Cardiovascular disease remains a leading cause of deaths due to noncommunicable diseases, of which ischemic heart disease forms a large percentage. The main therapeutic strategy to treat ischemic heart disease is reperfusion that could either be medical or surgical. However, reperfusion following ischemia is known to increase the infarct size further. Newer strategies such as ischemic preconditioning (IPC), ischemic postconditioning, and remote IPC have been shown to condition the myocardium to ischemia-reperfusion injury and thus reduce the final infarct size. Research over the past 3 decades has deepened our understanding of cellular and subcellular pathways that mediate ischemia-reperfusion injury. This in turn has resulted in the development of several pharmacological agents that act as conditioning agents, which reduce the final myocardial infarct size following ischemia-reperfusion. This review discusses many of these agents, their mechanisms of action, and the animal and clinical evidence behind them.
Keywords: acute myocardial infarction; cardiac pharmacology; heart disease; ischemia–reperfusion injury.