When the inflammation is less severe and is limited to the endo cardium there may be little or no disturbance of the breathing or of the cardiac action. In many cases subjective symptoms are entirely absent; and the sole indication of the existence of the endocarditis is the altered character of the heart's sounds, the alteration generally consisting in the development of one or more murmurs.
It has been said that such murmurs may be of anmnic origin. I do not think that nowadays they ever are so. They may sometimes have been so in the old days of free bleeding : but in the absence of such treatment it is scarcely possible for an anaemic murmur to be developed in the short time that suffices for the production of those which we are now considering. In acute rheumatism an anemic murmur could scarcely be developed till late in the case : those now under consideration generally appear in the early stage of the disease.
In the aortic valve we have seen that the morbid change consists in the thickening of its segments, and in roughening of their convex surfaces. During the systole of the heart these segments are thrown against the walls of the aortic outlet. Thickening of their fibrous tex ture must, therefore, cause a diminution of the calibre of this outlet— a diminution which is directly as the extent of the morbid change; while the deposition of fibrin on the surface of the valve not only further diminishes the aortic outlet, but, by presenting to the blood a roughened surface, interferes with the naturally smooth and easy passage of that fluid from the heart into the great vessels. The re sult and the physical evidence of this state of matters is the develop ment of a systolic murmur loudest at the base, and transmitted into the aorta. If one or more of these segments should be so altered as to render due closure of the valve impossible, some of the blood re gurgitates back into the ventricle from the aorta, and there is devel oped a diastolic murmur transmitted downward into the heart and most distinct at mid-sternal region.
Thickening of the fibrous structures of the heart is not limited to their valvular portion: the rings also suffer. The effect of this on the aortic ring is still further to diminish the calibre of its outlet and increase the signs of aortic obstruction.
In the mitral valve the morbid change consists in thickening of its structure, and in roughening of its auricular surface at the line of con tact of its segments.
Such morbid change in the mitral valve is apt to produce more serious disturbance of the valvular function than does a correspond ing change in the aortic. For in the aortic the thickening is partial;
the lunulte are not affected, and so long as they come well into con tact the valve continues to perform its function. But in the mitral valve there is no lunula; the whole segment is thickened. This means loss of mobility, loss of pliability, and consequent loss of adaptability—a condition which is exaggerated by the roughening of the surface of the valvular segments at their line of contact. The result is that the two segments do not come into close and perfect contact, a certain quantity of blood regurgitates back into the auricle, and there is developed a mitral systolic murmur.
Should the fibrous ring be sufficiently thickened to cause any nar rowing of the mitral orifice there will be developed a presystolic blow—the evidence of mitral obstruction.
Thickening of the rings gives rise to no friction and no roughen ing of the endocardial surface, and is for this reason more often recov ered from than thickening of a valve.
The absence of pain in rheumatic inflammation of the fibrous tex tures of the heart is one of the chief points of distinction between it and similar inflammation of the fibrous textures of the joints. Another distinction, and one of much more serious import, is that the results of rheumatic inflammation of the textures of a joint are generally transient and perfectly recovered from ; while those of like inflammation in the textures of the heart are apt to be permanent. Why is this? The poison which produces the inflammation is the same iu both; its mode of action is the same; the tissue on which it acts has in each the same structure, and a similar function. Why, then, should the results be so different? The temporary character of the injury to the textures of the joints has been ascribed to the ab sorbent effects of the pressure exercised on the effused products by the surrounding solid structures. The permanence of the damage to the textures of the heart has been ascribed to the absence of such pressure. "The permanence of the injury in the case of endocarclitis is simply due to the want of counter-pressure. In the joints the swol len membranes are pressed against the other solid structures as soon as the liquid effusion is removed. This pressure causes absorption of all the new products, whereas in the heart there is no direct pres sure of solids against the inflamed valves, which stand freely in fluid blood, so that the new products persist" (Wilks and Moxon).