Congestive heart failure remains a major public health problem, with recent estimates indicating that end-stage heart failure with two-year mortality rates of 70–80% affects over 60,000 patients in the US each year. In Western societies heart failure is primarily the consequence of previous myocardial infarction . As new modalities have emerged which have enabled significant reduction in early mortality from acute myocardial infarction there has been a paradoxical increase in the incidence of postinfarction heart failure among the survivors. Current therapy of heart failure is limited to the treatment of already established disease and is predominantly pharmacological in nature, aiming primarily to inhibit the neurohormonal axis that results in excessive cardiac activation through angiotensinor norepinephrine-dependent pathways. For patients with end-stage heart failure treatment options are extremely limited, with less than 3000 being offered cardiac transplants annually due to the severely limited supply of donor organs , and implantable left ventricular assist devices (LVADs) being expensive, not proven for long-term use, and associated with significant complications . Clearly, development of approaches that prevent heart failure after myocardial infarction would be preferable to those that simply ameliorate or treat already established disease.