Abstract

In association with consistent increases in stroke volume and a high incidence of systemic and/or pulmonary arterial hypertension, the cardiac work of very obese patients at rest was considerably greater than that predicted for normotensive subjects at ideal body weight. Although this change was effected chiefly by increased left ventricular work, and the latter was roughly correlated with the amount of excess body weight, variable increases in right ventricular work resulted in a lack of correlation between total cardiac work and the amount of excess weight. Though pulmonary hypertension secondary to an increase in left ventricular filling pressure usually occurred in the very obese patients of this series under conditions of moderate exercise, the increment in cardiac output per unit increment in oxygen consumption with exercise was within normal limits. Because of the need to move excess body weight, at any given level of activity the cardiac workload was considerably greater for the obese subjects than for individuals at ideal body weight. Cardiac enlargement and increased heart weight were found quite regularly in very obese subjects, increasing in rough proportion to the amount of excess body weight. The increased heart weight was due to muscular hypertrophy involving the left ventricle or both the left and right ventricles. Neither fatty infiltration of the myocardium nor isolated right ventricular hypertrophy was observed. Cardiac failure occurred in 8 per cent of the extremely obese patients in this series, involving a high cardiac output and left ventricular or biventricular insufficiency. It has been proposed that myocardial hypertrophy and failure derive from the increased cardiac workload present at rest and during exercise. Heart failure due to obesity generally responded well to bed rest, digitalis, diuretics, dietary sodium restriction and measures usually effective in managing heart failure due to other causes. Effective long term therapy necessarily involved weight reduction.

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