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Strategies for myocardial protection in cardiac surgery are directed at the prevention of procedure-induced ischemia/reperfusion injury as well as metabolic resuscitation in acute ischemic syndromes. Postreperfusion myocardial dysfunction remains a significant clinical problem, most importantly in certain high-risk patient groups. The large body of experimental evidence demonstrating a significant role for sodium-hydrogen exchange activation in myocardial ischemia/reperfusion injury suggests that the ability to pharmacologically inhibit the exchanger presents a promising new approach to current myocardial preservation techniques.