Obesity produces a variety of hemodynamic alterations that may cause changes in cardiac morphology which predispose to left and right ventricular dysfunction. Various neurohormonal and metabolic alterations commonly associated with obesity may contribute to these abnormalities of cardiac structure and function. These changes in cardiovascular hemodynamics, cardiac morphology, and ventricular function may, in severely obese patients, predispose to heart failure, even in the absence of other forms of heart disease (obesity cardiomyopathy). In normotensive obese patients, cardiac involvement is commonly characterized by elevated cardiac output, low peripheral vascular resistance, and increased left ventricular (LV) end-diastolic pressure. Sleep-disordered breathing may lead to pulmonary arterial hypertension and, in association with left heart failure, may contribute to elevation of right heart pressures. These alterations, in association with various neurohormonal and metabolic abnormalities, may produce LV hypertrophy; impaired LV diastolic function; and less commonly, LV systolic dysfunction. Many of these alterations are reversible with substantial voluntary weight loss.
Keywords: Bariatric surgery; Cardiac output; Central blood volume; Concentric and eccentric left ventricular hypertrophy and remodeling; Diet and exercise; Duration of obesity; Heart failure; Hemodynamics; Left ventricular; Left ventricular diastolic dysfunction; Left ventricular diastolic filling and relaxation; Left ventricular geometry; Left ventricular hypertrophy; Left ventricular systolic dysfunction; Left ventricular systolic function; Obesity; Obesity cardiomyopathy; Severe obesity; Sleep-disordered breathing; Systemic hypertension; Weight loss.