MYOCARDITIS: A CLINICAL STUDY.

BY THOMPSON ANDERSON, M.D.,

Director of Histological Laboratory, Medical Department of the University of Nashville.

Gentlemen:-This is practically a case report, so after giving briefly some general considerations of myocarditis that bear on the cases in question I shall ask you to assist me in untangling some knotted pathological and clinical threads which I have found in a particular type of myocardial affection.

Myocarditis may be either acute or chronic. I shall deal with the chronic variety alone. Under the name chronic myocarditis are included a number of morbid conditions and clinical pictures which, though differing widely in degree and nature, have yet this one point in common, that the ultimate result of the morbid process, and the one of paramount importance is a condition of cardiac insufficiency. Dispensing with those rather rare diseases of the myocardium, due to parasites as well as those due to neoplasms, pathological conditions of the heart muscle may be said to occur invariably as a result of one or more of the following causes: First, senile change; second, changes in the quality or quantity of the blood supplying the heart muscle; third, changes resulting from long continued functional derangement and strain.

Senile Change: The man who attains his allotted three-score years and ten without realizing that he has an apparatus to keep his blood circulating is an anomaly. And when the Psalmist concludes that "If by reason of strength they be fourscore years, yet is their strength labor and sorrow, for it is soon cut off and we fly away," he utters, unconsciously, perhaps, a pathological and clinical truism. Every man in his declining years is necessarily a victim of disturbed circulation in some degree. The change in his heart muscle may so keep pace with the other signs of his advancing years as to be inconspicuous, for they may be so marked as to cause decided symptoms and demand treatment. "The heart is the one or gan of the body whose sufferings are most apt to disturb the equanimity of the most imperturbable." We know that with each pulsation, life and intelligence are flashed to the farthest

outpost of our frame, and we also know that if the heart beats falter for a second or two we fall to the ground, pale, limp and almost inanimate-an almost which speedily becomes absolute if from any cause these heart beats are prevented from resuming their pristine vigor. With this knowledge ever before our eyes and clinched by many a startling fact, we cannot wonder that feelings of alarm are excited by any deviation from the normal which makes us cognizant of the movements of so important an organ, of which we are ordinarily so profoundly unconscious. Hence palpitation, intermission, irregularity and tremor cordis, all of which make themselves so disagreeably perceptible to our senses, appeal most forcibly to the imagination of the patient, and bring him more certainly to the physician than cardiac ailments of more serious import but of less obtrusive character. Symptoms such as those described always, and at every age, indicate some physical impairment, a matter of comparatively little moment in early life, but of very much more serious import after middle life. We must not forget, too, that at any age, but more probably in advanced life the physical impairment may be primarily due to failure of the trophic nerve centers.

Microscopically his heart may show varying degrees of fatty or other degenerations, fatty infiltration, hyperplasia of the interstitial connective tissue. One or all of these changes may be present in the heart at the same time, and while occurring as a result of irritation or malnutrition of the myocardium from some antecedent cause, become themselves causes of further impairment of nutrition and thus establish a vicious circle of interdependent and interacting factors of disease and decay. Inviting complications, they may cause death, or in themselves may become so extreme as to be fatal. Unless complicated by valvular insufficiency, anginoid attacks or some train of striking symptoms which suggest to the attendant a morbus. cordis, the condition presents so few and such insignificant symptoms that a high percentage of cases probably pass undiagnosed, despite the fact that the great majority of people pass middle life who present indications of cardio-vascular disturbance have no valvular lesion and probably no symptoms. which are strikingly suggestive of heart disease. But however insidious the onset and unobtrusive the manifestations, the progress is sure and soon or late the fatal termination occurs, perhaps suddenly and without warning or-non vi, sed

saepe cadendo-as more often happens, its advance is stealthy, hidden by the footprints of the passing years and making itself known by some vague symptoms only when the patient is already shrouded in the gloom of approaching dissolution. While every subject of senile change in the heart does not die as a result of that condition, it should always be borne in mind that an affection which might only embarrass and cripple the heart in a healthy man, may prove fatal in a man whose myorcardium has undergone degenerative changes.

Changes in the Quality or Quantity of Blood Supplying the Heart Muscle: Under this head will come those cases of chronic myocarditis induced by insufficient blood supply resulting from disease of the coronary arteries, from impairment of the general circulation, as well as those cases resulting from the changes in the quality of the blood; namely, (a) deficiency in the nutrition of the blood, and (b) the presence of toxic substances in the blood. Any of the above-named pathological changes may result from these causes, giving rise to the same symptoms that occur with degeneration of the heart muscle from any cause.

Long continued functional derangements and strain bring about chronic inflammation of the heart muscle by causing hypertrophy, dilatation, impairment of nutrition and continued disturbance of the nervous mechanism of the heart.

Whether one or all of the above causes act in producing myocarditis, and whatever the morbid changes present, the symptoms manifested are exceedingly variable and distressingly unreliable. Any attempt to associate a certain train of symptoms with any one of the above morbid changes is worse than useless. A patient with a fibroid heart may present practically the same symptomology shown by a victim of extreme fatty degeneration. They may both have few or no symptoms, or, on the other hand, may suffer with the most striking manifestations of extreme cardiac disability. The symptoms. most often found are feeble, irregular pulse, often slow, dys pnoea, sometimes anginoid pains, and when relative insufficiency complicates the above disease the symptoms of this condition are superadded.

The inadequacy of the morbid changes to the symptoms and termination of some cases will be strikingly shown in the following brief case reports. During the summer of 1902 I was called to see Lucinda H-, aged 49, who complained of slight

dyspnoea and occasional precordial oppression. The patient gave no history of rheumatism, syphilis or alcoholism. She had, indeed, been an unusually healthy woman and a hard manual laborer. For the last few months she had been bothered by occasional attacks of palpitation and paroxysmal dyspnoea. For a week or two the dyspnoea had been worse and more or less continuous. Some dropsy was present, but the most striking symptom was the arrhythmic pulse, which was irregular in force, intermittent, rather soft, with fifty beats to the minute. The arteries were somewhat firm. On physical examination the apex beat was neither visible nor palpable.

The woman had emphysema, was obese with a thick chest wall, consequently no enlargement of the heart could be made out. On auscultation the first sound of the heart was weak The aortic and pulmonary second sounds were accentuated No murmur was detected. Under the influence of digitalis the heart's action became more forcible but did not become regular. I beg you to bear this in mind-the patient grew steadily worse and after some weeks died. Being so fortunate as to secure the privilege of an autopsy, the following observations were made: Both the right and left sides of the heart were somewhat hypertrophied. The valves and their orifices seemed to be normal and competent. The heart muscle appeared to be healthy except along the course of the coronary arteries and auriculo-ventricular furrows, where there were decided increases in the sub-epicardial fat with some infiltration of the adjacent muscular tissue. The morbid changes certainly did not seem extensive enough to have produced fatal termination, since no obstruction was found in the cardiac vessels. My ante-mortem diagnosis was fatty degeneration; after the necropsy I had none. With this problem still unsolved, I saw case number two. A man of 55, a hard worker, an alcoholic, who complained of some precordial distress, at times anginoid in character. He got progressively worse, particularly palpitation and attacks of syncope.

The heart's action began to get weak and irregular. At this time his pulse was only fifty-five to the minute. This condition lasted for some weeks, gradually becoming more marked and the patient died after a prolonged attack of palpitation. When first examined his heart impulse was moderately forci ble, the apex slightly out to the left, the aortic second sound

was accentuated, no murmur was present. During the last weeks of his sickness his heart became weak and he devoloped dyspnoea and other signs of cardiac failure. The heart muscle responded to digitalis by an increase in the force of its systole, but the pulse remained irregular and this condition became very marked as the case neared its termination. The post-mortem examination revealed no incompetency of the valves. The coronary arteries were rather firm, but no more than was to be expected from this general arterio-fibrosis, which probably accounted also for the moderate amount of hypertrophy. The muscle was fairly healthy, but showed an increase of interstitial connective tissue in patches in the apical region; and of particular interest were some areas of fibroid degeneration seen in the upper part of the right ventricle, near the angle of the auriculo-ventricular and interventricular grooves on the surface of the conus arteriosus.

Neither this nor the previous autopsy had shed much light on the diagnosis. Indeed the pathology and the clinical findings appeared to be at cross purposes.

I was confronted by the incongruous picture of two patients who had died evidently of heart failure, but who did not show sufficient degeneration of the myorcardium to account for their untimely end, and in whom no indication of angina pectoris, valvular disease or disease of the coronary artery was to be found. Chagrined and vexed at this enigma, the more I pondered on the two cases the farther at sea I was. While in this state of dissatisfaction I received a letter from a friend in a charitable institution. He wrote as follows: "A strange coincidence which occurred yesterday taught me a lesson which I shall never forget. Two patients died in the hospital; one an old woman with phthisis, died of severe hemorrhage from the lung. At the autopsy we found a heart di lated excessively. The cardiac muscle had undergone fatty degeneration to such a degree, that in places one's finger could almost be pushed through it, and we are puzzled because she had presented practically no symptoms of this condition. The next patient, a man who labored on the place, had been apparently well except for occasional attacks of syncope, slight dyspnoea at times and a peculiar, irregular pulse, beating only forty times to the minute. I have just seen his heart and find nothing abnormal except a fibrous nodule about the size of a buckshot near the root of the right coronary artery."