Stem Cell Therapy in Myocardial Infarction Clinical Point of View and the Results of the REANIMA Study (REgenerAtion of Myocardium with boNe Marrow Mononuclear Cells in MyocArdial Infarction)

Abstract

The incidence of heart failure (HF) after acute myocardial infarction (AMI) is around 10-40% during the hospital stay depending on its definition (Weir & McMurray, 2006; Cleland & Torabi, 2005). Also, another 10-20% of patients will develop heart failure symptoms during the next few months and years (Torabi et al., 2008). The mortality of patients with heart failure symptoms after AMI is very high and it reaches up to 50% in 5 years (Weir & McMurray, 2006; Fox et al, 2006). The left ventricle dilatation occurs in even 30% in patients reperfused successfully with primary angioplasty during six months follow-up (Bolognese el al, 2002) and the occurrence of dilatation is more pronounced in patients with lower baseline left ventricle ejection fraction (LVEF). The incidence of HF after AMI has increased, and mortality decreased over time with the better reperfusion therapy (Velagaleti et al, 2008). According to these facts, it is extremely important to develop therapeutic modalities in order to prevent the remodeling of myocardium after infarction. The adult stem cell therapy is a relatively new and promising method of an infarcted heart healing and HF prevention. In the last two decades three important discoveries regarding different regenerative steps of damaged myocardium promoted the completely new era in the treatment of ischemic heart disease. First of all, several adult multipotent and pluripotent stem cells from different tissues may trans-differentiate in certain circumstances to cardiomyocytes or other needed cells, such as endothelial cells (Korbling M & Estrov Z, 2003; Muller et al, 2005). However, in vivo, this mechanism of heart regeneration seems to be negligible (Wagers et al, 2002; Murry et al, 2004), at least for the acute injury. The second is the fact that a significant number of cardiac cells are in the proliferative state in the areas of myocardium adjunction to infarction (Beltrami et al, 2001). The first source of these regenerative cells is very probably resident cardiac stem cells which are in the quiescent state out of injury, but in the time of infarction they proliferate and differentiate to cardiomyocytes, smooth muscle cells and endothelial cells (Bollini et al, 2011). And the third important discovery is that in the time of infarction,