Cardiovascular adaptation to obesity and hypertension

Hypertension and obesity are two disorders that are closely related; each occurs more frequently with the other than in an otherwise normal population. These two disorders, however, exert disparate effects on cardiovascular structure and function. The hallmark of essential hypertension is an increased total peripheral resistance, and hypertensive patients have a contracted intravascular volume and normal cardiac output but an increased left ventricular stroke work due to a high afterload. In contrast, obese patients have an increased intravascular volume, left ventricular filling pressure, cardiac output and a lower total peripheral and renal vascular resistance. Left ventricular adaptation will consist of eccentric hypertrophy in obesity regardless of the level of arterial pressure and concentric hypertrophy in lean hypertensive patients. Although obesity may mitigate the harmful effect of a chronically elevated total peripheral and renal vascular resistance and lessen target organ damage in essential hypertension, the combination of obesity and hypertension presents a double burden to the left ventricle and is associated with systolic and diastolic dysfunction and a propensity for high grade ventricular dysrhythmias. It is not surprising that congestive heart failure and sudden death are common sequelae of obesity hypertension. Weight reduction reduces arterial pressure by decreasing intravascular volume and cardiac output associated with a fall in sympathetic activity and reversal of cardiac hypertrophy. Therefore, weight loss unloads the heart from the two-fold burden caused by obesity and hypertension and should become a major goal in the prevention and treatment of heart disease.