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Reactive oxygen metabolites and the human myocardium.

Thrombolytic treatment in acute myocardial infarction achieves coronary patency in most patients.' Mortality in groups treated early after the onset of symptoms is significantly reduced,' but left ventricular function does not always improve.5 Myocardial necrosis during the period of vessel occlusion is partly responsible for the irreversible ventricular impairment that occurs even when the vessel is re-opened. In the dog the expanding area of myocardial necrosis induced by experimental coronary occlusion is surrounded by a potentially viable ischaemic zone.6 But viable ischaemic cells can be irreversibly damaged when coronary flow is reestablished. During reperfusion, molecular oxygen is converted to oxygen metabolites, which are toxic and can promote further tissue injury. In this way, reoxygenation of the myocardium may itself result in secondary deterioration in myocardial function-the "oxygen paradox".7 In animal models the extent of injury is reliably reduced and residual myocardial function appreciably improved by agents that either suppress the generation of oxygen derived free radicals or inhibit the damaging effects that these reactive oxygen metabolites produce.8 Direct evidence of injury by free radicals has yet to be shown in the human heart, but many studies of other mammals have linked reactive oxygen metabolites with myocardial injury. Many workers conclude from these studies that interventions directed against free radicals will improve myocardial function after thrombolysis for acute infarction and in other forms of myocardial revascularisation (coronary bypass graft surgery and coronary angioplasty) and during cardiac transplantation. Appreciation of such studies depends on an understanding of some simple biochemistry.