The main determinant of myocardial necrosis following an acute myocardial infarction (AMI) is duration of ischemia. Infarct size is a strong independent predictor of postinfarction mortality. Interventions able to protect the myocardium from death during an AMI (cardioprotection) are urgently needed. Myocardial injury associated with reperfusion (ischemia/reperfusion injury [I/R]) significantly contributes to the final necrotic size. Duration of ischemia can only be reduced by social and emergency medical services--hospital collaborative programs. However, for a given duration of ischemia, infarct size can be limited by reducing reperfusion injury. Despite the fact that several therapies have been shown to reduce I/R injury in animal models, translation to humans has been frustrating. The cost of developing new drugs able to reduce I/R injury is huge, and this is a major roadblock in the field of cardioprotection. Recent studies have proposed that old, inexpensive drugs--in human use for decades (e.g., β-blockers and cyclosporine, among others)--can reduce I/R injury when administered intravenously before coronary opening. The demonstration of such a cardioprotective effect should have a significant impact in the care of AMI patients.
© 2012 New York Academy of Sciences.