Disparate cardiovascular effects of obesity and arterial hypertension

• Published in: The American journal of medicine Vol. 74; no. 5; pp. 808 - 812
• Main Authors: Messerli, Franz H., Sundgaard-Riise, Kirsten, Reisin, Efrain, Dreslinski, Gerald, Dunn, Francis G., Frohlich, Edward
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.05.1983; Elsevier
• Subjects: Adult; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Catecholamines - blood; Clinical manifestations. Epidemiology. Investigative techniques. Etiology; Female; Hemodynamics; Humans; Hypertension - complications; Hypertension - physiopathology; Male; Medical sciences; Obesity - complications; Obesity - physiopathology; Renin - blood; Heart; Hypertension; Obesity; Limb; Exploration; Hemodynamics; Left ventricle performance; Artery
• ISSN: 0002-9343; 1555-7162
• DOI: 10.1016/0002-9343(83)91071-9

Since obesity and essential hypertension frequently coexist, a study was designed to analyze some of their cardiovascular effects. Twenty-eight obese patients, half of whom were normotensive and half with established hypertension, were matched for mean arterial pressure with 28 corresponding lean subjects. Systemic and renal hemodynamics, intravascular volume, plasma renin activity, and circulating catecholamine levels were measured. Obese patients had increased cardiac output (p < 0.001), stroke volume (p < 0.001), central blood volume (p < 0.02), plasma and total blood volume (p < 0.01), and decreased total peripheral resistance (p < 0.001). In contrast, cardiac output, central blood volume, and stroke volume of hypertensive patients were normal, but they had increased total peripheral (p < 0.001) and renal vascular resistance (p < 0.001) and a contracted intravascular volume. Left ventricular stroke work was elevated to a similar level In obesity (p < 0.001) and hypertension (p < 0.02), but the increase was caused by an expanded stroke volume in the former and by an increase in systolic pressure in the latter. It is concluded that the disparate effects of obesity and hypertension on total peripheral resistance and intravascular volume counteract and may even offset each other. Thus, obesity may mitigate the effects of chronically elevated total peripheral resistance (and therefore end-organ damage) in essential hypertension. Since both entitles affect the heart through different mechanisms, their presence in the same patient results in a double burden to the left ventricle, thereby gently enhancing the long-term risk of congestive failure.