Kardioprotektive Konditionierung

Abstract

The extent of myocardial infarction depends primarily on the size of the perfusion territory of the occluded coronary artery, then on the duration of coronary occlusion and on collateral perfusion, and finally on the hemodynamic situation, notably heart rate. Early reperfusion is mandatory for salvage of ischemic myocardium; however, reperfusion is a double-edged sword and causally contributes to the extent of infarction through reperfusion injury. Short cycles of ischemia and reperfusion before (preconditioning) or following (postconditioning) a sustained coronary occlusion with reperfusion reduce infarct size. Pre- and postconditioning are also operative in the human heart. Such cardioprotection is effected by a complex signal transduction, initiated by extracellular triggers (autacoids, cytokines, growth factors), which activate an intracellular mediator cascade. Intracellular mediation requires activation of protein kinases. Mitochondria are central elements of signal mediation, notably by free oxygen radical formation, but also end-effectors which are decisive for cell death or survival. Age, comorbidities, and drugs interact with cardioprotection.