THE HEART IN ACUTE INFECTIONS

J. G. CROSS, M. S., M. D.

Minneapolis

Acute infectious diseases have a tendency to produce degenerative and inflammatory changes, in other tissues than those primarily attacked by the infectious agent. Kidney, liver, spleen, and voluntary muscles are especially liable to undergo degeneration, and heart tissues are not excepted from this process. The causation of cloudy swelling in different organs in such diseases as septicemia, typhoid fever, pneumonia, scarlet fever, influenza, and acute rheumatism which are attended by prolonged fever, has been much discussed. Welch's1 experiments seemed to show that prolonged high bodily temperatures are capable of producing tissue degeneration. Naunyn, by slightly modifying the conditions surrounding his animals, kept them at as high temperatures for twice as long a period, without finding change in the same organs, and it is well known that cloudy swelling in the heart, and other tissues, takes place oftentimes in cases of diphtheria which have had no fever at all, and this occurs also sometimes in a febrile septicemia and typhoid. The fact that the nature and extent of degenerative changes depend upon the character of the infection. rather than upon the height of the temperature, indicates that some product of the infectious agent acting through the circulation is the cause. That in different infections there are specific toxins is shown by the selection of one group of tissues in one disease, and not in another. For example, endocarditis and pericarditis are common in rheumatism, while in typhoid fever they are rare.

Cloudy swelling is evident in the epithelium of the kidney and intestine after only a few hours of some toxemias,

but as a rule several days of the same infection must elapse before the heart structure is similarly affected. Cowan2 concludes that the poison causing the change is more concentrated in the excretory organs.

None of the heart tissues are exempt from the toxic action of infectious disease. Muscle, connective tissue, endothelium, or blood-vessels may be attacked, but by far the most frequent, as well as most important, degenerative change, is that which takes place in the muscle wall. For this reason, and also because endocarditis and pericarditis are already so much better understood, it is intended to discuss especially the muscle and connective tissue changes in the heart, which occur in acute infectious disease, together with their immediate and remote effects.

While acute infections produce in some instances both inflammatory changes in the heart, and also granular degeneration, cloudy swelling, and fatty changes, that most commonly found, and as a rule first produced, is cloudy swelling of the muscle fibres, parenchymatous degeneration. In its simplest form there is swelling of the fibers, the striæ disappear, and small granules are seen in the cell, which can be distinguished from fat granules by their reaction to ether and acetic acid. It is still unsettled whether cloudy swelling in the muscle cell is an antecedent stage of fatty change. Fatty and hyaline degeneration are found, however, more often in cases of severer clinical type and more prolonged

course.

The heart may not show any alteration in gross appearance unless parenchymatous change is general and considerably advanced, when the muscle looks pale, is somewhat soft, and the cavities perhaps dilated. Some writers refer to this condition as heart softening. Degenerative changes in the nuclei of the muscle cells, and the development of vacuoles and segmentation in the muscle fibers are also seen. In the interstitial tissues a round cell infiltration, particularly about the blood vessels, is the most common evidence of a toxic influence. In the blood vessels, the changes found include an obliterating endarteritis from swelling of the

intima and cellular infiltration of the outer coat. Hyaline degeneration of the media occurs, and hyaline thrombi in the smaller vessels may be present.

Degenerative changes in the nerve tissues of the heart have been demonstrated, especially in tetanus and diphtheria. While it is common to find in the same heart an inflammatory process, and also primary degeneration, there is no question but they may be the separate reactions of different tissues to the same toxin, if not to different and distinct bacterial products. At the same time it should be remarked that the muscle near an inflamed pericardium is always degenerate, with consequent lessened heart power, and changes in the nearby connective tissue of one sort or another are often present to still further hamper the action of the muscle cells.

SPECIAL PATHOLOGY

Endocarditis and pericarditis are prominent features of acute rheumatism, yet affections of the muscle wall of the heart are as common, and quite as important. Poynton3 has classified the latter as

A.

Affections of cardiac muscle.

1. Fatty degeneration of muscle fibers.

2.

3.

Loss of striation.

Nuclear changes.

B. Affections of blood vessels.

I. Cellular exudation around blood vessels.

2.

Exudation into, and swelling of interstitial tissues.

3. Perivascular fibrosis.

In 100 cases of rheumatic fever, 23 were found to present signs of alteration in the muscular wall. The muscle cells themselves show the most extensive degeneration. Inflammation of endocardium and pericardium are common, and in fact usual, accompaniments. Dilatation of the heart may follow upon the muscle degeneration. It is present as a rule in pericarditis, and is then responsible in a large measure for the great enlargement of cardiac dullness which oc

curs.

The most common, and sometimes the only heart change produced by diphtheria is parenchymatous degeneration, consisting in loss of striation, granular, fatty, and hyaline changes in the muscle cells affecting a greater or less number of fibers. There is great difference in the size and extent of lesions in specimens taken from different parts of the heart, as well as from different cases. The first parenchymatous changes are noted after the disease has lasted five to eight days. The more severe infections and those of longer duration lead to greater defects in structure. Interstitial changes also occur, more often in foci under the pericardium. There is also a degeneration of nerve tissues in the heart in diphtheria shown by later staining methods.

It is a frequent occurrence to find that there is a general parenchymatous degeneration of muscle fibers in hearts that show little or no macroscopic change from typhoid fever. Endocarditis and pericarditis are extremely rare. In typhoid fever there also appears to be a true myocarditis, with interstitial inflammation, and in some cases an obliterating endarteritis, considerably narrowing some of the branches of the coronary circulation, with resulting degeneration in the tissues whose nutrition is thereby diminished.

Endocarditis and pericarditis are relatively frequent in pneumonia. The heart muscle is not, as a rule, degenerated, unless in prolonged cases, but when it is structurally changed, dilatation is much more apt to follow.

Granular, hyaline, and vacuolar degeneration may result in scarlet fever (Ziegler1). V. Jürgensen states that a wall endocarditis, leaving the valves free is a frequent occurrence in the disease. In severe cases dilatation may come on early in the illness. Influenza and septicemia characteristically cause fatty degeneration in the heart muscle. The gonococcus has been cultivated from ulcers and vegetations on the heart valves.

EFFECTS

The effects of muscle defects in the heart are far-reaching. Especially in endocarditis and pericarditis the prognosis depends upon the condition of the heart muscle. If

the muscle is attacked by the toxemia of acute infection the immediate effect is to cause an amount of weakness of the heart in proportion to the extent of tissue involved and the degree of the structural change. These effects are found to vary with the intensity and duration of the infectious process. Neither inflammatory nor degenerative changes in the heart muscle in the course of acute disease give any regular series of symptoms or physical signs. Degenerative changes alone are difficult to recognize during life, but when in typhoid fever, septicemia, rheumatic fever, influenza, scarlet fever or pneumonia, the pulse becomes more frequent without a corresponding rise in the temperature, we are justified in suspecting some myocardial weakness. Of still more significance are irregularity and inequality of the pulse coming on under the same conditions. Next, the volume and strength of the first heart sound are diminished, and a soft, compressible, small pulse follows. At the same time. these signs cannot be referred absolutely to progressive muscle changes since the same effect may be caused by toxic impression of the vasomotor centers. In pneumonia this is frequently observed. In diphtheria it is impossible to distinguish clinically between lesions of the pneumogastric nerve in cardiac paralysis, and myocardial degeneration; death may occur from either cause. If myocarditis is present, there may be precardial distress. When dilatation follows, there are tangible signs in addition to the symptoms of acute cardiac insufficiency. Generally, with an increased frequency and lowered tension of the pulse, the apex beat may be observed to be slightly further to the left, the first sound becomes shortened, approaching the second in quality; the second pulmonary sound is more accentuated and in many instances the soft blowing murmur of a relative insufficiency systolic in time, is audible just inside the nipple. The opinion appears to be increasing that the dilatation of the heart in pneumonia is largely due to structural changes in the heart wall which allow it to stretch, brought about by the toxic action of bacterial products, rather than to the respiratory obstruction. The occurrence of sudden death in