ABSTRACT

Acute myocardial infarction (AMI) occurs in an estimated 500,000 Americans each year (1). Early reperfusion with fibrinolytic therapy or percutaneous coronary intervention (PCI) has been shown to significantly reduce mortality by salvaging ischemic myocardium and reducing infarct size (2). Reperfusion remains the most powerful method to reduce infarct size and the earlier that reperfusion occurs after coronary occlusion, the smaller the infarct size, the better the left ventricular function, and the lower the long-term mortality. Numerous clinical trials have also demonstrated that the degree of restoration of blood flow and myocardial perfusion is important (3). When complete and normal blood flow to the microcirculation is obtained, outcome is further improved. To date, PCI with adjunctive pharmacological therapy is most effective in restoring rapid and complete blood flow in the infarct artery (4). However, despite successful reperfusion, a significant number of patients fail to demonstrate benefit. Animal studies have demonstrated that reperfusion itself can result in adverse consequences that can lead to further myocyte death that might be avoided with adjunctive therapy (5,6). This chapter will discuss the proposed mechanisms for ischemia/reperfusion injury and the results of the clinical trials of various pharmacological agents that have been conducted to enhance myocyte salvage.