tion appears as a terminal or agonal event in various diseases not necessarily involving the myocardium primarily.] The transverse striations may be absent over large areas, while the nuclei also show changes. (Plate 4, Fig. I.) Here and there the nuclei are found increased in numbers, so that in a single muscle-cell several nuclei occur in rows; or they are found enlarged, ballooned, with a loose chromatin network. Through disintegration of the cells part of these nuclei become free. The most striking changes, however, are observed in the intermuscular connective tissue. The fixed connective-tissue cells proliferate and produce fibroblasts-large spindle-shaped or round, plasmatic cells with vesicular nuclei. These accumulate especially around the blood-vessels, forming numerous foci, while the surrounding muscle-tissue disintegrates more and more.

Gradually, these areas are transformed into fibrous scars, which remain after the inflammatory processes have subsided. In this manner various sized scars are developed without necessarily being preceded by infarction or necrosis of muscle-tissue, which, as it degenerates, is substituted by fibrous tissue. Myocardial scars, therefore, may develop in three ways: After infarction, after healing of an abscess, and as a termination of acute interstitial myocarditis (Plate 4, Fig. II); but their genesis is not yet exhausted, inasmuch as focal disappearance of musclesubstance, accompanied with chronic proliferative changes of the interstitial connective tissue, occurs in all cases of narrowing of the coronary arteries in endarteritis and arteriosclerosis-chronic fibrous myocarditis or arteriosclerotic myocarditis.

Infectious new growths, as syphilis and tuberculosis, are rare in the heart-muscle, but occasionally are observed. They do not present any special histologic peculiarities.

It also occurs in young individuals suffering from exhaustive diseases with general marasmus. The muscle-fibers appear more or less diminished in size, oftentimes to a considerable degree, and their striations are indistinct or have entirely disappeared, while the nuclei may have become flattened. Around the latter are found masses of amorphous, finely granular, yellowish-brown pigment. In severe cases the cells are completely filled with this pigment, or the pigment may be found free between the fibers, owing to the destruction of the cells. In cases not so far advanced transverse sections will not always show pigment in each individual cell, for the reason that the groups of pigment particles, like the nuclei, are found only at certain planes; fat-vacuoles are sometimes seen in the sarcoplasm at the same time. The pigment gives no iron reaction, and it is undoubtedly related to the pigment normally found in the heart-muscle.

In severe cases of general amyloid disease there is sometimes found in the myocardium amyloid degeneration of the blood-vessels of the intermuscular connective tissue. Hyaline degeneration may also be observed in the intermuscular connective tissue.

[Among the degenerative changes of the myocardium should be mentioned segmentation, or separation of the muscle-fibers along the cement lines into the individual cells that compose the fibers; and fragmentation, or the breaking of the fibers into fragments irrespective of the cement lines. These changes are terminal or agonal events in diseases of various kinds, and are found to a greater or less degree in about two-thirds of all hearts examined.]

Circulatory Disturbances of the Myocardium.

Embolism, Infarction.-Embolism of the coronary arteries of the heart occurs but infrequently, as the result

PLATE 2.

FIG. I.-Adipositas Cordis. Frozen section. Stained with hematoxylin and sudan III. × 80. 1, Transversely striated musclefibers, pressed together, diminished in size, and continuity interrupted; 2, fat-cells in rows between the muscle-fibers.

FIG. II.-Brown Atrophy of the Heart-muscle in Longitudinal Section.

FIG. III.-The Same in Transverse Section. 340. In the muscle-cells are seen masses of brownish, amorphous pigment. In the transverse section are seen round vacuoles in the sarcoplasm.

of detached pieces of thrombi or endocardial vegetations being swept into those vessels. Provided sudden death by obstruction of a larger stem does not occur, the results are anemic infarct; since the coronary arteries are, in the sense of Cohnheim, end arteries-in other words, do not form collaterals. The whole infarcted area undergoes anemic necrosis. Through coagulation of the albuminous substances, the area presents a homogeneous, dry, firm consistency, while the contours of the cells and transverse striæ of the muscle-fibers disappear, and the nuclei do not stain. Later, the musculature breaks up into a granular substance. The infarct, like necrotic tissue in general, acts upon the neighboring tissue as an inflammatory irritant, which causes the accumulation of numerous round cells, lymphocytes, and leukocytes around the periphery of the infarct, forming a compact wall. At this stage softening may take place in the infarct as the result of an infiltration of serous fluid throughout the area, the fluid being transuded from the surrounding blood-vessels that are in a state of stasis (Neelsen). This condition is designated as myomalacia cordis. The softened tissue can not, when extensive, withstand the blood pressure, a local bulging occurs, and an aneurysm of the heart develops.

It is much more common to observe that shoots of new