Protection of the myocardium against postischemic reperfusion damage.

Fifty years ago it was observed that a sudden restoration of antegrade flow in the ischemic myocardium can lead to a paradoxical deterioration of cardiac function. The implications of this observation were only fully understood during the last decade when, thanks to the improvement of angiographic methods and the development of thrombolytic agents, reperfusion could be demonstrated in humans. At present, it is generally accepted that reperfusion phenomena play an important role in ischemic heart disease and probably the reperfusion damage, which may occur as a consequence of thrombolytic therapy, reduces the finally observed effect of these agents. During the last few years, many agents have been studied for their potential to reduce reperfusion damage. Several groups of these agents and their mechanism of action are discussed in this report. Special attention is paid to the possible effects of angiotensin converting enzyme inhibitors in this situation, as this group of agents combine several interesting characteristics of other groups, among which are their effects on norepinephrine levels, prostaglandin synthesis, and free radicals.