[Reperfusion-induced arrhythmia and oxidative stress]

Abstract

Although recognized and reproduced in numerous animal models, reperfusion arrhythmias were not studied extensively in humans until the advent of methods of coronary reperfusion during the acute phase of myocardial infarction. Usually of ventricular origin, these arrhythmias are polymorphic and constitute imperfect but useful markers of coronary reperfusion. Their electrophysiologic mechanisms are complex and their molecular mechanisms unelucidated. Predisposing conditions are the duration and severity of the ischemia, biochemical modifications such as heterogeneous uptake of extracellular potassium, magnesium deficit, intracellular calcium overload and release of arrhythmogenic lipid metabolites or prostaglandins. The autonomic nervous system also plays a part by an increase in the number and response of alpha-adrenoceptors. Furthermore, experimental studies provide theoretical and pharmacologic arguments for the participation of free oxygen radicals (superoxide anion (02.-, hydroxyl radical OH.) in reperfusion arrhythmias in the animal. By its complexity, human myocardial infarction differs markedly from the animal models studied; it probably involves, apart from the free oxygen radicals, multiple thrombotic, humoral and nervous factors whose respective role in the production of reperfusion arrhythmias remains to be established. Some enlightenment should be obtained by analysis of rhythmic events during proposed controlled studies using anti-free radical agents to prevent these post-myocardial infarct acute events.