Pathophysiology of Myocardial Ischemia Reperfusion Injury: A Review

Abstract

Cardiovascular events are one of the leading causes of death in the world. Thrombolysis, percutaneous transluminal coronary angioplasty, and coronary bypass surgery are the general treatment strategies of cardiovascular events. All of these treatment strategies can cause a myocardial ischemia reperfusion (MI/R) injury, which is known to occur on the restoration of coronary blood flow after a period of myocardial infarction (MI). Although there is an only way to save the myocardium from necrotic and apoptotic damages, reperfusion achieved by the restoration of blood flow often aggravates cardiac dysfunction. It is believed that MI/R injury is related to the increased reactive oxygen species (ROS), calcium overloading, and the loss of membrane phospholipids especially during the reperfusion. The harmful effects of ROS on cardiac tissue during the MI/R can be prevented by endogenous antioxidant systems. Also, the complement system plays a crucial role in the inflammatory events of ischemic injury; thereupon it is important in the pathogenesis of the MI/R injury. Polymorphonuclear leukocytes in the reperfusion period are also associated with MI/R injury. Therefore these circumstances can increase the irreversible tissue damage. Although sometimes the reperfusion is provided, blood flow cannot be supplied to the myocardial tissue. This is called a no-reflow phenomenon. A lot of exogenous antioxidant agents can be used to prevent this process of injury. Due to these properties of antioxidants, a number of studies have been carried out and have been reported anywhere in the world. These studies demonstrated that these agents can be used in the MI/R-induced tissue damage and protect the heart against ROS-related myocardial injury.