BACKGROUND: Left ventricular remodeling after myocardial infarction (MI) results in ventricular dilation, fibroplasia, and decline in cardiac function. There is significant morbidity and mortality associated with this process, often leading to heart failure despite medical management. New therapies aimed at altering ventricular remodeling after MI are needed, and cytotherapy utilizing progenitor cells is a current area of investigation. THE PROBLEM: Many variables need to be considered to maximize the therapeutic benefit of cytotherapy, including the cell type, the method of delivery, the timing, and patient selection. Investigation into progenitor cell biology will continue to identify novel treatment strategies that then must be tested clinically to demonstrate safety, feasibility, and ultimately therapeutic benefit. BASIC/CLINICAL SCIENCE ADVANCES: Although progenitor cells have the potential to affect ventricular remodeling through multiple mechanisms, their major effect is likely due to actions of secreted factors. Hepatocyte growth factor, stromal-derived growth factor-1 alpha, and stem cell factor affect the mobilization of progenitor cells, which makes it possible to develop treatment strategies based on recruitment of endogenous progenitor cells. CLINICAL CARE RELEVANCE: There have been a number of randomized controlled trials demonstrating modest improvements in cardiac function using progenitor cell therapies after MI. In addition, clinical trials have used granulocyte-colony-stimulating factor as a treatment aimed at increasing progenitor cell mobilization. CONCLUSION: Progenitor cell therapy after MI has been shown to be safe and feasible with some improvements in cardiac function and clinical outcomes. Further investigation is needed to better understand the biology of progenitor cells and the effects of progenitor cell-based therapies.
BACKGROUND: Left ventricular remodeling after myocardial infarction (MI) results in ventricular dilation, fibroplasia, and decline in cardiac function. There is significant morbidity and mortality associated with this process, often leading to heart failure despite medical management. New therapies aimed at altering ventricular remodeling after MI are needed, and cytotherapy utilizing progenitor cells is a current area of investigation. THE PROBLEM: Many variables need to be considered to maximize the therapeutic benefit of cytotherapy, including the cell type, the method of delivery, the timing, and patient selection. Investigation into progenitor cell biology will continue to identify novel treatment strategies that then must be tested clinically to demonstrate safety, feasibility, and ultimately therapeutic benefit. BASIC/CLINICAL SCIENCE ADVANCES: Although progenitor cells have the potential to affect ventricular remodeling through multiple mechanisms, their major effect is likely due to actions of secreted factors. Hepatocyte growth factor, stromal-derived growth factor-1 alpha, and stem cell factor affect the mobilization of progenitor cells, which makes it possible to develop treatment strategies based on recruitment of endogenous progenitor cells. CLINICAL CARE RELEVANCE: There have been a number of randomized controlled trials demonstrating modest improvements in cardiac function using progenitor cell therapies after MI. In addition, clinical trials have used granulocyte-colony-stimulating factor as a treatment aimed at increasing progenitor cell mobilization. CONCLUSION: Progenitor cell therapy after MI has been shown to be safe and feasible with some improvements in cardiac function and clinical outcomes. Further investigation is needed to better understand the biology of progenitor cells and the effects of progenitor cell-based therapies.
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