Obesity and Cardiac Remodeling in Adults: Mechanisms and Clinical Implications

Abstract

Obesity, particularly severe obesity is capable of producing hemodynamic alterations that contribute to changes in cardiac morphology which may predispose to impairment of ventricular function and heart failure. These include a high cardiac output state in most, left ventricular (LV) hypertrophy, and LV diastolic dysfunction. Right heart involvement may result from LV failure, the hypercirculatory state, and sleep disordered breathing. In recent years experimental studies and some studies in humans suggest that certain neurohormonal and metabolic alterations that occur commonly in obesity may contribute to alterations in cardiac structure and function. These include activation of the renin-angiotensin-aldosterone and sympathetic nervous systems, hyperleptinemia due to leptin resistance, low circulating adiponectin levels, insulin resistance with hyperinsulinemia, and possibly cardiac lipotoxicity. This review will describe the ways in which these factors weave together to promote adaptations and maladaptations that result in alterations in cardiac structure and function which may contribute to the development of heart failure.