Ischemic heart disease (IHD) is the single largest cause of death worldwide. In the United States of America alone, there are over 1,000,000 heart attacks every year1.  Limitation of blood flow to the heart causes ischemia and irreversible death of the myocardial cells resulting in irreversible heart damage, progressive myocardial remodeling, reduced heart function and heart failure.  The size of a myocardial infarct is directly correlated with a decrease of heart function, the risk of developing heart failure and mortality. Infarct size may be significantly decreased with prompt reperfusion after the first symptoms, either by thrombolytic treatment or by percutaneous intervention. Indeed, restoration of arterial perfusion with thrombolytic and antiplatelet therapy during percutaneous coronary intervention (PCI) is the most commonly performed invasive therapeutic cardiac procedure in the management of IHD.  The decline in myocardial infarction (MI) acute mortality, achieved with primary PCI, has augmented the prevalence of HF among survivors, because of the development of substantial scarring despite reperfusion strategies. A major problem is that human adult cardiac myocytes fail to elicit an endogenous regenerative response after a MI, and there are no adjunctive pharmacological treatments that can be administered in conjunction with reperfusion injury to regenerate heart muscle at the time of or following an MI.