[Apoptosis--what is it? Significance in coronary heart disease and myocardial infarct].

Apoptosis is a physiological, highly conserved program of cellular suicide, characterized by nuclear condensation with DNA-fragmentation, by alterations in the distribution of cell membrane phospholipids, and by cellular shrink-age. Apoptotic cellular remnants engulfed by cell membranes are phagocytized largely without activation of inflammatory reactions. The apoptotic program is executed by a cascade of highly specific caspases, activated by complexation of initiatorcaspases in cytosolic signalling complexes at receptors of the TNF family or at impaired mitochondria. In many forms of cellular stress with damage of nuclear DNA and mitochondria, mixed forms of cell death are triggered with regulated activation of the apoptotic program and concomitantly, with induction of catastrophic necrosis. Such a mixed form of myocyte death is observed in myocardial ischemia and reperfusion. Antiapoptotic interventions can delay ischemic myocardial damage in experiments. Therefore, those interventions appear conceivable as future strategy for acutely enhancing the available time interval for therapeutic reperfusion. However, chronic inhibition of apoptosis for ongoing prevention of myocardial ischemic damage may not become a plausible strategy because of disturbances of the immune system, because of putatively infavorable effects on arteriosclerotic lesions and because of likely disturbances in the physiologic elimination of damaged mitochondria.