Abstract
CARDIAC SURGERY frequently involves ischemia and reperfusion of the myocardium, which can lead to perioperative damage, arrhythmia, and dysfunction. In noncardiac surgery, cardiac complications are the major cause of morbidity and mortality. This is a consequence of the high underlying prevalence of cardiovascular disease and the metabolic responses to surgical stress and pain, which alter physiology and may trigger a cascade of prothrombotic biochemical events. Myocardial oxygen consumption also is increased during the perioperative period, which affects the oxygen supply/demand balance, and intraluminal shear forces in the coronary artery may be increased, producing a “perfect storm” for atheromatous plaque rupture and subsequent coronary artery thrombosis. Intense research has been directed toward preventing or ameliorating myocardial ischemiareperfusion injury, stemming from the groundbreaking work of Murry et al. They “conditioned” the heart to tolerate the effects of acute ischemia-reperfusion injury by inducing brief nonlethal episodes of ischemia and reperfusion to the heart before sustained lethal myocardial ischemia. The subsequent dramatic reduction in myocardial injury is now referred to as ischemic preconditioning, and it has become apparent that similar levels of cardioprotection can be achieved by applying the stimulus during or after the lethal ischemia (preconditioning or postconditioning, respectively).
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