Volume 3 — DISEASES OF THE BLOOD, AND OF THE HÆMATOPOIETIC SYSTEM.

DISEASES OF THE BLOOD AND BLOOD-GLANDULAR SYSTEM. DISEASES OF THE THYROID GLAND.

DISEASES OF THE SPLEEN. SIMPLE LYMPHANGITIS.

DISEASES OF THE SUBSTANCE OF THE HEART.

BY WILLIAM OSLER, M.D.

Malpositions of the Heart.

We shall consider only such alterations as affect the whole organ; faulty position of individual parts comes under the section upon Malformations. It may, however, be mentioned that cases are known of complete transposition of the chambers, the pulmonary artery and cavæ being connected with the left, the aorta and pulmonary veins with the right side, the valves being also transposed.¹

¹ Pazannuzzi, London Med. Record, 1877.

Malpositions of the heart result either from errors of development, or, more commonly, from changes in contiguous organs, usually the effect of disease.

Of the congenital anomalies only a few are of practical interest. The heart may be placed vertically in the chest, as in the foetus, the apex beating at the lower end of the sternum; or, more rarely, the organ lies transversely. Dextrocardia, the condition in which the heart is on the right side of the body, is much more important, and is usually associated with the transposition of the abdominal viscera—situs inversus viscerum. In these cases the apex-beat is in the region of the right nipple; a distinct area of dulness can be obtained to the right of the sternum, in which situation the heart sounds are loudest; and, lastly, there is pulmonary resonance in the place of normal cardiac dulness. In the great majority of cases—70 out of 78²—the abdominal organs are also transposed, the liver on the left side, the spleen on the right; but in a few instances the heart alone has been misplaced, and under such circumstances care is needed to diagnose the condition from dislocation of the organ due to old-standing lung disease with retraction.

² Gruber, Virchow's Archiv, 1865.

More serious congenital malpositions, but of less practical importance, are the cases of ectopia cordis, which may exist in all grades, from simple failure of closure in the sternum—fissura sterni—to the most extreme condition, in which the naked heart lies outside the chest-wall. Hodgen³ and March⁴ have each described remarkable examples of the latter condition. In other instances the heart lies free in the neighborhood of the neck, or it may be in a congenital umbilical hernia.

³ American Practitioner, xviii. p. 107.

⁴ Trans. of the New York State Medical Society, 1859.

The malpositions with which we are more immediately concerned arise from disease of the heart itself or its membranes, or from disease of contiguous organs.

We judge of the situation of the heart by the site of the apex-beat, by the position and extent of the area of dulness, and by the character of the sounds. So constant in health is the position of the apex-beat in the fifth intercostal space that in our examination of the heart we seek first to determine its existence as affording the most important information of the normal situation of the organ. The area of dulness is a much more variable guide, depending as it does so greatly on the degree of distension of the lungs. When, as sometimes happens, neither apex-beat nor area of dulness can be obtained, the position of maximum intensity of the heart sounds becomes an important indication.

In regard to the effect of respiratory movements in the position of the heart, with each inspiration it is drawn down slightly by the descent of the diaphragm, and it is separated from the chest-wall by the inflation and descent of the left lobe of the lung—in deep inspiration to such a degree as to obliterate the area of dulness and to prevent the systolic impulse from reaching the intercostal space.

The effect of gravity on the position of the heart is well illustrated by the more forcible and extended beat when the chest is bent forward or when the person is turned toward the left side—procedures frequently resorted to when from any cause the apex-beat is obscure.

Of diseases of the heart itself, dilatation and hypertrophy are very common causes of displacement, and in general enlargement the organ may occupy a very considerable part of the left side of the chest, and the apex-beat in the seventh or eighth space in the axillary line. Hypertrophy of the left ventricle alone pushes out the apex-beat, while enlargement of the right ventricle gives a stronger impulse toward the left border of the sternum and a more marked pulsation below the ensiform cartilage. Hypertrophy and dilatation of the auricles increase the width of the cardiac dulness, and may cause marked pulsation in the second and third spaces on either side of the sternum.

In pericardial effusion the heart is pressed backward and the apex slightly raised.

To understand clearly the effects upon the position of the heart of disease of contiguous organs, we must bear in mind their mutual relations. Situated in the mediastinum between the lungs on either side, it is subject to the elastic traction of these organs, which counterbalance each other, but if from any cause the elastic tension of one lung is suppressed, as in pneumothorax or in pleural effusions, then the other lung may also collapse to a slight degree, and pull over the mediastinum and with it the heart. The pericardium is firmly fixed below to the diaphragm, chiefly to the central tendon, to a slight extent also to the muscular substance, but the union with the diaphragm is so intimate that there can be but little movement of the attached portion. The mobility of the heart is measured by that of the mediastinum and pericardium, and through these alone the displacing forces act. The limits of dislocation are determined by the attachments of the central tendon, of the inferior cava, and the great vessels at the root. Within the pericardium the heart has a certain degree of mobility, but this is confined, as regards pressure or traction effects, to rotation upon its axes.

Of the malpositions due to changes in contiguous organs, the following may be considered:

Changes in the Chest-wall.—The gradual incurvation of the ribs and costal cartilages in some cases of rickets may alter the position of the heart.

Curvature of the spine, particularly cases which narrow to a great extent the upper outlet of the thorax, may produce very considerable displacement of heart and great vessels. There may be areas of extensive pulsation on either side of the sternum, and the condition may simulate aneurism of the aorta, as in a case reported by Bramwell.⁵

⁵ Lancet, 1878, i.

In certain affections of the lungs the position of the heart is much altered. In emphysema, when extensive, the apex is directed more to the right, and the organ is somewhat lower than normal, on account of the depressed condition of the diaphragm. The heart may also occupy a more transverse position. The area of cardiac dulness may be greatly reduced by the distended left lung, and there is usually forcible epigastric pulsation, due to the lower position of the organ and the hypertrophy of the right ventricle which almost always accompanies emphysema.

The most marked displacement is produced by fibroid induration of the lung, with contraction—cirrhosis. As the process of condensation goes on, the chest-wall is gradually flattened, and the mediastinum, with the heart, drawn toward the affected side. When the left lung is involved, the heart may be completely to the left of the median line, and is usually drawn upward as well. There may in such cases be a very wide area of impulse, as the heart occupies the position of the left lung in front. In cirrhosis of the right lung the organ is drawn toward the right side, and the area of visible impulse may be in the third and fourth interspaces to the right of the sternum. In the process of slow traction the heart revolves upon itself and the left chambers come uppermost. In many cases of chronic phthisis, when the anterior margin of the left lung is involved, the retraction from induration may leave a large portion of the heart exposed and increase the area of visible pulsation; sometimes, when there is much contraction of the upper lobe, the organ is drawn up and to the left, and the apex-beat may be in the fourth interspace.

The pressure of a pneumonic lung may depress the diaphragm and draw down the heart.

Abnormal conditions of the pleuræ are frequent causes of cardiac displacements. In pneumothorax there is collapse of the lung on the affected side, and the elastic traction of the sound lung draws over the mediastinum and heart. It is not that the heart is pushed over, as so often stated, but the tension of the other lung, being unopposed, pulls the mediastinum toward the sound side. Later, when, as usually happens, effusion takes place, the pressure assists in the displacement. In pleuritic effusion dislocation of the heart to one side is almost constant if the amount of fluid is at all considerable. Here pressure plays the most important part, and the heart is gradually pushed over by the effusion; but the elastic tension of the lung on the sound side is also concerned in the result. In right-sided effusion the whole organ may be to the left of the median line, and from the depression of the diaphragm it is usually lower in the chest, so that the apex-beat may be in the sixth, rarely the seventh, interspace in the axillary line. When the exudation is on the left side, the dislocation is more marked, and there may be a cardiac impulse at the right nipple or even beyond it. A common error is to regard the pulsation as due to the apex, but it is invariably caused by some portion of the right chambers, usually the ventricle. Even in the most extensive effusion the apex is probably never pushed beyond the right border of the sternum, and the relative position of apex and base is not changed. This I have carefully noted in several autopsies.⁶

⁶ Fig. 76 of Sibson's article on "Displacements of the Heart" in Reynolds's System of Medicine gives an incorrect idea of the position of the organ in these cases, as the apex is represented as beating beneath the right nipple.

In the gradual absorption of a pleuritic effusion, serous or purulent, the heart may not only regain its normal position, but is in many instances drawn toward the affected side by the contracting false membranes.

Of conditions of the mediastinum producing displacement, two only need be mentioned—aneurism and tumor. Very large aneurisms of the arch usually press the heart downward, and its axis may be transverse; but much depends on the direction of growth, and a slight lateral and downward dislocation is most frequently met with. Tumors do not necessarily cause displacement, but when large there may be some dislocation in the direction of the growth of the mass. Most extensive masses of mediastinal cancer may occur without any disturbance of the position of the heart.

Diseases of the abdominal viscera not uncommonly produce dislocation of the heart, generally upward. Extensive peritoneal effusion, gaseous or fluid, forces up the diaphragm, and with it the heart, which may assume the transverse position, and the apex beat as high as the third interspace. Gas much more readily than fluid rapidly lifts the diaphragm and produces upward dislocation of the heart. Diaphragmatic hernia of intestines or stomach may push the heart up or to one side.

Conditions of the liver not infrequently affect the position of the heart. Abscess or hydatid cysts of the left lobe may push the organ up and to the left. More rarely large hepatic tumors drag the diaphragm down, and with it the heart. Very great splenic enlargement, as in leukæmia, may push up the diaphragm and lift the heart.

Other abdominal growths, as large retro-peritoneal and ovarian tumors or aneurism of the abdominal aorta, may occasionally produce the same effect. Knowsley Thornton has given in Fothergill's work on the Heart an excellent account of the upward displacement of the heart in ovarian disease.

As a very rare circumstance, the heart is displaced by accidental injury to the chest-walls. The case which Stokes relates of this kind was probably, as he subsequently suggested, due rather to the effects of the pleuritic effusion which followed the accident.

The dislocations of the heart when gradually induced rarely disturb to any serious extent the functions of the organ.

Myocarditis.

Inflammation of the heart-muscle is rarely primary; usually it is associated with endo- or pericarditis, strain,⁷ embolic processes, disease of the arteries, or the presence of certain poisons—diphtheritic, rheumatic, etc.—in the blood.

⁷ Some French writers refer specially to the occurrence of myocarditis from strain or prolonged muscular exercise—myocardite des surmenes. Peter (Maladies du Coeur, Paris, 1883) gives two cases (without autopsy), and quotes a case from Revilliod, whose work (La Fatigue, Lausanne, 1880) I have not been able to consult.

We may recognize three forms—acute suppurative, acute interstitial, and chronic myocarditis. By many writers the parenchymatous degeneration so frequent in fevers is regarded as an inflammation, but it is the result of a process which we can scarcely term inflammatory.

Acute suppurative myocarditis is almost invariably associated with pyæmia or with malignant endocarditis, and in most instances may be regarded as embolic. In severe pyæmia from any cause foci of suppuration are not infrequently met with in the walls of the ventricles. There may be multiple abscesses or a single purulent collection varying in size from a pea to a walnut. Numerous miliary abscesses are not so often met with in ordinary pyæmia as in endocarditis. If large, the abscess may burst into the heart or into the pericardium and excite inflammation of this membrane; or, indeed, without perforation, as I saw in one instance. The calcareous nodules occasionally found in the muscle-substance have been regarded as healed abscesses. Suppurative myocarditis is a frequent result of malignant endocarditis, and we meet with it either in the form of miliary abscesses, scattered in numbers through the substance, or as large solitary abscesses at the bases of vegetative outgrowths or in connection with excavating ulcers of the endocardium, valvular or mural. The small embolic abscesses vary in size from a pin's head to a pea, and may occur in extraordinary numbers in the muscle-substance of all the chambers. They present usually a central grayish-white focus of suppuration surrounded by a zone of deeply-congested and hemorrhagic tissue. Microscopically, there is a central infiltration of leucocytes with destruction of the muscle-fibres, and in every instance colonies of micrococci can be readily discovered. These abscesses are identical in character with those occurring in the kidneys, intestines, and brain. Sometimes at the base of large endocardial outgrowths, particularly of the aortic segments, abscesses are found extending deep into the muscle-substance, and even perforating the wall. These occur most often in the left ventricle, but occasionally in the right, as in a case of stenosis of the pulmonary valves at the Montreal General Hospital, in which there was an abscess cavity in the wall of the right ventricle the size of a marble, situated at the base of some endocardial vegetations. The acute ulcer of the heart is of the nature of a suppurative myocarditis, having its starting-point, in the great majority of cases, in the endocardium. It may perforate the wall of the ventricle, as in the cases of Mackenzie⁸ and Keating.⁹ The blood-pressure in the abscess-cavity may dilate the wall, and form what is known as acute aneurism of the heart.

⁸ Path. Soc. Trans. London, xxxiii.

⁹ Trans. of the College of Physicians of Philadelphia, 1879.

Acute interstitial myocarditis occurs in connection with the infectious fevers, and also with pericarditis, more rarely endocarditis. It is characterized by the presence of numerous round cells in the interfibrillar tissue, multiplication of the corpuscles, and degeneration, granular or fatty, of the muscle-fibres. The coarse appearances are—a relaxed state of the cardiac walls, pale or turbid condition of substance, in extreme instances a sodden, soft friable state, so that the muscle readily tears on pressure. In acute pericarditis the superficial myocardium, for a line or two beneath the membrane, frequently presents this condition in a typical manner; it looks pale and turbid, contrasting strongly with the deeper parts, and on examination presents infiltration of leucocytes, swelling of the interstitial tissue, sometimes effusion of blood-corpuscles, and a swollen, granular, or fatty state of the muscle-fibres. Although the process may be intense, suppuration rarely occurs, whereas in myocarditis supervening upon inflammation of the endocardium it is, as we have seen, not uncommon. A similar diffuse interstitial process is met with in many of the fevers. In rheumatism, typhus, scarlet fever, small-pox, and diphtheria the myocardium may be found relaxed and soft, the chambers dilated, the substance pale, easily torn, in some instances extremely soft; and this condition has been variously described as inflammatory or degenerative. While not denying that such a state of the muscle-fibre may be brought about by the action of the fever or the influence of some specific poison without any signs of inflammatory action, yet in other instances changes have been found which are evidently of the nature of a myocarditis. In these cases the intermuscular connective tissue is swollen, infiltrated with round cells and nuclei, the vessels are dilated, and often there are minute extravasations and the muscle-fibres are granular and fatty, with indistinct striæ and nuclei. As Leyden¹⁰ has pointed out, this condition probably affords an explanation of some of the cases of sudden death in diphtheria. It may occur without the coarse or microscopic appearance of degeneration of the muscle-fibres, and when of any duration may produce areas of atrophy. Though usually diffuse, it may be patchy and limited in distribution. Martin¹¹ has described in cases of sudden death in diphtheria and typhoid fever an acute endarteritis of the small branches of the coronary arteries, which probably has a close relationship with this acute interstitial myocarditis.

¹⁰ Zeitschrift für klinische Medicin, Bd. iv.

¹¹ Revue de Médecine, 1881.

The SYMPTOMS of acute myocarditis are those of cardiac weakness and irritability, and it is the conditions under which these occur which make us suspect involvement of the myocardium rather than any special features pertaining to the disease. We may reasonably suspect its presence in a case of rheumatism, puerperal fever, or other specific fever when the patient complains of cardiac distress or actual pain, with shortness of breath, and on examination we find a weakened impulse, feeble, indistinct first sound, and a small, irregular pulse. The area of heart-dulness is increased, and there may be a murmur due to muscular incompetence. There is usually fever, but this is generally due to the primary affection. The symptoms are those of a weak and dilated heart, and are peculiar only in the mode of onset and the circumstances under which they arise. A point of note observed by Stokes is the weakening or disappearance of organic murmurs during an attack of acute myocarditis. In acute pericarditis grave implication of the myocardium may be suspected when the pulse gets small and rapid, dyspnoea urgent, and the cardiac pain is increased. Such symptoms, in the absence of copious effusion, would appear to indicate extension of the inflammation to the heart-muscle. Even the occurrence of suppuration has no distinctive symptoms, as it almost invariably occurs as part of a pyæmic process, and the cardiac weakness which supervenes may be regarded as an outcome of the septic or febrile condition. The bursting of an abscess into the pericardium will excite violent pericarditis. In the case of Kortüm, referred to by Friedrich,¹² an abscess in the septum burst into the ventricle; the symptoms, which developed suddenly during a lecture, were a sense of constriction in the chest, dyspnoea, and lividity, and death occurred in six hours.

¹² Virchow's Handbuch, Bd. v.: "Herzkrankheiten," S. 275.

The DIAGNOSIS can rarely be made with certainty; at the best we can suspect its presence under the conditions above mentioned.

The course of suppurative myocarditis is always unfavorable, but the fatal termination of the case is usually dependent on concomitant causes. The possibility of recovery in some instances of abscess of the heart is suggested by the occurrence of caseous and cretaceous masses, probably the remnants of collections of pus.

The chief danger in interstitial myocarditis is heart paralysis and sudden death, as occur in diphtheria and occasionally in rheumatism. From mild grades of the disease recovery may take place, and even when general and severe it has often been some indiscretion which has induced the collapse, as sudden sitting up in bed or getting out to attend to the calls of nature. Possibly the slight intramuscular scars and spots of atrophy furnish evidence of past acute myocarditis.

When suspected, the TREATMENT should consist of absolute rest, muscular and mental, with careful feeding and stimulation. If a rheumatic case upon the alkaline or salicylate treatment, the remedies should be stopped. I saw sudden death from heart failure in a case of acute rheumatism in which during four days the full alkaline treatment of Fuller was followed, and in which, by mistake, a much larger quantity of the bicarbonate of soda was given each day than had been intended. Strychnia and small doses of quinine may be given. Shall digitalis be employed in acute myocarditis? Upon this point authorities differ. If we regard it as simply increasing the force of the muscular contractions, we can understand the fear of straining a weakened heart; but digitalis has important trophic influences, and, while it stimulates the vigor of the contraction, improves the nutrition of the heart-muscle and renders it better able to contract. After all, the question amounts to the giving of digitalis in dilatation, and with a weak first sound and feeble action the careful administration, in conjunction with stimulants, will be found beneficial. Peter¹³ speaks highly of the application of a blister in the region of the heart.

¹³ Loc. cit.

Chronic Myocarditis (Fibroid Heart).

A condition characterized by the substitution in areas of variable extent of a fibrous connective tissue for the muscular substance. It is an interstitial growth, comparable to the cirrhosis of other organs, and the muscle-elements in the affected regions are wasted or entirely destroyed. The process may occur in a mild grade throughout the organ, but it is more common to find it distributed in certain parts which seem specially prone to this form of degeneration.

The conditions under which it is most likely to occur are those which we find in connection with arterio-sclerosis. It is an affection of adult and advanced life, and is met with most frequently associated with disease of the coronary arteries. In chronic valvular affections it is very common, and may be part of the so-called cyanotic induration or an extension from the thickened endocardium. Sometimes it seems a part of a general arterio-capillary fibrosis. In a few cases there is direct extension from the pericardium. Rheumatism is in this way indirectly responsible; possibly some of the cases are directly traceable to acute interstitial myocarditis occurring in this disease. Chronic alcoholism, syphilis, and gout are prominent factors in the etiology. Some of the most marked cases give no clue in the history or habits of any conditions which we could reasonably connect with the disease. Males are more often affected than females. The tendency to arterio-sclerosis seems to run in some families. Mental anxiety is not without influence, and when the disease is established seems very liable to bring on the anginoid attacks. The situation and extent of the fibrosis are very variable. The papillary muscles and the columnæ carneæ of the left ventricle are most frequently affected, less often the corresponding structures on the right side. The middle portion of the muscular bundles and the apices of the papillæ are first involved. In the latter the process may extend almost to their bases, but on section it will be found that it is more advanced in the superficial than the deep parts. This change is very common in cases of valvular disease with hypertrophy, especially mitral stenosis, but it often occurs in elderly persons who have had no special heart symptoms.

Beneath patches of pearly-white thickened endocardium local fibrosis may occur, often seen at the upper part of the septum in left ventricle, and in the dilated and thickened left auricle of mitral stenosis, and occasionally in other parts. This is usually regarded as an extension from a chronic endocarditis. More rarely the fibrosis extends from a thickened pericardium, but cases are on record of the conversion of the outer layers of the muscular fibres into a firm, hard tissue. We frequently meet with scattered areas of fibrosis in septum and ventricular walls without any implication of peri- or endocardium. During foetal life an endo-myocarditis may occur in the conus of the right ventricle, less frequently in the left, and produce very great narrowing by the gradual contraction of the newly-formed tissue. But the condition to which the term fibroid heart can be most properly given is an extensive affection of the left ventricle, involving most commonly the anterior wall near and at the apex and the lower part of the septum. In these cases there may be marked bulging at the apex, and on section the wall cuts with great resistance, and a dense fibrous tissue of a grayish-white appearance occupies the position of the myocardium. In extreme cases a large part of the septum and anterior wall is in this state, and may present only traces of muscular tissue. There is usually thinning, sometimes thickening, of the affected portions, and the septum bulges toward the right ventricle. The endocardium is opaque, often much thickened, and directly continuous with the fibrous tissue. The columnæ carneæ may be narrow and flattened, and the lacunæ between them very small. The chamber is usually dilated. The upper third of the septum and the base and posterior wall of the ventricle in such cases present a marked contrast to the affected parts, and may look natural, but more commonly are hypertrophied. The other chambers may not show any special change or there may be scattered areas of fibrosis. The thinning and dilatation at the apex and septum are the conditions which precede and lead to the formation of cardiac aneurism. The valves may be normal, but in many cases there is sclerotic endocarditis and retraction. The histological appearance varies much with the stage of the process. When early or where advancing, the muscle-bundles are seen separated by round and elongated cells. The process is usually more marked about groups of fibres, which gradually become isolated by the increase of the growth, and in this way one often sees streaks or patches of muscle-tissue surrounded by the fibrous elements. The destruction of the muscle-cells is apparently by pressure; they gradually waste and present the condition of brown atrophy, the pigment of which remains and indicates the position of the fibres. The intimate pathology of the process is of great interest. Doubtless in some instances we may attribute the fibrosis to an extension of an indurative process from the endo- or pericardium, but the researches of Tautain,¹⁴ Martin,¹⁵ Huber (Karl),¹⁶ and others have thrown a new light on the subject, and it seems probable that in most instances the fibroid degeneration is associated with changes in the coronary arteries. The former describes an endarteritis and a periarteritis of the small vessels, leading to disturbance of nutrition and increase of the connective tissue (sclérose dystrophique). Huber in a considerable number of cases has traced the connection between the arterio-sclerosis, chiefly of the smaller twigs, and the indurative process. The region supplied by the obliterated arteriole is in the condition of an infarct and undergoes an anæmic necrosis, and subsequently by a proliferating myocarditis is transformed into a fibroid area. The condition is well described and figured by Ziegler.¹⁷ Why this obliterating endarteritis should be so limited in the majority of cases to the vessels of the left ventricle is not very clear. The parts most distant from the aorta seem most liable to the process, as the apex and the tips of the papillæ; and it is interesting in this connection to note that the left coronary artery is more frequently diseased than the right.

¹⁴ Thèse de Paris, 1878.

¹⁵ Revue de Medicine, 1883.

¹⁶ Virchow's Archiv, Bd. lxxxix.

¹⁷ Pathologische Anatomie, Lief. ii., 1884.

In the milder grades of fibrous myocarditis, when only the apices of the papillæ and thin layers beneath the endocardium are involved, the heart does not appear to be seriously affected; but when of any extent the vigor and force of the contractions are impaired, and the ventricle is unable to do the work of a healthy muscle. Compensatory hypertrophy is not readily established, possibly on account of the arterial sclerosis on which many of the cases seem to depend, although in rare instances, as in a specimen referred to by Quain,¹⁸ there may be very great muscular hypertrophy. Dilatation of the left ventricle is much more apt to follow, as the fibroid walls have not the resisting power of muscular tissue, and the patients finally present a clinical picture of heart failure. The gradual yielding of the fibroid region may result in aneurism.

¹⁸ "Lumleian Lectures," Lancet, 1872, i.

There are no characteristic symptoms to indicate the condition. The fibroid heart is a weak heart, and it is scarcely possible to distinguish it from fatty degeneration. A feeble, irregular, sometimes slow, pulse, dyspnoea on exertion, and painful anginoid attacks—symptoms which may have persisted for many years—are special clinical features in many cases. In a patient I examined some years ago for Palmer Howard of Montreal—a typical instance of the condition under consideration—the first symptoms began eight years before death with angina, and there were repeated attacks of cardiac asthma. A careful study of the case was made by Howard¹⁹ extending over several years, and weak heart, dyspnoea on exertion, and anginoid attacks were the prominent symptoms.

¹⁹ "Fibroid Disease of the Heart," Canada Med. and Surgical Journal, vol. viii., 1880.

Several very careful studies of the disease have been made within the past few years.²⁰ Among the symptoms the following may be specially considered. The first place seems accorded by all to the cardiac weakness, and in consequence the pulse is feeble. By some (Rühle) irregularity is regarded as a special feature (delirium cordis), but Ebstein refers to three cases in which the pulse was always regular. Juhel-Renoy also speaks of it as frequent and regular. In many cases the number of beats appears about normal; in others there is a great increase; while in a third set the pulse may be very slow, sinking to 40 or 50 per minute. It is evident that in regard to regularity and frequency of the pulse there are very great differences. In this connection it is interesting to refer to the case of thrombosis of the coronary artery reported by Hammer,²¹ in which the pulse sank to 8 per minute.

²⁰ Rühle, "Zur Diagnose der Myocarditis," Deutsches Archiv f. klin. Med., Bd. xxii.; Ebstein, Zeitschrift für klinische Medicin, Bd. vi.; Leyden, Ibid., Bd. viii.—a most important and exhaustive article; Welch, in a paper read before the Medical Section of the American Medical Association, Washington Meeting, 1884; Juhel-Renoy, Archives gén. de Médecine, Juillet, 1883.

²¹ Wiener Med. Wochenschrift, 1878, No. 5.

Angina is a most important symptom; attacks may recur for years, and death may take place in a paroxysm. Asthmatic attacks are very common: a feeling of impending suffocation, and gasping for breath amounting in some instances to urgent dyspnoea. Oedema of the lungs may occur in these attacks. Fainting and pseudo-apoplectic attacks are frequent symptoms. The physical signs are not very definite or constant. The apex-beat may be displaced and weak, perhaps unrecognizable. With an increase in the area of dulness this is a sign of dilatation. A systolic murmur at the apex is not infrequent. There may be the bruit de galop; gradual heart failure, with general dropsy, is the mode of termination in a considerable number of cases.

The DIAGNOSIS can rarely be made with certainty. The combination of weakened heart, atheromatous arteries, and angina attacks occurring in a person above fifty years of age is certainly suggestive of the existence of this condition; but, as will be seen, this group of symptoms occurs also in fatty degeneration, although the anginoid attacks are probably not so frequent.

In spite of the admirable clinical memoirs above referred to, we are still in need of careful studies of an extensive series of cases, whereby we can get information which will enable us to distinguish more clearly than we can at present the diseases of the myocardium from one another. In this respect our pathological knowledge is in advance of our clinical.

The TREATMENT is largely that of cardiac dilatation and angina, which will be elsewhere considered. The condition is a chronic one, and often associated with hypertrophy, and many of the symptoms are dependent upon failing compensation. Under such circumstances digitalis is indicated, but when there are attacks of angina caution must be exercised in its use.

The Degenerations of the Heart-Muscle.

Under this division we shall consider the following conditions, all of which are characterized by an alteration in the quality and an impairment of function in the affected tissue: 1. Anæmic necrosis; 2. Parenchymatous degeneration; 3. Fatty changes, infiltration and degeneration; 4. Brown atrophy; 5. Amyloid degeneration; 6. Hyaline degeneration; and 7. Calcareous degeneration.

1. Anæmic necrosis is a condition which results in the heart-muscle when a branch of the coronary artery is blocked either by a thrombus or an embolus, or is obliterated by a progressive sclerosis. The region supplied by the affected vessel is deprived of blood and undergoes a process of infarction. In some instances the tissue is not infiltrated with blood, as in an ordinary infarct, but has a pale yellowish color and is very soft. When there is extravasation the color is more reddish-brown. Histologically, the muscle-cells are found in a state of granular degeneration, and on staining the nuclei do not take the tint, and the whole tissue ultimately assumes the homogeneous granular aspect of coagulation necrosis. There may be fatty degeneration in the contiguous muscle-fibres, and finally, as with infarcts in other organs, fibroid induration takes place. This process, as before mentioned, plays an important part in the production of the fibroid patches scattered through the myocardium. When fresh, the softening of the affected region may be marked, and the name myomalacia cordis which Ziegler²² has suggested is so far suitable, but it seems more appropriately applied to that condition of general softening of the organ met with in severe fevers. This process most frequently affects the left ventricle, and if extensive may lead to rupture.

²² Loc. cit.

The clinical aspects of this condition, as induced by sclerosis of the coronary arteries, have been recently studied with great care by Leyden.²³ In acute cases death occurs in a few hours with symptoms of intense angina pectoris and heart failure. The subacute cases are characterized by recurring anginoid attacks lasting from a few minutes to half an hour. There may be attacks of asthma with heart weakness, and signs of oedema of the lungs. The clinical picture is that of angina pectoris, and the patient may have had similar attacks on previous occasions.

²³ Zeitschrift f. klin. Med., Bd. vii., 1884.

2. Parenchymatous Degeneration.—The relation of inflammation of the heart-substance to this degeneration is still somewhat indefinite. I have under Myocarditis described an acute interstitial form characterized by inter-fibrillar swelling with exudation and proliferation of corpuscles, and often granular or fatty degeneration of the muscle-cells. These changes may certainly be regarded as inflammatory, and they are met with either in association with endo- or pericarditis or in connection with specific fevers. Under the term parenchymatous degeneration or cloudy swelling Virchow described²⁴ a change of frequent occurrence in the heart-muscle and elsewhere, which I think should be distinguished from myositis, although the two processes may lead to alterations difficult to distinguish macroscopically. It is characterized by a pale, turbid state of the cardiac muscle, general, not limited, and a relaxed, soft, brittle condition of the walls. The turbidity and softness are the special features; there are no peri- or endocardial changes—simply the loss of color and consistence. It is the softened heart of Laennec and of Louis; and Stokes speaks of an instance in which "so great was the softening of the organ that when the heart was grasped by the great vessels and held with the apex pointing upward, it fell down over the hand, covering it like the cap of a large mushroom."²⁵ Microscopically, the fibres are indistinct, the protoplasm occupied by fine granules which obscure the striæ, and sometimes the nuclei. Proliferative changes rarely occur, although swelling and multiplication of the nuclei and the interstitial cells have been described. The granules may be extremely minute, or so large that they are mistaken for fat. They are generally uniform in size, and are scattered irregularly through the fibres. In extreme grades the entire fibre may be occupied by them, and no trace of structure can be seen. Dilute acids and alkalies dissolve the granules, but they resist the action of ether, indicating their albuminous nature. This condition is met with in the infectious diseases—typhoid, typhus, small-pox, pyæmia, remittent fever, etc.—particularly when the disease is protracted and the temperature high. Apparently, we must regard it as an expression of the effect of the poison upon the metabolism of the fibres, inducing a separation of albuminous particles in a granular form. That the high temperature alone does not produce it is demonstrated by its absence in many other diseases in which this condition prevails. The relation to fatty degeneration is not clear. It would appear to precede the development of this change.

²⁴ Archiv, vi.

²⁵ Diseases of the Heart, Am. ed., p. 373.

The effect of this degeneration is virtually the same as that of myocarditis, already described. It produces the weak heart of fever so well described by Stokes,²⁶ with indistinct impulse, feeble or imperceptible first sound, and progressive diminution of contractile power. There is often a great reduction in the number of beats, which may sink to 40 or 50 per minute. In severe cases of typhoid fever we often have an opportunity of studying the progressive enfeeblement of the heart with weakening or disappearance of the first sound.

²⁶ Loc. cit., chap. vii.

To Stokes we are indebted for the suggestion of the use of alcohol in this condition, and the experience of the past forty years has fully confirmed this practice of the Dublin school.

3. Fatty Heart.—Two conditions of the heart are recognized under this heading—viz. fatty infiltration and fatty degeneration.

Fatty Infiltration.—Cor adiposum, Lipomatosis cordis, and Fatty hypertrophy or overgrowth are synonyms found in the older and more recent works.

A condition in which there is an excess of fat beneath the pericardium and a growth of the same between the fibres of the myocardium. There is normally a certain amount of fat in the cardiac groves, particularly the auriculo-ventricular, and along the coronary arteries. An excess is not infrequently met with in connection with general atrophy, whether the result of disease or the natural decay of old age. Here it serves as padding, and has no pathological significance. In very corpulent persons there is always much subpericardial fat; it forms a part of the general obesity, and in this state an excessive accumulation may lead to a dangerous or even fatal impairment of the contractile power of the heart. Obesity is the expression of a morbid tendency, generally hereditary, to the deposition of fat in the connective tissues. A sedentary life and the consumption of food rich in carbohydrates favor this tendency, but we see it arise under conditions just the opposite when the predisposition to polysarcia is marked. Males are more usually affected than females, at least in Great Britain and Germany.

In the inspection of the bodies of very corpulent persons we find the mediastinum occupied by masses of fat which may completely cover the pericardium. The entire heart may be enveloped in a thick sheeting of fat, through which not a trace of muscle-substance can be seen. Along the groves, the regions of normal deposit, the layer may be an inch or more in diameter. In some cases the muscle-substance beneath seems but slightly involved; there may be superficial infiltration and penetration of columns of fat between the bundles, but the thickness of musculature is normal, and apart from the excessive deposition there is not much amiss. In other instances the muscle-substance is seriously affected; on section of the ventricular wall the fat is seen to infiltrate the entire muscle, separating strands of fibres and reaching almost to the endocardium. There may be places, indeed, in the thinner parts of the ventricular walls in which there appears to be complete substitution of the muscle by fat. Even the papillary bundles may contain adipose tissue. The chambers are usually dilated and the entire organ soft and relaxed. Microscopically, the fat-cells are everywhere seen infiltrating the muscle-tissue, separating the fibres and inducing atrophy. In some cases, even when the condition is advanced, the muscle-fibres appear normal, but in the majority fatty degeneration is also present. Often in these cases the coronary vessels will be found atheromatous.

The SYMPTOMS of fatty overgrowth will depend greatly on the degree of infiltration, the state of the muscle-fibres—whether normal or degenerated—and on the presence or absence of coronary atheroma. Many very fat persons enjoy excellent health and have actively beating hearts, which fail them only on severe exertion, when they get out of wind and experience cardiac distress, perhaps palpitation. The pulse is good and the heart sounds are clear. The signs of heart failure (which may be due either to excessive infiltration or secondary degeneration of the muscle, or both combined) in obese persons are generally very marked—breathlessness on slight exertion, amounting oftentimes to dyspnoea; attacks of asthma of a distressing nature coming on without cause or after a full meal; cough, with or without bronchitis; dizziness and pseudo-apoplectic attacks. Sudden death from syncope or rupture of the heart is common. Dropsical symptoms and cyanosis may supervene. The physical signs are those of heart weakness; impulse imperceptible or very diffuse; area of dulness increased, but often hard to delimit, with fat chest-walls and fatty mediastinum; sometimes a soft systolic murmur at apex; radial pulse rapid, weak, and irregular, in some instances very slow.

The DIAGNOSIS of the condition with such a series of symptoms in an excessively stout person can offer but little difficulty.

The TREATMENT in the early stage should be directed to reducing the general obesity, and such persons should be warned against taking too violent exertion or subjecting the heart to unusual strain. Moderate exercise, mental quietude, and careful dieting may do much toward postponing heart failure, which, when established, calls for the treatment which shall be described under Dilatation.

Fatty Degeneration.—An anomaly or disturbance of nutrition in which minute particles of fat accumulate in the protoplasm of the muscle-fibres, and impair the functional activity of the organ.

This is one of the most common of post-mortem conditions, and in mild grades is met with in a great variety of diseases. The fat is a product of the metabolism of the protoplasm of the muscle-fibres, and in a normal state it (or its immediate antecedents) is oxidized; but when either there is increased transformation or reduced oxidation the products accumulate in the protoplasm, and are evident as minute molecules or as distinct fine oil-droplets. The condition of cloudy swelling or parenchymatous degeneration appears in many cases to precede that of fatty degeneration, and sometimes the granules are of such a size, so abundant, and resemble fat so closely that chemical tests alone can distinguish between them.

A practical division of fatty degeneration is into—1, cases in which the process has attacked a normal heart; and 2, cases in which we find it associated with valvular disease and hypertrophic states of the muscular walls.

In the first group we have (a) The degeneration which accompanies the failing nutrition of old age, of wasting diseases, and of cachectic states. (b) The fatty change in the heart-muscle so often a sequence to, or coexisting with, the parenchymatous degeneration of fevers. (c) The extreme fatty degeneration so constantly associated with profound anæmia. (d) Certain poisons, particularly phosphorus; arsenic, lead, and antimony also act in the same way. The slow poisoning by alcohol is a very frequent cause of a gradually fatty degeneration of the heart. And (e) some local causes are important in inducing this change in the previously normal organ. Pericarditis is almost invariably associated with involvement of the superficial myocardium, either inflammatory or degenerative. Disease of the coronary arteries is a frequent and important cause of fatty metamorphosis. When due to the general conditions above mentioned, the affection is widely distributed in the organ; when the result of gradual narrowing of the vessels by atheroma, the distribution is in the regions supplied by the affected vessels.

The second group comprises those cases in which the fatty degeneration involves the muscle-substance in a condition of hypertrophy, and is an important element in inducing the disturbance of compensation upon which so many heart symptoms depend. Here the process may be more local, affecting, for example, the left ventricle chiefly, as in the hypertrophy from aortic valve disease or in association with contracted kidneys, or the right ventricle in chronic lung affections and mitral stenosis. More rarely we find the process confined chiefly to the auricles, but there may be advanced changes of this nature in the hypertrophied left auricle in mitral stenosis. The fatty degeneration of an hypertrophied heart may be induced by any of the general causes above referred to, but there are also special ones to which it is liable. The chronic congestion which accompanies a dilated heart affects the walls of the organ as well, and diminishes the vigor of the coronary circulation. In emphysema and in mitral stenosis, and other diseases which induce a dilated state of the right heart, fatty degeneration, sometimes combined with fibroid change, is, as Jenner pointed out,²⁷ very common. This state of the right chambers also interferes with the proper oxygenation of the blood in the lungs, and so acts in a double way. Degenerative changes in the coronary arteries are specially prone to accompany valvular diseases, on which the majority of cases of hypertrophy depend, and we have here one of the most serious causes of fatty degeneration in this state. And, finally, we see this change in some hypertrophied hearts without being able to ascertain any exciting cause: a nutritive breakdown occurs, of which the fatty degeneration is the expression. Possibly in such cases the trophic nerve-influences may be at fault.

²⁷ Medico-Chirurgical Transactions, xliii.

Defective oxidation, in whatever way brought about, seems the common factor in all forms of fatty degeneration. The process may be almost confined to the heart or be more or less general in the solid viscera and voluntary muscles. The diaphragm is sometimes much involved with the heart, even when the other muscles show no signs of the change. There certainly seems to be a special proneness to fatty degeneration in the heart-muscle which may perhaps be associated with its incessant activity. So great is the need of an abundant oxygen-supply that it early feels any deficiency, and in consequence is the first muscle to show nutritional changes.

Fatty degeneration is met with at all ages. I have seen it in the hypertrophied right ventricle of a new-born infant, with stenosis of the pulmonary artery. The cases dependent upon vascular changes are most frequent after middle life. Males appear more frequently affected than females. The form associated with anæmia is an exception to this rule. Stout persons are not more liable to be affected than thin ones; indeed, it is often, to use Paget's phrase, "a lean degeneration." Sedentary habits, worry, grief, and other depressing emotions are believed by some to have a predisposing influence. Persons with gouty and arthritic tendencies are more prone to this change.

The anatomical condition is very characteristic even to the naked eye, and the microscope may be required only in corroboration. It may be local or general. In the former case the left ventricle is most frequently affected, the right ventricle more rarely, and the auricles very seldom. The amount of subpericardial fat may be slight. If the process is advanced and in all the chambers, the heart looks large and is flabby and relaxed. It is pale, of a light yellow-brown tint, buff color, or, as it is sometimes expressed, a faded-leaf color. The consistence is greatly diminished, and the substance tears easily and the finger can be readily thrust through the wall. Extreme grades are met with in profound anæmia and in phosphorus-poisoning. The fatty degeneration of coronary disease and of valvular affections is usually more local, and the heart has often a brownish-yellow tint from the coexistence of brown atrophy. In the left ventricle the papillary columns and the layers of muscle just beneath the endocardium are most affected, and in a curious streaked or patchy way—the tabby mottling of some authors. A similar change may be seen in the right ventricle, particularly in the hypertrophy from mitral disease. In the auricles the right may show patches on the musculi pectinati, but on the left, which is most often affected, the thick endocardium usually obscures it. Chemically, it has been shown that in fatty degeneration the heart may contain from 3 to 5 per cent. more fat than normal.

On microscopical examination of teased portions of the muscle the fibres are broken and irregular, and there is much free fat, in form of droplets, among them. The appearance of the fibres will vary with the intensity of the process; in mild grades there are minute scattered droplets in the protoplasm, not obscuring the nuclei or the striæ; but in an advanced condition the fibres seem occupied completely with minute globules, and no trace of structure can be seen. The patchy distribution of the fatty degeneration in many cases, usually evident to the naked eye, is corroborated by the microscope, and one may obtain portions of the muscle with scarcely a normal fibre, while in a contiguous bit the fibres are little if at all affected. In some instances of general fatty degeneration in anæmia, and even in fevers, as diphtheria, the process is so advanced that it is difficult to find any normal-looking fibres. Brown atrophy is a frequent accompaniment of fatty degeneration.

The effect of this change upon the heart is seen in a diminution of its functional power; the contractile force is weakened and the organ rendered incapable of doing its work efficiently. If the change occurs in a previously normal heart, much will depend on the rapidity with which it has supervened. Repeated hemorrhages or poisoning by phosphorus will induce in a few days an extreme degree of weakness rarely seen in the fatty degeneration of chronic anæmia—perhaps equally extensive. As a consequence of the enfeebled action of the heart, the arteries are not well filled during the systole, and there is anæmia of the organs. The mural weakness readily permits of dilatation, with imperfect emptying of the chambers and distension of the venous system. In hypertrophy the failing compensation is frequently due to the onset of fatty degeneration. During a sudden strain or a more continued effort than usual there may be heart failure, asystolism, or the walls may tear and sudden death occur from rupture.

The SYMPTOMS of fatty degeneration of the heart are by no means definite, being those of defective cardiac power. It is often met with post-mortem when not expected, and on the other hand we may fail to find it even when the symptoms seem to point very clearly to its existence. In chronic anæmia, in chlorosis, in fevers and wasting diseases the process may be extreme, without leading to any more marked symptoms than feeble action of the heart, palpitation on exertion or excitement, with signs of slight dilatation, and a soft mitral systolic murmur from incompetency of the valves. In cases of idiopathic anæmia, in which the fatty degeneration is perhaps more marked than in any other condition except phosphorus-poisoning, the pulse is frequently full, though soft, and regular so long as the patient is quiet. The symptoms of fatty degeneration in cases of valvular disease with hypertrophy are simply those of failing compensation, and we see the same process in the non-valvular hypertrophy of chronic Bright's disease. But, apart from these conditions, fatty degeneration occurs as part of a process of general failure of nutrition, premature or senile. These form the cases of idiopathic fatty heart which seem so constantly to be associated with atheromatous changes in the coronary vessels. English writers have dealt specially with this form, which certainly appears to be more prevalent in Great Britain than on this continent or in Europe. In these cases there may be general obesity, but as often the subjects are of spare habit, with full atheromatous arteries, and other indications, perhaps, of early senility. They are usually persons who have lived freely and taken stimulants in excess. Among the symptoms believed to indicate fatty degeneration in these cases are—weak, irregular action of the heart, with a small intermittent pulse; cardiac pain, sometimes anginoid in character; dyspnoea, particularly on exertion, as in ascending an incline; signs of cerebral anæmia, indicated by vertigo or pseudo-apoplectic attacks and loss of mental power; the presence of an arcus senilis; and, as a final symptom, Cheyne-Stokes respiration.

Persistent irregularity in the action of the heart in a person with atheromatous arteries, and dyspnoea on exertion, without signs of valvular affection, are certainly suggestive of degeneration of the muscle-fibres of the heart. In some instances there has been noted a greatly diminished number of beats, 40 or 50 per minute, or even slower. Irregular action of the heart may, however, persist for years without indicating any serious mischief.²⁸ The yellow fatty arcus senilis is believed by many physicians to indicate a weak fatty heart, and it does occur in many persons of soft flabby habit of body with degenerated arteries and evidences of premature decay; but by itself it is of no value as a sign of vascular degeneration. It must not be confounded with the opaque white calcareous arcus not uncommon in elderly people, and met with occasionally in middle-aged persons. The Cheyne-Stokes breathing so often referred to as specially associated with fatty heart is, in my experience, a much more frequent concomitant of uræmic states.

²⁸ In the spring of 1882, I saw, for Geo. W. Campbell, a gentleman aged eighty-two, a man of remarkable vigor, mental and bodily. He had an extraordinarily irregular yet full pulse, with atheromatous arteries—a condition which he assured me had been constantly present for close upon forty years, and had been a source of needless anxiety to many physicians, and for some years to himself.

The physical signs of fatty degeneration of the heart are a weak impulse, often diffuse, and if the patient is thin the area of dulness may be found increased. In stout persons it is difficult to determine dilatation on account of the fat inside and out. The sounds on auscultation are generally weak, distant, and muffled, but in the fatty degeneration of anæmia the first will often be found sharp and distinct, though short and more like the second sound. A soft murmur, systolic in character, is not infrequently heard at the apex, and believed to be due to muscular incompetency.

The DIAGNOSIS is beset with difficulties, and in most cases we have to be content with probabilities, except in the instances due to anæmia, etc. Permanent weakness of impulse and the symptoms it entails, with signs of degeneration of tissue as shown by atheromatous arteries, are the most suggestive features, but even about them there are uncertainties. My own errors and a contemplation of those of several very eminent clinicians, taken in connection with the fact that some of the most typical cases of fatty heart which come under my observation have been instances of sudden death in persons pursuing their avocations, have made me very cautious in the diagnosis of this condition.

The PROGNOSIS depends entirely on the circumstances under which the degeneration has developed. In the weak fatty heart of chlorosis and anæmia, with a return to a normal blood-condition, the nutrition of the heart is improved and its action strengthened. Doubtless many cases of failing compensation are due to it, and a subsidence of the symptoms under rest, digitalis, and careful feeding may simply mean improved nutrition of heart-muscle and disappearance of the fat which clogs its action. Where due to atheromatous changes, no permanent improvement can be expected; and in these cases, particularly if combined with fatty infiltration, rupture or fatal syncope may occur. In not a few of such cases the persons have not complained either to their physicians or friends of cardiac distress. The case of the celebrated Scotch divine, Chalmers, described by Begbie,²⁹ is an illustration of advanced fatty heart with sudden death in a man of extraordinary vigor of mind and body.

²⁹ Contrib. to Pract. Med., 1862.

The TREATMENT should be directed to the removal of the cause when possible, as the anæmia, febrile condition, etc. In all cases rest, quiet, and avoidance of excitement are to be rigidly enforced. Sudden exertions may prove instantly fatal. In the cases where there is hypertrophy with or without valvular disease, and the failing compensation is due to this cause, digitalis acts well, and should be combined with stimulants. In the senile and atheromatous cases great care must be exercised: the bowels should be kept loose, and the patient cautioned not to strain at stool or make any sudden exertion. He should lead a very quiet, regular life, and exercise great moderation in food, drink, and venery. Warm and Turkish baths are most dangerous. Iron, arsenic, and nux vomica are remedies from which benefit may be expected. Digitalis is, as a rule, contraindicated. We must remember that, as Sir William Jenner has remarked, fatty degeneration is sometimes a preservative lesion, and induces a due proportion between the cardiac strength and the arterial resistance, reducing the former when there is great atheroma and brittleness of the vessels. The application of blisters is often of use in allaying the pain, and nitrite of amyl should be given in the anginoid attacks.

4. Brown atrophy is a very common degenerative change in the heart-muscle, particularly in the hypertrophied organ of valve affections. In old people and in persons dead of wasting diseases it seems invariably present. When advanced, the color of the muscle is quite distinctive—a dark red-brown and the consistence may be greater than normal. Microscopically, the fibres present a central accumulation of brown pigment, generally arranged about the nuclei and extending up and down the cells. The cement-substance between the cells is often unusually distinct in these cases, and seems more fragile than in healthy muscle. The composition of the pigment has not, so far as I know, been determined, but it is doubtless, like that of the brown induration of the lung and red atrophy of the liver, derived from the hæmoglobin, and possibly, as in these latter conditions, is connected with feeble venous circulation.

5. Amyloid degeneration of the heart is occasionally met with, but rarely in so advanced a grade as to be recognizable macroscopically. It occurs in the intermuscular connective tissue and in the blood-vessels, not in the fibres, and occasionally may be extensive, as in a case mentioned by Ziegler.³⁰

³⁰ Pathologische anatomie, 3te Aufl., Lief. i., §59.

6. The hyaline degeneration of Zenker is sometimes seen in the heart-muscle in cases of prolonged fever. The affected fibres are swollen, homogeneous, translucent, and the striæ very faint or entirely absent.

7. Calcareous degeneration may occur in the myocardium, involving the fibres and forming a definite calcareous infiltration of the protoplasm, as well figured and described by Coats.³¹ It is a rare condition, whereas extensive calcified plates in endo- and pericardium are by no means uncommon.

³¹ Pathology, 1883.

Spontaneous Rupture of the Heart.

Laceration of the wall of the heart is usually associated with fatty infiltration or degeneration, most frequently the latter. It is doubtful if in any instance the healthy muscle has broken. Rare causes are—acute softening, in consequence of embolism of a branch of a coronary artery; abscess from pyæmia; or an acute ulcer of the endocardium. Cysts simple or hydatid are mentioned, but the extreme rarity of causes other than fatty changes may be inferred from the statistics of Quain,³² who states that of 100 cases of rupture collected by him, fatty degeneration was noted (microscopically) in 77, and in the others there was softening in all but 2, or no mention was made of the condition of the wall.

³² Loc. cit.

Males are more frequently the subject of this accident than females, and the great majority of cases occur in persons over sixty years of age—two-thirds of the eases tabulated by Quain.³³

³³ Loc. cit.

The rent may occur in any of the chambers, but the most frequent site is the left ventricle on the anterior wall, not far from the septum. Statistics give, for 55 cases,³⁴ 43 in left ventricle, 7 in right ventricle, and 3 in right auricle and 2 in the left auricle.

³⁴ Elleaumé, Essai sur les Ruptures du Coeur, Paris, 1857.

The break is generally a ragged, irregular rent in the course of the fibres, and the trajét may be oblique and crossed by strands of muscle. The internal orifice may be larger than the external; the opposite is rarely the case. Two or more rents have been found. Usually the fissure is not very long—from a quarter of an inch to an inch—but there are cases of long rents extending from base to apex. Clots usually block the orifices, and the pericardium also contains large coagula. Evidence is sometimes found to indicate that the tear has occurred slowly, as attempts at repair may be present.

The wall in the vicinity of the break has usually been found in a state of degeneration, and we can readily understand how sudden and violent contractions might strain a weak part and tear the substance. Perhaps irregularity in the contractions may be an important factor, such as we may suppose occurs when a wave of contraction reaches a patch of advanced fatty change or softening from embolism.

The accident usually takes place during exertion or excitement. Many cases are reported during straining at stool, others while lifting weights, running, or during coitus. Cases are mentioned as occurring during sleep or while at rest.

There may be no preliminary symptoms, and without warning the patient falls, and with a few gasps or a cry is dead. This occurred in 71 of the 100 cases collected by Quain. In other instances there is great pain in the præcordial region, a sense of suffocation and anguish, with vomiting, and life may be prolonged several hours. In one instance the patient lived eleven days.³⁵ Probably in such cases there is a small rent at first which gets blocked with clots, and only a small amount of blood oozes into the pericardium with each systole. The symptoms may be those of simple heart failure, as in a case I examined for Burland of Montreal, in which the patient lived thirteen hours after the onset of the symptoms, and was able, though with difficulty, to continue his walk up a rather steep hill.³⁶ Death appears to occur from shock or syncope, sometimes from compression of the heart by the extravasated blood. In the case just mentioned the amount of blood in the pericardium was very much less than I have seen in cases of rupture of an aneurism into this sac.

³⁵ Barth, Archiv. générales, 1871.

³⁶ This was a case which illustrated well the latency of many cases of fatty heart. The patient was an active merchant, aged sixty, who had never complained of cardiac trouble, and had only a short time before his death effected a reinsurance upon his life for a large amount.

In protracted cases the nausea and vomiting may for a short time lead to the supposition that the case is one of severe indigestion, but, as mentioned above, in the great majority of cases death occurs at once, and in the others there can rarely be any question of diagnosis, and still less of treatment.

Atrophy of the Heart.

DEFINITION.—A diminution in size and weight of the organ, due to degeneration and atrophy of the muscular fibres.

The old writers applied the term phthisis of the heart to this condition. The decrease is always in weight, and usually in size; it is doubtful if there is an atrophic and dilated heart in which, with the wasting, the size is maintained by the dilatation. In many of the degenerations, particularly fatty and fibroid, there is local atrophy of the muscle-fibres and yet the weight and size of the organ are not changed.

The varieties which have been recognized correspond to those of hypertrophy—viz. the simple, eccentric, and concentric forms, but the two latter are probably only conditions of contraction or dilatation in a wasted heart. The post-mortem contraction in the small left ventricle of persons dead of chronic disease may be excessive; and here, as in concentric hypertrophy, the examination must be made with care.

ETIOLOGY.—The atrophy is either congenital or acquired. The congenital atrophy which is most frequently seen in women is in association with defective development of the arterial system and the generative organs. This is occasionally very marked in chlorosis, and is described and figured by Virchow in his monograph on this subject.³⁷ But apart from this general hypoplasia of the heart and vessels in women, we sometimes in the post-mortem room find in a man, dead perhaps of an acute disease and without any cardiac symptoms, a heart small out of all proportion to the size and general nourishment of the body. Many of the older writers mention this. Gowers refers to a case which Allan Burns narrates, in which the heart of an adult was not larger than that of a child of six or seven. Morgagni has a similar observation.

³⁷ Ueber die Chlorose, Berlin, 1872.

The great majority of the cases are secondary or acquired, and are met with in the wasting diseases, as cancer, phthisis, prolonged suppuration, and diabetes. The cardiac wasting is part of the general marasmus which affects the whole body. In about half the cases of phthisis the heart is small.³⁸ In cancer of the pylorus the most extreme wasting has been found. Disease of the coronary arteries is an occasional cause, but it most frequently produces local atrophy or degeneration. Compression by pericardial effusion, fatty infiltration, and pericardial adhesions are mentioned as rare causes.

³⁸ Quain, loc. cit.

A rough guess at the proportional size of the heart may be made by comparing it with the closed right fist of the person. Weighing gives the most accurate test, and in each instance regard must be had to the size of the body. In some instances the organ has weighed only two or three ounces. The heart figured by Bramwell,³⁹ one of the smallest on record, weighed only 2 ounces and 2 drachms. Quain⁴⁰ refers to one, from a girl aged fourteen, which weighed only 1 ounce 14 drachms.

³⁹ Diseases of the Heart, 1884.

⁴⁰ Loc. cit.

Usually, in secondary atrophy, the visceral pericardium is wrinkled and the coronary arteries prominent and tortuous—two features of great importance in determining atrophy and in distinguishing between the acquired and congenital forms. The pericardial fat is variable in amount. Microscopically, brown atrophy is the most constant change; fatty degeneration much less common. Senile atrophy may present very similar appearances. The heart may be tough and firm from an increase in the fibrous elements. The pericardial fluid I have often noticed to be much increased.

There are no characteristic SYMPTOMS. The heart-muscle may be able to fulfil the requirements of the wasted frame. A feeble impulse and diminished area of dulness may be present, but in the marasmus of middle-aged or elderly people emphysema of the anterior margin of the lung may seriously interfere with a proper examination. The increased pericardial effusion occurs toward the end. The heart sounds are feeble and the pulse weak. Palpitation is frequent, and there may be the usual signs of anæmia, dizziness, etc.

The condition may be suspected, but is rarely diagnosed during life.

The PROGNOSIS depends upon the disease to which the atrophy is secondary, to the amelioration of which also the treatment must be directed.

Hypertrophy of the Heart.

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 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.

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 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.

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

⁴³ Guy's Hospital Reports, 1836.

The hypertrophy of the left ventricle in connection with contracted kidneys is more frequent and more marked. Traube suggested⁴⁴ 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 hold⁴⁵ 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 Johnson⁴⁶ 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.

⁴⁴ Gesammelte Beiträge, Bd. ii.

⁴⁵ Medico-Chirurgical Transactions, lv., 1872.

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. 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.

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, states⁴⁸ 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.

⁴⁸ Journal of Physiology, iii.

(8) That the heart becomes hypertrophied during pregnancy has been specially insisted upon by French writers, Larcher⁴⁹ 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 Cohnstein⁵¹ connects it with the hydræmic and chlorotic conditions of the blood, so liable to develop during pregnancy.

⁴⁹ Archives générales, 1859.

⁵⁰ McDonald, Heart Disease during Pregnancy, London, 1878.

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.

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.

⁵² New York Medical Record, 1883.

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. Hepp⁵³ 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 Moxon⁵⁵ and Gowers⁵⁶ find that the fibres are not increased in size. Letulle⁵⁷ thinks that there is a process of progressive hyper-nutrition of the fibres.

⁵³ Henle's Zeitschrift, 1854.

⁵⁴ Zielonko, Virchow's Archiv, lxii.

⁵⁵ Pathological Anatomy, London, 1875.

⁵⁶ Reynolds's System.

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 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 Shroetter⁵⁸ 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.

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 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.