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blood-vessels and proliferative connective-tissue cells grow into the periphery of the infarct, which becomes gradually infiltrated with granulation tissue-that is to say, the infarct becomes organized, the necrotic muscle-tissue is substituted by a connective tissue at first richly cellular and vascular. (Plate 3, Fig. I.) Later, the blood-vessels disappear through obliteration, and the large, plasmatic, epithelioid" fibroblasts give way to small spindle-shaped cells and long connective-tissue fibers. Minute extravasations of blood lead frequently to a deposit of brownish pigment. In this way the infarcted area is gradually replaced by a connective-tissue scar, which is outlined from the surrounding muscle-tissue by an irregular line. Myocardial scars may also develop in another way, which will be described later.

Embolism takes the course previously described when the embolus acts in a purely mechanical way. Should, however, the embolus contain micro-organisms, as in the case of pyemia or mycotic ulcerative endocarditis, then acute inflammatory changes ensue, and there results an embolic abscess. (Plate 3, Fig. II.) Microscopically, we find in the center of the latter staphylococcal or streptococcal masses, as well as fragments of necrotic muscle-tissue, the nuclei and striæ of which have disappeared. In the early stages the coccal emboli are still seen inclosed within the blood-vessels. Naturally, the walls soon break down, and the bacteria then lie free in the tissue. They are usually surrounded with numerous leukocytes with lobulated and fragmented nuclei. The muscle-tissue at this area has entirely disappeared. Around the margin of the abscess the leukocytes may be seen as irregular shoots into the intermuscular connective tissue. Sometimes the abscess undergoes healing; this takes place when the bacteria do not flourish, but undergo destruction. The pus-cells break down through fatty degeneration, and the contents of the abscess are then entirely absorbed, while from the per

PLATE 3.

FIG. I.-Infarction of the Heart muscle, Organizing. X70. 1, Heart-muscle still containing nuclei; 2, young connectivetissue cells growing into the infarcted area, and infiltrated with numerous small flakes of brownish pigment; 3, new shoots of bloodvessels; 4, necrotic heart-muscle.

FIG. II.-Embolic Abscess in a Papillary Muscle of the Mitral Valve in Septicopyemia. Stained by Gram's method. 1, Heart-muscle infiltrated with small round cells; 2, abscess cavity filled with leukocytes; 3, colonies of cocci in the center of the neighboring abscesses; 4, remains of necrotic muscle cells.

iphery granulation tissue grows into the cavity, which is finally replaced by scar tissue, as described in simple infarction. In this way also myocardial scars are formed.

Besides the previously described form of myocarditis which leads to such rapid softening of larger or smaller areas of muscle-tissue, there occurs another form, the real interstitial myocarditis. The latter is not circumscribed, but more diffuse in character, and is not accompanied by direct necrosis. Apart from the processes in the endocardium which may extend directly to the heart-muscle, this form is principally observed in connection with the acute general infectious diseases. Through the action of bacterial products or toxins, there is produced first nutritional disturbances and later inflammatory changes. Primarily, we find in these forms quite frequently such degenerative changes of the muscle-fibers as cloudy swelling, areas of fatty degeneration, vacuolations, and transverse tears of the cement lines-the so-called "myocardite segmentaire" of Renaut. [Segmentation and fragmentation of the heart muscle-fibers are of common occurrence. The existence of a distinct form of segmentary myocarditis, as laimed by Renaut, has not been established. Segmenta