ABSTRACT
Introduction Modern reperfusion strategies and advances in pharmacological management of acute myocardial infarction (AMI) have resulted in an increasing proportion of patients surviving the acute event. Many of these patients eventually develop adverse left ventricular remodeling and heart failure. None of our current therapies addresses the underlying cause of the remodeling process, i.e. the damage to the cardiomyocytes and the vasculature in the infarcted area. The alleged transdifferentiation capacity of adult stem cells and the recent discovery of endogenous cardiac repair mechanisms have suggested that cardiac repair (i.e. replacement of necrotic or scarred tissue with viable myocardium) might be achieved in the clinical setting.1
