Heart, Myocardium - Necrosis

The peracute to acute stage of myofiber necrosis (Figure 1, Figure 2, Figure 3, Figure 4, and Figure 5) consists of focal to multifocal hyaline, cytoplasmic eosinophilia of cardiomyocytes with loss of cellular and nuclear detail. A few marginating neutrophilic inflammatory cells may be present, and it may be accompanied by interstitial edema. Focal loss of preexisting fibers (i.e., myocytolysis) may also be present. Within a few hours of initial damage, infiltration of macrophages digesting the necrotic myofibers may be present. With time, larger areas of myocardial necrosis become fibrotic.

Necrosis can be one of the morphologic manifestations seen in cardiotoxicity (i.e., myofiber vacuolation, mononuclear cell infiltration, and fibrosis) or may be the predominant component in relatively early stages of spontaneous cardiomyopathy. Necrosis may also result from ischemia (infarct); these areas tend to be larger and are typically well circumscribed (Figure 6 and Figure 7). These lesions may have an inflammatory reaction at the margins and become fibrotic with time. Infarcts are caused by occlusion (e.g., by ligation or thrombosis) of a coronary artery that result in regional ischemic/coagulative necrosis of cardiomyocytes supplied by that vessel. The extent of the infarct is determined by the level at which the vessel is occluded, the volume of myocardium supplied by the vessel, and the collateral circulation to that region of the heart. There is no regional predilection for the formation of infarcts. Chemically induced models of heart infarction, without documentation of coronary vessel thrombosis, have been proposed in the literature.