these orifices leads to great enlargement of the ventricle. Pulmonary stenosis is the most common lesion; incompetence is not often met with. Lesions of the tricuspid valves in the adult are almost always associated with mitral disease. When the dilated hypertrophy of the right ventricle reaches a certain grade in cases of mitral disease or pulmonary lesion, tricuspid incompetence develops.

(4) Among other causes which may be mentioned are pericardial adhesions, which some think tend specially to the production of right-sided hypertrophy and extensive pleuritic adhesions. Atheroma of the pulmonary arteries is more often a consequence than a cause of hypertrophy.

The auricles are usually dilated and hypertrophied; simple hypertrophy is probably never seen. In the left auricle this condition develops in lesions at the mitral orifice, particularly stenosis when it compensates for the obstruction. In free mitral regurgitation the hypertrophy is not so marked.

The right auricle hypertrophies when there is greatly increased blood-pressure in the lesser circulation, whether due to mitral stenosis or pulmonary lesions, and incompetency at the tricuspid orifice. Stenosis of the auriculo-ventricular orifice is a less frequent cause. The dilatation is always excessive.

MORBID ANATOMY.--In general hypertrophy the entire organ is increased in size and weight; more commonly we find the condition limited to two or three chambers or to one side. The estimation of slight grades of enlargement is difficult, but where the increase is marked the process is simple enough. The volume of the heart varies in different individuals according to their age and size. The normal heart is about the size of the closed fist, and, as Virchow suggests, a fair estimate can be made by comparing the two together. By careful weighing we get much more accurate information. The heart of an average-sized man weighs about 9 oz., of a woman about 8 oz. In great hypertrophy the organ may weigh three or four times the normal amount. A heart which weighs over 12 oz. in a man, and over 10 oz. in a woman, may be considered hypertrophied. Hearts weighing from 16 to 20 oz. are not uncommonly met with. Weights above 25 oz. are rare. The heaviest hearts on record are described by Beverley Robinson of New York,[52] 53 oz.; Dulles of Philadelphia, 48 oz.; and there are several cases described in the _Transactions_ of the London Pathological Society of the organ weighing as much as 46 oz.

[Footnote 52: _New York Medical Record_, 1883.]

{624} Next to weighing, careful measurement of the thickness of the walls is the best means of determining hypertrophy. When there is great dilatation of a chamber the walls, though actually thick, may look proportionately thin; and on the other hand, when rigor mortis is present the cavity may be very small and the walls appear enormously thick. In this case measurements should not be made until the heart has been soaked in water and thoroughly relaxed. The normal thickness of the left ventricle is about half an inch (12 or 13 millimeters), being thicker toward the base. It is well to measure in two or three places, not including the papillary muscles. A thickness of 10 lines or over (20 to 25 mm.) indicates hypertrophy. It is rare to meet with the wall thicker than 1 inch (25 mm.), even in very great hypertrophy. The right ventricle is thinner than the left, and has an average diameter of from 2 to 3 lines (4 to 7 mm.). A thickness of from 6 to 9 lines (13 to 20 mm.) may be met with in great hypertrophy. It is very rare to see a diameter of more than three-quarters of an inch, but cases are reported of a thickness of over an inch. The left auricle has a normal thickness of about a line and a half (3 mm.), which in considerable hypertrophy may be nearly doubled. The wall of the right auricle is even thinner than the left, rarely exceeding 1 line in diameter. In hypertrophy the sinus does not present a marked increase in thickness, but the appendix, particularly the musculi pectinati, may be greatly developed and measure from 2 to 3 lines in diameter.

The shape of the heart is much affected by the degree of hypertrophy in different cavities. Great enlargement of the ventricles broadens the apex, and the conical shape is lost. In the enormous hypertrophy and dilatation of aortic insufficiency the increased breadth and rotundity of the apex becomes very marked. When the right ventricle is chiefly affected, it occupies a large share of the apex, and the transverse diameter of the organ is increased. When due to mitral stenosis the contrast between the large broad right ventricle extending well to the apex and the small left chamber is very striking.

When not degenerated the muscle-tissue of an hypertrophied heart is of a deep-red color, firm, and usually cuts with slightly increased resistance. The right ventricle often has a peculiarly hard, leathery feel, which was noticed by Rokitansky. In simple hypertrophy of the left ventricle the papillary muscles and columnæ carneæ may be increased in size, but the former often appear flattened in great eccentric enlargement. The trabeculæ are usually much more developed in the right ventricle and in the appendix of the right auricle than in the left chambers. Very often the tissue looks pale, and may be soft from the occurrence of fatty degeneration.

The histological characters of the changes in hypertrophy have been much studied, particularly with a view of determining the question of numerical increase. Hepp[53] described an increase in the thickness; but most recent observers regard the hypertrophy as due to numerical increase, resulting from the development of new fibres, either by the splitting of the old ones (Rindfleisch) or their growth from interfibrillar nuclei.[54] Wilks and Moxon[55] and Gowers[56] find that the fibres are not increased in size. Letulle[57] thinks that there is a process of progressive hyper-nutrition of the fibres.

[Footnote 53: _Henle's Zeitschrift_, 1854.]

[Footnote 54: Zielonko, _Virchow's Archiv_, lxii.]

[Footnote 55: _Pathological Anatomy_, London, 1875.]

[Footnote 56: _Reynolds's System_.]

[Footnote 57: Quoted by Peter, _loc. cit._, p. 280.]

The toughness of the hypertrophied muscle is due to the increase in the connective tissue, which is more marked as a rule in the right than the left ventricle. Sometimes, indeed, it is not at all noticeable in the latter, which may be soft and tears readily with the finger.

SYMPTOMS.--Hypertrophy is a conservative process, usually secondary to some valvular or arterial lesion, and is not necessarily accompanied by any {625} symptoms. So admirable is the adjusting power of the heart that, for example, an advancing stenosis of aortic or mitral orifice may be for years perfectly counterbalanced by a progressive hypertrophy, and the subject of the affection be happily oblivious to the existence of heart trouble. Particularly is this the case with mitral stenosis and the consequent hypertrophy of the left auricle and right ventricle. While leading quiet lives and not straining the heart with violent exertion, such persons may not suffer in any way, or perhaps only experience a little shortness of breath when going up stairs. Indeed, the hypertrophy is in almost all instances an unmixed good, and many of the symptoms which arise are to be attributed to its failure, or, as we say, disturbance of compensation.

The left ventricle is most often involved, and the clinical features of hypertrophy are best seen when it is affected. Inspection may reveal decided bulging of the præcordia, producing in extreme instances marked asymmetry of the chest. This is most frequent in persons under twenty years of age, and it may occur without any pericardial adhesions, which Shroetter[58] thinks are invariably associated with this condition. The intercostal spaces may be widened, and the area of visible impulse is much increased. On palpation the character and position of the apex-beat give most important results. It is stronger, more forcible and heaving, and may lift the chest-wall. With each systole the hand or the ear applied over the heart may be visibly raised. A slow heaving impulse is one of the best signs of simple hypertrophy; when there is large dilated hypertrophy the forcible impulse is often more sudden and abrupt. A second, weaker, impulse can sometimes be felt, due possibly (as Gowers suggests) to a rebound from the aortic valves. The area of impulse is greatly increased, and the beat may be felt in the sixth, seventh, or eighth interspace from an inch to three inches outside the nipple. The downward dislocation of the apex is an important sign in hypertrophy of the left ventricle; simple outward displacement may be due to enlargement of the right ventricle.

[Footnote 58: _Ziemssen's Encyclopædia_, vol. vi.]

In moderate grades of hypertrophy, as seen in chronic Bright's disease, the apex-beat may be in the sixth interspace in the nipple-line or a little outside it.

Percussion gives an area of increased dulness, due to the much larger portion of the heart which comes in contact with the chest-wall. The dulness in the parasternal line may begin at the third rib or in the second interspace, and the transverse limits extend from half an inch to two inches beyond the nipple-line, and an equal distance beyond the middle line of the sternum. The dull region is more ovoid than in health. When carefully delimited and measured, there may be in the colossal hypertrophy of aortic valve disease an area of dulness from seven to eight inches in transverse extent. In moderate grades a transverse dulness of four inches is not uncommon.

On auscultation the heart sounds, when there is no valve disease, may not present any special changes, but the first is often prolonged and dull; but when there is dilatation as well, it may be very clear and sharp. Reduplication is not uncommon, particularly in the hypertrophy of renal disease. A peculiar clink--the tintement métallique of Bouillaud--may sometimes be heard, with the impulse most frequently just to the right of the apex-beat. The second sound is clear and loud, sometimes ringing in character or reduplicated. When the hypertrophy depends upon valvular lesions the sounds are of course much altered, and replaced or accompanied by murmurs.

The pulse of simple hypertrophy not dependent on valvular lesions is usually firm, full, and strong, of high tension, and regular. It may be increased {626} in frequency, but often is normal. In eccentric hypertrophy the pulse is full, but softer, and usually more rapid. So long as the hypertrophy is maintained the pulse is regular; one of the earliest signs of failure and dilatation is irregularity and intermittence. The various modifications of the pulse in connection with valve disease are considered elsewhere.

Among symptoms which patients complain of most frequently are unpleasant sensations about the heart--a sense of fulness and discomfort, rarely amounting to pain. This may be very noticeable when recumbent and on the left side. Actual pain in simple hypertrophy is rare, but in the irritable heart from tobacco and in neurasthenics with slight enlargement it is often a very troublesome symptom. Palpitation is not often complained of, nor do patients always have sensations from the violent shocks of a greatly hypertrophied organ; others, again, will have very uneasy feelings from a moderately exaggerated pulsation. The general condition of health has much to do with this: we are not in health conscious of our own heart's action, but one of the very first indications of nervous exhaustion from excesses or over-study is the consciousness of the heart's action, not necessarily accompanied by palpitation. Flushings of the face, noises in the ear, flashes of light, and headaches are not uncommon.

There are certain untoward effects of long-continued hypertrophy of the left ventricle which must be mentioned, chief among which is the production of atheromatous degeneration of the vessels. Particularly is this the case when the hypertrophy results from increased peripheral resistance. The heightened blood-pressure in the arteries (which is expressed by the word strain) gradually induces an endarteritis and a stiff, inelastic state of those vessels most exposed to it--viz. the aorta and its primary divisions. In overcoming the peripheral obstruction the hypertrophy "ruins the arteries as a sequential result" (Fothergill). It is in this way that prolonged muscular exertion acts injuriously, and leads to two common morbid conditions in athletes and persons whose employment necessitates violent exercise of the muscles--viz. aneurism and sclerosis of the aortic semi-lunar valves, with incompetency. Syphilis certainly does not embrace the entire etiology of aneurism, the occurrence of which in soldiers, strikers, foundrymen, etc. can be traced to arterial strain. So also with the sclerosis of the semi-lunar valves--just enough, perhaps, to produce incompetency; how common it seems to be in strong, well-built men whose excesses have been on the cinder-path or on the river! The increased aortic tension, with the more forcible recoil and closure of the semi-lunar valves, would seem to be factors in the production of this condition. Aortic incompetency is the special danger of athletes, and no inconsiderable number of the cases of this lesion occurring in men without rheumatic or syphilitic history may be traced to over-use of the muscles.

Another special danger is rupture of the blood-vessels, particularly of the brain. In the condition of general arterial degeneration associated with contracted kidneys and hypertrophied left heart apoplexy is common; indeed, we may say that in the majority of cases of cerebral hemorrhage there is sclerosis of the cerebral vessels, often with the development of miliary aneurisms, and the rupture is directly induced by the forcible action of the heart.

Hypertrophy of the right ventricle in the adult is rarely induced by valvular disease on the right side, but is a result of increased resistance in the pulmonary circulation, as in cirrhosis of the lung and emphysema, or in stenosis of the mitral orifice. When the compensation is perfect, and the hypertrophy fully maintains the equilibrium of the circulation, there are no symptoms. Extra exertion, as in ascending stairs or running, may induce shortness of breath, but in many respects hypertrophy of {627} the right ventricle is the most enduring and salutary form in the whole range of cardiac affections. For long periods of years the effects of mitral stenosis may be counterbalanced completely, and only sudden death by accident or an acute disease reveals the existence of extensive unsuspected heart disease. In the hypertrophy secondary to pulmonary disease, particularly emphysema and cirrhosis, there may be sensations of uneasiness in the cardiac region, with cough and shortness of breath; but so long as the dilatation is moderate the symptoms are not marked. With great dilatation and tricuspid regurgitation come the venous engorgement, oedema, and pulmonary troubles. The increased pressure in the lesser circulation not uncommonly leads to atheroma of the pulmonary artery, and the full state of the capillaries leads ultimately to a deposition of pigment and increase in the fibrous elements in the lung--the brown induration. Pulmonary congestion and apoplexy from thrombosis or embolism are more often associated with dilatation. Hæmoptysis may result from rupture of vessels during sudden exertion.

The physical signs of hypertrophy of the right ventricle are not so marked as those of the left. Bulging of the lower part of the sternum and left cartilages is occasionally met with. The apex-beat is forced to the left, but is not so often displaced downward. The most marked impulse may be in the epigastrium, in the angle between the ensiform cartilage and the seventh rib or beneath the cartilages of the sixth and seventh ribs. The pulsation is rarely the strong heave of left-sided hypertrophy, and is apt to be diffuse, not punctuate, particularly if there is much dilatation. In thin-walled chests there may be pulsation in the third and fourth right interspaces. The area of dulness is increased in the transverse direction, particularly toward the right, where it may extend an inch or more beyond the border of the sternum. On auscultation the first sound at the lower part of the sternum is louder and fuller than normal, but the differences are not very marked unless there is much dilatation, when it is clearer and sharper. The second sound is accentuated in the pulmonary artery on account of the increased tension, and there may be reduplication. The pulse at the wrist is usually small. The jugular pulsation occurs when there is tricuspid incompetence, which arises when the eccentric hypertrophy reaches a certain grade.

Hypertrophy of the auricles is always associated with dilatation. It is most common in the left chamber, which hypertrophies in mitral stenosis and incompetency, and assists materially in restoring the balance of the circulation and protects the lungs. There are no special physical signs, and we usually can only infer its presence by the existence of mitral stenosis and a presystolic murmur. Increased dulness may be determined at the left of the sternum, and there may be a presystolic wave in the second left interspace.

Hypertrophy and dilatation of the right auricle occur not infrequently, and are almost invariably associated with a similar condition in the right ventricle, and incompetency of the tricuspid. In emphysema, cirrhosis of the lung, chronic bronchitis, and in mitral disease, it is very common, much more so than the statement of some authors would lead us to expect. In comparison with the left auricle the greater development and hypertrophy of the appendix and its musculi pectinati is very striking. The latter may be distributed over the anterior wall of the sinus to a much greater extent than in health. There may be increased dulness in the third and fourth interspaces, with pulsation presystolic in rhythm. Usually there are signs of venous engorgement, jugular pulsation, and other evidences of dilatation of the right heart.

The DIAGNOSIS of cardiac hypertrophy does not usually present any serious difficulties. Increase in size, more forcible contraction, with displacement of {628} the apex-beat, and the character of the pulse, are the most important signs. There are certain conditions which require to be carefully distinguished. Neurotic palpitation, from whatever cause, may be accompanied with forcible contraction, but it has not the heaving impulse of genuine hypertrophy. Actual enlargement of the organ may, however, result from prolonged over-action, as in Basedow's disease, in the smoker's heart, and the irritable heart of neurasthenics, but it is usually slight. Increased dulness in the cardiac area may be due to a variety of causes, some of which may simulate hypertrophy, as pericardial effusion, aneurism, mediastinal growths, or displacement of the heart from pressure or the existence of malformation of the chest; but with the exercise of ordinary care the diagnosis can usually be made. There are two opposite conditions which not infrequently give trouble. When the left lung is retracted from pleurisy, phthisis, or cirrhosis, there is a large surface of the heart exposed, and the pulsation may be extensive and forcible, and at first sight resemble hypertrophy. There is usually in this condition some dislocation upward and to the left. The history of pulmonary or pleuritic disease, and the evident fixture of the lung on deep inspiration, will usually suffice to prevent mistake. A similar exposure of the heart occurs without any disease in very narrow-chested persons with ill-developed lungs; and here, though the area of dulness may be much increased, yet the normal position of the apex and the absence of forcible heaving impulse, pulse signs, and of any obvious cause of hypertrophy will afford satisfactory criteria for a diagnosis. Just the reverse occurs in some cases in which a moderate cardiac hypertrophy is masked by emphysema of the lungs or of their anterior borders. The area of dulness may be normal, or even diminished, and the pulsation diffuse and chiefly epigastric. The general condition, state of the pulse, and character of the sounds would help in the diagnosis, but it is sometimes a matter of no little difficulty.

The symptoms and physical signs above narrated sufficiently indicate the points of difference between hypertrophy of the two sides of the heart.

In all cases the greatest possible care should be exercised in ascertaining the presence or absence of conditions likely to cause hypertrophy.

The COURSE of a case of ordinary hypertrophy may be divided into three stages: 1st. The period of development, which varies much with the nature of the primary disease. Thus in rupture of an aortic cusp or in sudden overstrain from exertion it may require months, or even years, before the hypertrophy becomes fully developed. In these cases it may never do so, and then death results. On the other hand, in sclerotic affections of the valves with stenosis or incompetence the hypertrophy develops pari passu with the lesion, and may continue to counterbalance a progressive impairment of the valves. 2d. The period of full compensation, the latent stage, during which the heart's vigor meets all the requirements of the circulation. There may be no signs whatever of heart weakness, but the hypertrophied muscle completely equalizes the valvular or other defects. It may last an indefinite period of years. In some cases this fortunate period is never fully attained, and indications of incomplete compensation remind the individual that he has a heart affection. 3d. The period of disturbed compensation, which sooner or later awaits all victims of hypertrophy. It may come suddenly during an extra exertion, and death follow from acute dilatation; or more commonly it takes place slowly, and results from degeneration and weakening of the heart-muscle, with consequent dilatation and all its evils. There may be repeated failures before the end is reached, represented clinically by attacks of cardiac dyspnoea and dropsy.

The breaking, as it is called, of a compensatory hypertrophy may be induced by many causes. Among the most important is failure of general or local (cardiac) nutrition. In many a chronic heart case readmitted to {629} hospital, perhaps for the third or fourth time, with dyspnoea and dropsy, exposure, poor food, and whiskey are responsible for the failure. Gradual sclerosis of the coronary arteries leading to fatty or fibroid changes is a fruitful source of disturbed compensation. It is well known that during or after an acute illness, pneumonia, fever, or a bronchial attack the first symptoms of heart disease may be manifested. Mental emotions, severe grief, or fright have been known to bring on symptoms of heart failure in hypertrophy. One of the most frequent causes is sudden or prolonged muscular exertion, which may disturb a compensation perfect for years, and induce death in a few days.[59] The intimate pathology of broken compensation is not always clear. It certainly does not always depend on degeneration of the muscle-fibres, so far as microscopical examination can tell, and in many cases we are forced to conclude that the ganglia are at fault and the breakdown is nervous, not muscular.

[Footnote 59: Traube, _Gesammelte Beiträge_, Bd. iii.]

The PROGNOSIS depends entirely upon the nature of the cause which has induced the hypertrophy. When remediable or removable, the heart may return to its normal size, as after pregnancy, acute Bright's disease, and some cases of hypertrophy from deranged innervation and muscular exertion. When the cause is irremediable, as in chronic valve disease, sclerosis of the arteries, or obliteration of pulmonary capillaries, the case is quite different. Here the prognosis depends largely on the capability of maintaining in its integrity a sufficient hypertrophy to compensate for the obstruction: so long as this keeps up all is well; the evils come with failure of the hypertrophy and increase of the dilatation. Conditions of general and local nutrition are all-important factors, and when these can be supported to the highest possible degree the prognosis is favorable. Ill-health may be indicated at once by the onset of cardiac symptoms, pointing to disturbed compensation. Much depends on the seat of the original disease. Mitral stenosis carries with it as good prognosis, quo ad longevity, as aortic stenosis,[60] and the latter much better than aortic insufficiency. The nutrition of the muscle of the heart demands a full and constant supply of blood, but in aortic incompetency the rapid regurgitation does not permit of the complete distension of the coronary vessels,[61] and the strain is such that atheroma of these arteries is very apt to follow and still further diminish the blood-supply. Hence the prognosis in aortic insufficiency for enduring hypertrophy is bad. The hypertrophy which accompanies general arterial degeneration, though compensating for peripheral obstruction, carries with it certain dangers, as already {630} indicated, in the liability to cause rupture. With care such patients may survive for years, though exposed to risks other than cardiac.

[Footnote 60: Brückes held that the coronary vessels were filled in diastole alone, but there can be no question that blood also enters during the systole. The sigmoid valves certainly do not in the majority of cases cover the orifices of these arteries during this act. Undoubtedly, however, the heart-vessels are more distended in diastole. The pallor of the muscle in systole is a proof that the coronary vessels are not well filled at this period.]

[Footnote 61: This is not the usual statement, but my experience--limited, it is true--seems to point to the conclusion that mitral stenosis may also exist for many years without exciting symptoms of heart disease. It may, I think, be safely affirmed that a larger number of persons with mitral valve disease live in blissful ignorance of the existence of serious heart lesion than any other group of cardiac cases. Particularly is this the case in women. Two points have attracted my attention in this connection: the frequency with which we find evidence of stenosis--as shown by the presystolic thrill and rough murmur--in women complaining, perhaps, of shortness of breath on exertion and slight cardiac distress--symptoms which are readily relieved--and the discovery post-mortem of stenosis of the mitral orifice in cases of sudden death by embolism or from some intercurrent disease occurring in persons in whom heart disease had never been suspected. The narrowing may be extreme--an orifice only 13 millimeters in width in one case in which a woman was stricken with hemiplegia while attending to her household duties. Such cases, and they are not very uncommon, teach us how perfect compensation may be in this lesion.]

The TREATMENT of hypertrophy consists largely of measures directed toward its maintenance in a degree proportionate to the extra work which the heart has to do. In organic disease the well-being of the patient depends on this: we cannot remove the cause, but we can by careful hygienic and dietetic regulations maintain the balance between the defect and the compensation. The original lesion is usually beyond control, and the special indications are to moderate certain dangers associated with hypertrophy, and to promptly meet the earliest symptoms of heart failure. The utmost moderation in food, drink, and exercise must be enjoined. Quiet, regular habits are all important; excesses of all kind quickly lead to impairment of the heart's action. In the hypertrophy associated with arterial and renal disease a special danger exists in the tendency to rupture of vessels. In these cases vigorous heart-beat, with very high tension in the peripheral arteries, indicates mischief which may be met by taking prompt measures for the reduction of the high pressure. A brisk cathartic may avert an apoplectic attack, and there are cases in which the old practice of bleeding--formerly so much in vogue for hypertrophy--is justifiable. Palpitation and shortness of breath are among the earliest signs of failing compensation, and call for the treatment to be considered under Dilatation. The condition of hypertrophy from organic disease is not directly amenable to treatment; we cannot diminish the size of the organ, but we can regulate its action by measures which control the contractions when from any cause they become too forcible or irregular. More particularly is this the case in hypertrophy due to disturbed innervation. When vigorous, rest and the administration of cardiac sedatives, such as aconite or veratrum viride, will generally suffice to reduce the force of the contractions. The palpitation and irregular action in cases of irritable heart from over-exertion, the abuse of tobacco, or sexual excesses may subside with the removal of the cause. The steadying action of small doses of digitalis is often well seen in these cases.

Dilatation of the Heart.

DEFINITION.--An increase in the size of one or more of the chambers, with or without thickening of the walls.

VARIETIES.--Two varieties may be recognized: (1) dilatation with thickening, and (2) dilatation with thinning. Dilatation with thickening is the most common, and corresponds with the dilated or eccentric hypertrophy and the active dilatation of some writers. Those cases of dilatation with walls of apparently normal thickness--simple dilatation of authors--also belong to this category, for if the chamber is distended, and yet the walls maintain their normal diameter, they must of course be hypertrophied. The dilatation with thinning--passive dilatation--is specially met with in the auricles, and is characterized by increase in the size of the chamber and attenuation of the walls.

The diastole of the heart is partly an active, partly a passive act. The cavities behave as would rubber balls, and their distension after contraction is partly due to their elasticity. The heart is a suction- as well as a force-pump. In the ventricles, for example, after systole the active dilatation draws blood from the auricle--must do so, in fact, in the very process of dilating--and then the auricular systole completes the process, fully accomplishing the diastole. Dilatation occurs during this period, and results from distension beyond the limits of the contractile power of the wall. More blood is contained in the cavity than the muscle of the wall can {631} control--_i.e._ expel--but if the organ is healthy, hypertrophy ensues and the chamber accommodates itself to the altered condition. It is the heightened pressure during diastole which is dangerous; during systole the pressure may be extreme, and yet no dilatation may ensue, as in aortic stenosis, in which condition the size of the chamber may remain normal, and yet the walls hypertrophy to meet the greatly-increased resistance to the outflow of the blood during the systole. In the auricles, however, the increased tension during contraction may be accompanied with considerable dilatation, as in mitral stenosis.

ETIOLOGY.--There are two important causes in the production of dilatation: increased pressure within the cavities, and impaired resistance due to disease of the muscular substance of the heart. They may act singly, but are often combined. Weakened walls may yield under normal distending force, or normal walls may yield under a heightened blood-pressure, or both factors may prevail.

1. Increased endocardiac pressure--which results, as before stated, either from an augmented quantity of blood to be moved or an obstacle to be overcome--is the most frequent cause of dilatation. It does not necessarily cause it. Simple hypertrophy may be the result, as in the early period of aortic stenosis and in the hypertrophy of the left ventricle in Bright's disease.

Most of the important causes of increased endocardiac pressure have already been considered under Hypertrophy, but we may refer to one or two more particularly.

The size of the cardiac chambers is variable in conditions of health. With slow action of the heart the dilatation during diastole must be much more full and complete than with rapid action. Physiologically, the limits of dilatation have been reached when the chamber cannot be emptied during the systole. We find this as an acute, transient condition in severe exertion--during, for example, the ascent of a steep mountain. There may be great distension of the right heart, as shown by the increased epigastric pulsation, and even increase in the cardiac dulness. The safety-valve action of the tricuspid valves may here come into play, and by permitting regurgitation into the auricle relieve the lungs. Rest causes it to pass off, but if it has been extreme, the heart may suffer a strain from which it may recover slowly, or, indeed, the person may never again be able to undertake severe exertion. In the process of training the getting wind, as it is called, is largely a gradual increase in the capability of the heart, particularly the right chambers. A degree of exertion can be safely maintained in full training which would be quite impossible under other circumstances, because by a gradual process of what we may call physical education the heart has strengthened its reserve force--widened enormously its limits of physiological work. Endurance in prolonged contests is measured by the capabilities of the heart, and its essence consists in being able to meet the continuous tendency to overstep the limit of dilatation.

We have no definite information as to the nature of the change in the heart which occurs in the process of training, but it must be in the direction of increased vigor, muscular and nervous. The large hearts often noted in athletes may be due, as already mentioned, to the prolonged use of their muscles; but probably no one can become a great runner or oarsman who has not naturally a large and capable heart. Master McGrath, the celebrated greyhound, and Eclipse, the race-horse, both famous for endurance rather than speed, had very large hearts.

Over-training and heart-strain are closely connected with this question of excessive dilatation during severe muscular effort. Both mean the same thing in many cases. A man, perhaps not in very good condition, calls upon his heart for much extra work during a race or the ascent of a very steep {632} mountain, and is seized with cardiac pain and a feeling of distension in the epigastrium, and the rapid breathing continues an unusual time, but the symptoms pass off after a night's quiet. An attempt to repeat the exercise is followed by another attack, or indeed an attack of cardiac dyspnoea may come on while he is at rest.[62] For months such a man may be unfitted for severe exertion, or may be permanently incapacitated. He has overstrained his heart and has become broken-winded. We see the same thing sometimes in horses. What exactly has taken place in these hearts we cannot say, but their reserve force is lost, and with it the power of meeting the demands exacted in maintaining the circulation during severe exertion.[63] The heart-shock of Latham[64] includes cases of this nature--sudden cardiac breakdown during exertion and not due to rupture of a valve. It seems probable that some cases of sudden death in men and animals during long-continued violent efforts, as in a race, are due to over-distension and paralysis of the heart.

[Footnote 62: In _St. George's Hospital Reports_, 1872, Clifford Albutt gives his own experience.]

[Footnote 63: H. C. Wood tells me he believes that wind in athletes is in large part a question of vagus control, and that he has noticed in races of dogs used in hunting and other violent exercise the vagi are more sensitive and powerful than in sedentary breeds. He thinks that a similar difference exists between tame and wild rabbits.]

[Footnote 64: _Diseases of the Heart_, New Sydenham Soc. ed.]

In the various forms of valvular disease we meet with numerous examples of dilatation. In aortic incompetency during diastole blood enters the left ventricle from the unguarded aorta and from the left auricle, and the amount of blood at the termination of diastole subjects the walls to an extreme degree of pressure, under which they inevitably yield: in time they augment in thickness, and we have the typical eccentric hypertrophy of this condition.

In mitral regurgitation a certain quantity of the blood which should have been driven into the aorta is forced into the auricle from which it came, dilating it; and then in the diastole of the ventricle a larger amount is returned from the auricle, and with increased force, by the hypertrophied walls of this chamber. In mitral stenosis the left auricle is the seat of greatly-increased tension during systole, and dilates as well as hypertrophies; the distension too may be enormous. Dilatation of the right chamber is very common, and is produced by a number of conditions, which were considered under Hypertrophy. All circumstances which permanently increase the tension of the blood in the pulmonary vessels will cause it--mitral stenosis, emphysema, etc. The dilatation seems easily produced, but the accompanying hypertrophy may hold it in check for years. We may here refer to the extreme distension of the right chambers in pneumonia, particularly when the consolidation is extensive. The passive dilatation may be very great and the walls much thinned, and we see the same in states of asphyxia. Valvular lesions of the right heart are not frequent causes of dilatation. When the causes which bring about the dilatation act suddenly, the degree of distension may be great, and there is much more difficulty in the establishment of compensation, as in rupture of an aortic cusp.

2. Impaired nutrition of the heart-walls from degeneration or inflammation may lead to such a diminution of the resisting power that dilatation readily occurs.

In fevers the loss of tone due to parenchymatous degeneration or myocarditis may lead to a condition of acute dilatation which may prove fatal. It is a well-recognized cause of death in scarlatinal dropsy,[65] and may occur in rheumatic fever,[66] typhus, typhoid, erysipelas, etc. The myocarditis accompanying acute endo- or pericarditis may lead to dilatation, especially in the latter disease. The cavities are usually large in fatty degeneration or {633} infiltration from the relaxed and atonic state of the walls. In anæmia, leukæmia, and chlorosis the dilatation of the chambers may be considerable. In fibroid degeneration the wall generally yields where the process is most advanced, as at the left apex. The impaired nutrition in coronary disease may lead to dilatation. Under any of these circumstances the walls may yield with normal blood-pressure, or if increased tension is present the effect is the more readily produced.

[Footnote 65: Goodhart, _Guy's Hospital Reports_, Series iii. vol. xxiv.]

[Footnote 66: Samuel West, _Barth. Hospital Reports_, xiv.]

Pericardial adhesions are usually spoken of as a cause of dilatation, acting by traction from without, and we generally find in a case of extensive and firm union considerable hypertrophy and dilatation. In this condition there is usually some impairment of the superficial layer of muscle which may permit of over-distension.