ABSTRACT

Introduction In recent years there has been considerable interest in the pathophysiology of myocardial ischemia-reperfusion injury. The possibility that the heart may be rendered more resistant to the damaging effects of ischemia is an attractive therapeutic goal. This has been driven partly by epidemiologic data that confirm the place of coronary artery disease as the leading cause of death in the developed world. Over the past ten years, the widespread adoption of thrombolytic therapy and invasive, revascularization procedures have revolutionized the management, and improved the prognosis, of acute myocardial infarction (MI). However, other than this rapid and complete restoration of blood flow to the ischemic myocardium, there have been no therapeutic interventions available to enhance myocardial tolerance to ischemia and counter the threat of myocardial necrosis. In this context, interventions aimed at modifying the symptoms of angina, such as beta-blockers, calcium antagonists and nitrates, have met with little success.