Obesity is reaching epidemic proportions in the United States. Obesity adversely affects the circulatory system with resultant endothelial dysfunction, which promotes systemic hypertension, coronary artery disease, and vascular calcification. It is believed that the release of adipokines is responsible for this effect. In addition, obesity causes intrinsic changes in the heart including an increase in left ventricular (LV) mass, LV hypertrophy, LV dilatation, left atrial dilatation, and diastolic, as well as systolic dysfunction in some cases. The combination of increased adipose cells and an increase lean muscle mass in obese patients results in high cardiac output and an accompanying increased circulating volume leading to these adaptive changes. Weight loss by means of caloric restriction or surgery results in favorable hemodynamic changes referred to as "reverse remodeling." Regression of LV mass and chamber size has been shown universally. However, some studies have failed to reveal improvement in diastolic function possibly because of confounders such as nutritional deficiency that may occur after weight loss surgery. Some evidence seems to suggest that the greatest regression of LV mass and LV hypertrophy may occur when weight loss is combined with beta-adrenergic blocker therapy (in those who have an indication for the drug) when compared with other antihypertensive drugs versus weight loss alone.