The Cleveland

Medical Journal

VOL V

OCTOBER, 1906

No 10

Myocarditis in Acute Infectious Diseases

BY JOHN H. LOWMAN, M. D.,

Professor of Medicine in Western Reserve University

That the heart is affected in acute infectious diseases has been known since the first quarter of the last century when Louis made his observations on typhoid fever at the Charité in Paris. The later French and German clinicians confirmed these discoveries of Louis. Then similar myocardial changes were observed in diphtheria and scarlet fever, so that now it is well established that myocarditis is not an uncommon complication in these diseases. Schmaltz last year demonstrated myocarditis in 38% of his scarlet fever cases. Not so much work has been done in this direction in influenza, tonsilitis and pneumonia, but there is no doubt but that myocarditis exists also in these affections as well. It has been the custom to speak of heart failure, weak heart, acute dilatation of the heart in acute respiratory conditions but the cause of the heart disturbances and even the sudden death occasionally observed is in all probability due to acute myocarditis. And I wish on this occasion to call attention to the presence of myocarditis in pneumonia and especially to the value of the systolic murmur at the base of the heart over the pulmonic area as a sign of its presence.

Louis says that in the first week of typhoid fever the heart has the color of a dead leaf. In the second week the right side of the heart is dilated and flaccid. He calls attention also to the fact that this flaccidity and dilation of the right side and left auricle are in marked contrast to the contraction of the left side. Andral, Chomel, Stokes and Leyden confirm these observations. Romberg in an extensive review and study of the subject proves

Read before the Cleveland Academy of Medicine

that this heart disturbance is due to a true myocarditis and that it is a parenchymatous myocarditis in diphtheria and interstitial myocarditis in typhoid fever and a mixed form in scarlet fever. In diphtheria the pathological changes may be fully established by the fourth day, and in scarlet fever somewhat later. By the second or third week the progressive process ceases and resolution and repair begin and proceed at a reasonable pace. The interstitial form is more apt to lead to permanent results as shown by the persistence of heart murmur and clinical changes. Rosenberg states that the process is less frequent in scarlet fever. And I am satisfied from the time that my attention has been attracted to the subject that it develops much more frequently in pneumonia also. For this reason I am impelled to call attention to it here.

In the course of any. acute infectious disease the heart should receive the closest attention. The first sign of myocardial weakness that is manifested is an accentuation of the pulmonic second sound. Romberg declares that even this early sign alone may be an indication of an insufficiency of the mitral valve. This is of course a very advanced position. Ordinarily an accentuation of the pulmonic second tone is explained by an increased tension in the smaller circulation due to the weakness of the left ventricle and the consequent fullness and tension in the left auricle. The blood does not leave the ventricle with the same facility and consequently cannot leave the auricle with the same freedom. Whence come naturally a hightened tension in the pulmonic veins, lungs and pulmonic arteries, and the tension in the pulmonic arteries explains the forcible closure of the semilunar valves in the right auricle and the accentuation of the pulmonic second tone. This early weakness of the left heart is probably one factor in the explanation of the constant lowered tension in the general circulation as shown by the tonometer. A mitral insufficiency would be followed and is always attended by these same phenomena. It is therefore exceedingly difficult to state when an accentuation of the pulmonic second is an indication of an insufficiency of the mitral. It is interesting however that some acute observer should say that it is such an indication, although it is difficult to prove.

The next sign which frequently appears is a reduplication of the heart, this can be similarly explained by the increased tension in the smaller or pulmonary circulation and diminished tension in the larger or systemic circulation. The pulmonic valves

close earlier than the aortic and consequently a double second or split second is observed. When the heart beats slowly, say 40 beats to the minute, one can easily hear that the first tone in the doubled second is louder over the pulmonic area, and it is not difficult to convince oneself that the reduplication of the tone is due to the advance of the pulmonic closure. When an accentuation of the pulmonic second tone is followed in a day or two by a reduplication of the second tone the suspicion of myocarditis is deepened. It can positively be surmised that there are grave lesions in the myocardium and that other symptoms confirmatory of this will probably follow sooner or later. The third sign which is apt to manifest itself is a systolic murmur at the base heard with greatest distinctness over the pulmonic area. The significance of this sound (or noise as it should be called) is most interesting. The pulmonic area with its murmur is still known as a terra incognata and has not been satisfactorily explained.

Since Potain's masterly treatise on extra-cardial murmurs this basic murmur has frequently been called a cardio-pulmonic murmur. There is undoubtedly a cardio-pulmonic murmur that is dependent on the heart movement but due to conditions of the lung. But the so-called hæmic or febrile murmur need not always be explained on that hypothesis. Balfour says that a systolic murmur in the pulmonic area is sometimes an indication of senile myocarditis. This fact was known also to Skoda. Yet the text books fail to make mention of this explanation. Sahli however admits in his recent work the possibility of a murmur in the pulmonic region being due to mitral regurgitation. This murmur frequently appears in typhoid fever and has for want of a better name been called the febrile murmur. It will develop while a patient after the first week is in transit from his house to the hospital. I have frequently observed such patients in their beds at home in the morning without the murmur and in the evening demonstrated the murmur in the hospital. Sometimes this murmur will disappear but more frequently it will persist during the illness, and be present when the patient leaves the hospital. It is often explained as a cardio-pulmonic murmur, but a more probable explanation is, that it is due to a myocarditis with a dilatation of the ostium arteriosum.

With the development of the murmur at the systole over the pulmonic area the apex moves to the left. There may however be a murmur present without a displacement of the point of maximum impulse. The last and most significant sign in the

early development of the disease is the systolic murmur in the apical region. The systolic murmur at the apex, especially when transmitted to the axilla, has long been regarded as a sign of mitral insufficiency. The murmur is heard sometimes over the entire præcordium; it is transmitted to the pulmonic area and resembles the hæmic murmur there. Thus it is well known that a mitral insufficiency can produce a distinct murmur at the base over the pulmonic area systolic in time. The only contention is whether a mitral insufficiency can produce a systolic murmur at the base without a murmur at the apex, and whether there can be definite signs of mitral insufficiency without a displacement of the left ventricle. I am satisfied that this is possible and it will only require the narration of one typical case of myocarditis following pneumonia to prove this.

The pulse rate is modified in myocarditis in various ways. The first indication of the onset of the disease may be a slow pulse. I have seen as low as 35 beats per minute. Pulse rate of 40 to 45 and 50 are common. The onset may again be accompanied by a rapid pulse rate and the first indication of trouble will be a pulse rate of 120 or 130. The slow pulse will change sometimes to the rapid one, but the rapid pulse not so frequently to the slow pulse. Arrythmia may be present in any case but is not relatively so often present as in chronic myocarditis with a commencing failure in compensation. The changes in the pulse and the position of the heart not infrequently appear late, even after convalescence is established. There may therefore be no clinical signs apparent unless the heart is closely inspected. In fact there may be in mild cases no marked changes in the pulse or the position of the apex at any time and the heart complication pass through its entire cycle to recovery with no marked clinical phenomena. Close observation of such cases will however demonstrate the fact that the pulse is erratic and becomes now fast, now slow, and that the apex of the heart move outwards temporarily from slight causes, as sitting up in bed, unusual activity, bad night, restlessness or a difficult defecation.

The duration of toxic myocarditis is often from four to six weeks in the young, strong and vigorous. But a dilatation of the heart following an infectious disease, and due to a myocarditis, may also be and not infrequently is persistent. This persistent dilatation I have known to follow influenza. It is occasionally called the convalescent heart but is undoubtedly a myocarditis. In arterio-sclerosis of the heart without physical signs a perma

nent dilatation with a mitral murmur may be introduced by influenza or pneumonia or even tonsilitis. In this latter disease tonsilitis with a persistent fever, showing a decided infection, myocarditis is not an uncommon and is an unsuspected cause of a slow convalescence.

As resolution of the heart muscle reestablishes itself after the acuteness of the disease passes, the physical signs of the heart disappear in the inverse order they appeared. In a typical case, they are not by any means uncommon, and the systolic murmur at the apex diminishes in intensity until it becomes inaudible. The apex moves inward, the murmur at the base, which may have been very loud, grows fainter, but persists after the murmur in the apical region has disappeared. The double second tone may or may not continue through resolution. Finally no changes from the normal heart tone is heard but the accentuation of the pulmonic second tone. The question of endocarditis and endomyocarditis will naturally present itself and the problem of a differential diagnosis between these possibilities and myocarditis will obtrude itself. A complete and satisfactory solution of the matter certainly is not always possible. But when in the course of a convalescence the signs of heart dilatation gradually appear, as above described, and there is no fever, one naturally decides in favor of myocarditis, and when the signs disappear in four or five weeks this conclusion must certainly be confirmed.

The frequency with which myocarditis follows pneumonia I am unable to state. I have however seen many instances of it. It may not be uninteresting to survey rapidly a typical case of this complication of pneumonia which I was able through the courtesy of Dr H. J. Gerstenberger to follow in a boy of ten, who had frank pneumonia which began with a severe abdominal pain suggesting appendicitis. The case passed on uneventfully to crisis. and convalescence. As resolution was about established and five days after the fever had disappeared, a change was noted in the heart tones and the pulmonic second tone was observed to be accented, in two days the second sound was reduplicated and a systolic murmur was heard at the base of the heart. The next day the pulse dropped to 40 beats per minute, at which point or immediately thereabout it remained for several weeks, the murmur grew more distinct each day until it became very loud and unusually conspicuous. Even at this time there was no apical murmur and no displacement of the apex of the heart. Six days after the first signs at the base the apex moved to the left and the