Obesity is both a risk factor and a direct cause of heart failure (HF) in adults. Severe obesity produces hemodynamic alterations that predispose to changes in left ventricular morphology and function, which, over time, may lend to the development of HF (obesity cardiomyopathy). Certain neurohormonal and metabolic abnormalities as well as cardiovascular co-morbidities may facilitate this process. Substantial purposeful weight loss is capable of reversing most of the alterations in cardiac performance and morphology and may improve functional capacity and quality of life in patents with obesity cardiomyopathy.