Myocardial Infarction

Molecular mechanisms of myocardial remodeling involves rearrangement of normally existing structure of heart include size, geometry, shape, composition and function of the myocardium and heart. Myocardial remodeling occurs mainly due to physical, mechanical stimuli like cardiac overload, ischemia and stretch as well as at chemical level includes misbalancing of atrial natriuretic peptide, renin-angiotensin system, aldosterone, endothelin, nitric oxide production, catecholamine and TNF-α. Myocardial infarction, heart failure and other cardiac diseases are major causes of myocardial remodeling. Myocardial infarction at molecular level involves extracellular matrix (ECM) proteins, elevated peripheral blood mononuclear cell counts, muscle LIM(Lin11, Isl-1, Mec-3) protein-calcineurin signaling; late exercise effects on cardiac remodeling following myocardial infarction, influence of AIN-93(American Institute of Nutrition) diet with myocardial infarction are major factors responsible for pathogenesis of myocardial remodeling.  Heart failure with adaptive versus maladaptive imbalance processes and neuro-hormonal imbalance activation are major causes of myocardial remodeling. Additional factors influence remodeling includes cardiac myocytes, fibroblast proliferation, collagen degradation and apoptosis. This review mainly focuses on pathophysiology involved in myocardial remodeling after myocardial infarction and heart failure as well as various effects of cardiac autocrines. Keywords: Myocardial Remodeling, Cardiac Autocrines, Myocardial Infarction, Heart Failure, Cardiac myocytes proliferation.