PATHOLOGY
The part of the heart most affected is the part which has the most work to do—the left side of the heart—and of this side the left ventricle and therefore the mitral and aortic valves; the most frequent valve to be inflamed and to stiffer permanent disability is the a mitral valve, the valve which in its inflamed condition is subjected to the greatest amount of pressure and therefore irritation. Not infrequently soft systolic murmurs are heard at the pulmonary and tricuspid valves during acute endocarditis. It is rare, however, that these valves are so affected during childhood or adult life as to be permanently disabled.
Whether a diminished alkalinity of the blood in rheumatism has anything to do with the cause of the frequent complication of endocarditis has not been determined. Whether the administration of alkalies to the point of increasing the alkalinity of the blood is any protection against the complication of endocarditis has also not been positively demonstrated, although clinically such treatment is believed by a large number of practitioners to be wise.
A chronic endocarditis with permanent lesions of the valves may become an acute inflammation with an infectious provocation.
It has been shown that even in a few hours after endocarditis has started, little vegetations composed of fibrin, with white blood cells, red blood pigment and platelets, may develop. Practically in all instances such vegetations develop, and later become more or less organized into connective tissue. These little vegetations, generally minute, perhaps not exceeding 4 mm. in height, are irregular in contour like a wart. Some of these may have small pedicles, and as such, of course, are more likely to become loosened and fly off into the blood stream. It is of interest to note that these little vegetations are more likely to be on the left side of the heart than the right; on the valves than any other part, and on the mitral valve than on the aortic. The consequence is a more frequent permanent disability of the valves of the left side of the heart, and of these more frequently the mitral. Although these little vegetations and excrescences sooner or later become mostly connective tissue, still fibrin and white blood cells may form thin layers over them, more or less permanent. In this fibrin are frequently found bacteria, even when there has been no recent acute inflammation. The deeper layers of the endocardium during acute inflammation may become infiltrated with young cells, with resultant softening and destruction of the intercellular substance. This softening and some swelling of the lower layers of the endocardium allow the pushing up of these extravasated blood cells which, being covered with fibrin, makes the little vegetations above described; and as just stated, the fibrin may form a more or less permanent cap. If this cap is disintegrated or lost and the cells under it washed away in the blood stream, ulceration takes place, which may be more or less serious, even to the perforation of a valve or actual erosion of one of its cusps, and the parts of the valves most seriously affected are the parts which strike against each other on closure; as previously stated, the parts subjected to the greatest strain and the greatest amount of friction during the inflammation are the parts most seriously affected afterward.
If a perforation has occurred, it may make a permanent leak. If an erosion of the edge of the valve has occurred, it may make permanent insufficient closure. If the valve has become thickened and stiffened during the cicatricial healing, it may not only be incompetent, but may not open perfectly, and a narrowed orifice may be the consequence. During the healing of these granulating ulcers there may be thickening of the part or shrinking of the tissue, and the valve may become shortened by adhesion to the wall, or the cusps of the valve may adhere together so that the valve becomes permanently unable to open properly or to close properly, or to do either.
Not infrequently and probably more frequently than we recognize, recovery without any of the pathologic lesions just described follows mild endocarditis. The occurrence of simple endocarditis is undoubtedly frequent during acute disease, and is unrecognized because there are no lesions of the heart at the time or subsequently; but valvular lesions only too frequently follow the endocarditis which occurs with rheumatism. Occasionally the ulcerations become serious, and ulcerative endocarditis or malignant endocarditis develops on the mild inflammation. In this form the little vegetations are liable to become loosened, fly off into the blood stream, and cause emboli in different parts of the body.
Recently Fraenkel [Footnote: Fraenkel: Beitr. z. path. Anat. u. z. allg. Path., 1912, iii, 597.] concluded that the microscopic nodules which occur in endocarditis in the myocardium, and which consist of the several varieties of white blood corpuscles first referred to by Aschoff in 1904, are characteristic only of acute rheumatism. Fraenkel found these nodules in the myocardium in a case of chorea, showing the close relationship between it and rheumatism.
While repeated careful examination of the heart during acute infections will generally show signs of endocarditis if it is present, even if there are no subjective symptoms, the disease may be so insidious as not to be noted until a valvular lesion occurs. Often, however, during the course of the disease, especially in rheumatism, there is a slight increase in fever and there is a discomfort complained of in the region of the heart, frequently accompanied by slight dyspnea. Real pain is seldom present unless the pericardium is affected. If the myocardium is much inflamed at the same time, the heart becomes more rapid and the blood tension lowered, and the apex beat diminished in intensity and perhaps not palpable. If there is pain, with or without pericarditis, it is often referred to the epigastrium, especially in children. The patient is often nervous, restless and sleepless. In simple endocarditis emboli rarely occur. If they do, of course the signs will be in the part in which the infarct occurs. Besides the diminished intensity of the apex beat and its greater diffusion, the valve sounds may be muffled, and sooner or later there may be systolic murmurs over the different orifices. Of course systolic murmurs may be due to a disturbed condition of the blood, but if they occur with the above-mentioned symptoms and signs, endocarditis should be diagnosed. If the heart becomes seriously weak and the patient suffers much dyspnea, myocarditis should be known to be present with the endocarditis. If there is a diastolic murmur, there can be no question of serious endocarditis having occurred. Unexplainable palpation during acute illness liar been thought to be a distinct symptom of endocarditis.