Reperfusion injury is of increasing importance due to new techniques of restoring blood flow to acutely ischaemic areas by means of thrombolysis, angioplasty, or acute coronary artery bypass surgery. Reperfusion of ischaemic myocardium can results in the acceleration of surrounding reversibly injured myocytes and endothelial cells to irreversibly injured cells. The complex group of phenomena associated with reperfusion include: no-reflow, arrhythmias, "stunned" myocardium-impaired contractile power and abnormalities of relaxation. Experimental studies have demonstrated that microvascular damage may play an important role in the pathogenesis of this phenomenon. The causal factors of reperfusion injury are not clarified, but include free radicals, calcium and various inflammatory mediators. The deleterious effects of reperfusion are related importantly to the action of oxygen-derived free radicals. These effects can be reduced or even prevented with scavengers of free radicals. However, the value of these agents in patients remains to be tested. Prophylactic chronic treatment of patients at high risk of coronary occlusion with a beta-adrenergic blocking agent or a calcium antagonist slow cell death causing limitation of infarct size.