Abstract
Myocardial ischemia-reperfusion injury associated with cardiac surgery is an acute inflammatory process in which activated leukocytes and endothelial cells play a critical role. Recent data indicate that the release of cytokines is crucial in inducing leukocytes and endothelial cells activation during cardiopulmonary bypass (CPB). Some inflammatory cytokines can be produced locally from the heart, particularly interleukin (IL)-8, which may further enhance leukocyte activation and accumulation in the injured myocardium. In fact, postoperative levels of cardiac troponin-I, a highly specific marker of myocardial injury, correlated strongly with IL-8 values in patients undergoing coronary artery bypass grafting (CABG). Off-pump CABG is associated with less IL-8 production compared with conventional procedure, which may in turn reduce the degree of myocardial injury. On the other hand, reduced release of IL-8 and cardiac troponin-I has also been discovered following the use of heparin-coated CPB circuits. In addition, the balance between pro- and anti-inflammatory mediators may be even more crucial in determining the extent of injury. Hence, avoiding the use of CPB or improving the biocompatibility of CPB may lead to better myocardial preservation. Research along these lines is expected to help in the development of ideal therapeutic strategies to minimize the inflammatory response and subsequent myocardial injury associated with cardiac surgery.
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