Heart Failure

Heart Failure (HF) is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. This is further subdivided into HF with reduced left ventricular ejection fraction (HFrEF) or HF with preserved left ventricular ejection fraction (HFpEF) previously known as diastolic HF. HF may be caused by disease of the myocardium, pericardium, endocardium, heart valves, vessels, or by metabolic disorders. Most patients with HFrEF should be routinely treated with guideline directed medical therapy (GDMT) that includes an angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) and a ?-blocker. Selected patients should also receive loop diuretics, hydralazine/nitrates, or aldosterone antagonists. The benefits of these medications on slowing HF progression, reducing morbidity and mortality, and/or improving symptoms are clearly established, Digoxin is potentially beneficial in symptomatic patients with HFrEF already receiving optimal medical therapy to decrease HF hospitalizations. There is little clinical trial evidence to guide which treatment are optimal to use in HFrEF.

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.