ABSTRACT
Ischemic heart disease accounts for approximately 50% of all cardiovascular deaths and is the leading cause of congestive heart failure.1 With 1.1 million myocardial infarctions and more than 400000 new cases of congestive heart failure each year in the USA, cardiovascular disease severely impacts on men and women. For patients diagnosed with congestive heart failure, a consequence of chronic heart failure, the 1-year mortality rate is 20%. Myocardial necrosis is due to myocardial infarction and is, by nature, an irreversible injury.2 After coronary artery occlusion the cardiomyocytes are destroyed irreversibly.2,3 The extent of the infarction, with respect to the loss of cardiomyocytes, depends on the duration and severity of the perfusion defect.4 However, the extent of infarction is also modulated by a number of factors, including collateral blood supply, medications and ischemic preconditioning.5 Beyond contraction and fibrosis of myocardial scar, progressive ventricular remodeling of non-ischemic myocardium can further reduce cardiac function in the weeks to months after the initial event.6 Many of the therapies available to clinicians today can significantly improve the prognosis of patients with acute myocardial infarction.7 Although angioplasty and thrombolytic agents can relieve the cause of the infarction by prompt reperfusion of the occluded artery, the time from onset of occlusion to reperfusion determines the degree of irreversible myocardial injury.8 However, post-infarction heart failure remains a major challenge, resulting from ventricular remodeling processes, characterized by progressive expansion of the infarct area and dilatation of the left ventricular (LV) cavity.9
