Mechanisms of myocardial reperfusion injury

Reperfusion of the ischemic myocardium results in irreversible tissue injur y and cell necrosis, leading to decreased cardiac performance. While early reperfusion of the heart is essential in preventing further tissue damage d ue to ischemia, reintroduction of blood flow can expedite the death of vuln erable, but still viable, myocardial tissue, by initiating a series of even ts involving both intracellular and extracellular mechanisms. In the last d ecade, extensive efforts have focused on the role of cytotoxic reactive oxy gen species, complement activation, neutrophil adhesion, and the interactio ns between complement and neutrophils during myocardial reperfusion injury. Without reperfusion, myocardial cell death evolves slowly over the course of hours. In contrast, reperfusion after an ischemic insult of sufficient d uration initiates an inflammatory response, beginning with complement activ ation, followed by the recruitment and accumulation of neutrophils into the reperfused myocardium. Modulation of the inflammatory response, therefore, constitutes a potential pharmacological target to protect the heart from r eperfusion injury. Recognition of the initiating factor(s) involved in myoc ardial reperfusion injury should aid in development of pharmacological inte rventions to selectively or collectively attenuate the sequence of events t hat mediate extension of tissue injury beyond that caused by the ischemic i nsult. (C) 1999 by The Society of Thoracic Surgeons.