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Accumulating evidence suggests that programmed cell death plays an important role in myocardial infarction. The occurrence of programmed cell death has clearly been shown in several clinical (1,2,3) and experimental settings involving myocardial injury. Experimental data in vivo and in vitro suggest that cardiomyocytes are able to undergo apoptosis during hypoxia (4,5), hypoxia-reoxygenation (6,7), myocardial infarction (8,9), ischemia-reperfusion (10,11), and heart failure (12,13). Based on these studies the present concept of myocardial injury attributes the major portion of cell loss during cardiac ischemia and reperfusion to primary necrosis (14,15). However, based on the observation that apoptosis can be the early and predominant form of cell death in infarcted human myocardium, the possibility of apoptosis as inducer of secondary necrosis has already been raised (9,16). Thus, investigating the …