ABSTRACT

Introduction Ischemic heart disease is the leading cause of mortality in the Western world. Myocardial infarction (MI) is frequently complicated by maladaptive left ventricular (LV) remodeling, which is characterized by ventricular dilatation and diminished cardiac performance. This may contribute to the progression into congestive heart failure. The current treatment option to reduce ischemic cardiovascular damage is to provide reperfusion of the infarct-related coronary artery by, for example, percutaneous transluminal coronary angioplasty (PTCA) or thrombolysis. The other option is to revascularize the ischemic area by coronary artery bypass grafting (CABG). These therapies have successfully reduced MI size and decreased the mortality of acute MI. However, when patients present late ( > 12 hours after MI) or fail to respond to therapy, a transmural MI will develop, characterized by cell death (Figure 6.1). The prevalence of congestive heart failure continues to increase and remains associated with a more than 10-fold elevated risk of death, despite the introduction of multiple treatment strategies to reduce the infarct size and LV remodeling. The search for alternative therapies remains necessary. At present, cell transplantation appears a promising treatment to repair the damaged myocardium and restore cardiac function, augmenting the inadequate intrinsic repair mechanisms within the diseased heart. Cell transplantation therapy might enhance the formation of vascular structures and serve as

a source of new cardiomyocytes to restore ventricular wall thickness and improve the contractile function of the heart. Additionally, transplanted cells may activate resident progenitor cells in the heart via a paracrine pathway.