Effects of Granulocyte-Colony Stimulating Factor and Bone Marrow Mononuclear Cells on Cardiac Function and Remodeling in the Porcine Reperfused Myocardial Infarction Model

Introduction Since ventricular remodeling after myocardial infarction (MI), which causes ventricular dysfunction, is strongly associated with the prognosis, the prevention of remodeling is an important therapeutic concern in the management of myocardial infarction. Ventricular remodeling is usually determined by infarct size, ventricular loading condition, and infarct artery patency. Although rapid reperfusion of the infarct-related coronary artery is of great importance in salvaging myocardium and limiting infarct size, there are cases of delayed reperfusion and those of irreversible myocardial damage or ventricular dysfunction even after optimal reperfusion in clinical settings. Medically, angiotensin converting enzyme inhibitors and beta blockers can prevent ventricular remodeling and reduce mortality in patients with myocardial infarction. However, the loss of myocytes and the resulting scar formation are irreversible processes and cannot be regenerated by these agents.