What is apoptosis? Relevance in coronary heart disease and infarction?

Apoptosis is a physiological, highly conserved program of cellular suicide, characterized by nuclear condensation with DNA-fragmentation, by alteratio ns in the distribution of cell membrane phospholipids, and by cellular shri nkage. Apoptotic cellular remnants engulfed by cell membranes are phagocyti zed largely without activation of inflammatory reactions. The apoptotic pro gram is executed by a cascade of highly specific caspases, activated by com plexation of initiator-caspases in cytosolic signalling complexes at recept ors of the TNF family or at impaired mitochondria. In many forms of cellula r stress with damage of nuclear DNA and mitochondria, mixed forms of cell d eath are triggered with regulated activation of the apoptotic program and, concomitantly, with induction of catastrophic necrosis. Such a mixed form o f myocyte death is observed in myocardial ischemia and reperfusion. Antiapo ptotic interventions can delay ischemic myocardial damage in experiments. T herefore, those interventions appear conceivable as future strategy for acu tely enhancing the available time interval for therapeutic reperfusion. How ever, 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 arterio sclerotic lesions and because of likely disturbances in the physiologic eli mination of damaged mitochondria.