A REVIEW ON CARDIAC REMODELLING

Abstract

Heart failure (HF) is a worldwide health problem that affects approximately 26 million individuals. It is known that heart disease progresses to HF, and there is a link between cardiac remodelling and the development of HF. The term "remodelling" was used for the first time in 1982 by Hockman and Buckey, in a myocardial infarction (MI) model. Cardiac remodelling refers to changes in the size, shape, structure, and function of the heart. This can happen as a result of exercise (physiological remodeling) or after injury to the heart muscle (pathological remodeling).{3} The injury is typically due to myocardial infarction. Chronic hypertension, congenital heart disease with intracardiac shunting, and valvular heart disease may also lead to remodelling. Between the physiological and pathological remodelling, the physiological remodelling is reversible and the pathological remodeling is irreversible. Cardiac remodelling is considered to be not only an adaptive event but also a maladaptive phenomenon. In the acute phase of a myocardial stress, cardiac remodelling acts as an adaptive response that enables the heart to maintain cardiac output; however, after the prolonged stressful stimulus, this continuous process leads to progressive decompensation. The cardiac myocyte is the major cell involved in remodeling. Fibroblasts, collagen, the interstitium, and the coronary vessels to a lesser extent, also play a role. The most used methods to detect these changes are echocardiography, ventriculography, and nuclear magnetic resonance. Several markers may indicate a remodelling process, including changes in the expression of myosin heavy chain isoforms, with an increase in alpha- and a decrease in beta-myosin heavy chain, increased expression of GLUT-1, alpha-actin, natriuretic peptide, galectin, caveolin, neuronal nitric oxide synthase, angiotensin-converting enzyme, a decrease in GLUT-4, SERCA2a, and a shift from glucose to fatty acid oxidation.Medications may attenuate remodelling , Angiotensin-converting enzyme (ACE) inhibitors, Beta blockers (Carvedilol), may actually reverse the remodelling process by reducing left ventricular volumes and improving systolic function.