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.