Chest
Volume 90, Issue 2, August 1986, Pages 275-279
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Today's Practice of Cardiopulmonary Medicine
Cardiovascular Adaptation to Obesity and Hypertension

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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.

Section snippets

Systemic Hemodynamics in Obesity and Hypertension

Systemic vascular resistance seems to be an indicator of the severity of systemic hypertensive vascular disease since it reflects either reversible arteriolar spasm or less reversible arteriosclerosis.10 Systemic vascular resistance can be calculated by dividing mean arterial pressure by cardiac output and is proportional to the radius of the blood vessel to the fourth power, to blood viscosity, and to the vessel length (Poiseuille's law). Although obesity and hypertension are related, the two

Hypertension

Substantial evidence exists to show that the fundamental response to an isolated increase in afterload consists of left ventricular hypertrophy (LVH) without chamber dilatation or concentric hypertrophy.20, 21, 22 These cardiac adaptive changes occur very early in hypertensive disease and can be seen in about 50 percent of juveniles whose blood pressure is elevated only to the borderline level.22 Since hypertrophy of the myocardial wall decreases the ventricular wall stress,23 it is a common

Obesity-Hypertension Connection

It is postulated that mild obesity may protect a given patient from the deleterious effect of hypertension by reducing systemic vascular resistance and thus decreasing hypertensive target organ damage.35, 36, 37, 38, 39 There are indeed some data to support this hypothesis. As mentioned earlier, we have shown that systemic vascular resistance and renal vascular resistance are lower in obese patients than in lean subjects having similar arterial pressures.6, 18, 19, 40 Likewise, there is an

Weight Reduction

Weight reduction in the obese hypertensive patient is clearly associated with a fall in arterial pressure, but the underlying mechanism remains obscure. The reduction in pressure has been attributed to alterations in body fluid partitions by reduced sodium intake47 and falls in the renin and aldosterone levels.48 Also, weight loss reduces the sympathetic drive to the cardiovascular system,49, 50 allowing a redistribution of the intravascular volume from the cardiopulmonary area to the

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