Myocardial ischemia-reperfusion injury (MIRI) is defined as the restoration of blood flow to the myocardium after a brief interruption of blood supply, causing more severe damage to the ischemic myocardium.

Myocardial injury in the setting of an acute myocardial infarction (MI) is the result of ischemic and reperfusion injury. Reperfusion therapies, including primary percutaneous coronary intervention and fibrinolytic therapy, promptly restore blood flow to ischemic myocardium and limit infarct size.

Myocardial ischemia–reperfusion injury (MIRI) is an independent aggravating factor leading to adverse cardiovascular events shortly after myocardial ischemia, cardiac surgery, or circulatory arrest. MIRI is a field of extensive research, given that it can account for up to 50% of the final size of a myocardial infarct in experimental models [ 3 ].

Injuries due to reperfusion may offset the benefits of coronary blood flow recovery, especially in older patients and in patients with prolonged ischemia. Mitochondrial dysfunction and the resultant oxidative stress are the key mechanisms for the development of cardiac damage during ischemia and reperfusion.

The reversible post-ischemic contractile dysfunction that occurs on reperfusing acute ischemic myocardium is referred to as myocardial stunning. This form of reperfusion injury results from the detrimental effects of oxidative stress and intracellular calcium overload on the myocardial contractile apparatus (7).