Ischemia-Reperfusion Injury of the Heart: Moving forward with our Knowledge

Ischemia Reperfusion (I/R) injury is a consequence of reperfusion of the ischemic myocardium when reperfusion is carried out beyond a certain time period of the ischemic insult. The I/R injury is associated with impaired heart function as well as myocardial cell damage and is generally seen to occur during coronary angioplasty, cardiac by-pass surgery, cardiac transplantation and thrombolytic therapy. Several mechanisms including the occurrence of oxidative stress, activation of inflammatory processes, development of intracellular Ca2+- overload, depletion of high energy stores and increased activities of proteolytic enzymes have been suggested to explain the I/R-induced cardiac dysfunction. While contractile failure, apoptosis and necrosis in the heart may be due to cationic redistribution and metabolic alterations as a consequence of oxidative stress and intracellular Ca2+- overload, marked alterations in cardiac gene expression and translation mechanisms may play a critical role in attenuating the recovery of ischemic myocardium. This article therefore is focused on understanding changes in the metabolic and molecular processes occurring in the heart due to I/R injury. Furthermore, current and potential pharmacologic as well as non-pharmacologic interventions are indicated for preventing the I/R injury in the heart.