Weight reduction of 39-84 kg reduced resting cardiac output (7.9 to 6.2 L/min), but exercise left ventricular filling pressure remained abnormal (20 mm Hg), indicating persistent dysfunction.
Observational (n=9)
Does weight reduction improve left ventricular hypertrophy and dysfunction in markedly obese patients?
While the circulatory effects of gross obesity are largely reversible with weight loss, evidence of left ventricular dysfunction persists, suggesting myocardial hypertrophy and reduced ventricular compliance do not regress significantly.
Weight reduction programs usually improve the exercise capacity of patients with chronic exogenous obesity. However, the reversibility of left ventricular hypertrophy and dysfunction associated with obesity is unknown. Accordingly, an analysis was made of hemodynamic data obtained by cardiac catheterization and standard chest roentgenograms in nine markedly obese patients before and after weight loss of 39 to 84 kg (24 to 55% of control weight) over periods of 4 to 34 months. In each case body oxygen uptake (360 to 297 ml/min), blood volume (7.8 to 6.1 liters), cardiac output (7.9 to 6.2 liters/min), and arteriovenous oxygen difference (4.6 to 4.0 vol. %) were significantly reduced after weight loss. Systemic arterial pressure declined (102 to 87 mm Hg) while systemic vascular resistance changed insignificantly (1,067 to 1,141 dynes-sec-cm -5 ). In seven subjects comparable chest roentgenograms before and after weight reduction revealed decrease in the cardiothoracic ratio, suggesting a reduction in left ventricular dimensions. These results have been interpreted as indicating that the circulatory effects of gross obesity are largely reversible with weight loss. Despite reductions in left ventricular stroke work, stroke volume, and cavity size at rest, the average left ventricular filling pressure rose with exercise to a comparable and abnormal level (20 mm Hg) both before and after weight loss. Thus, evidence of left ventricular dysfunction persisted, suggesting that myocardial hypertrophy and reduced ventricular compliance did not regress significantly with weight loss over periods as long as 3 years.
Alexander et al. (1972) conducted an observational in Chronic exogenous obesity (n=9). Weight reduction vs. Baseline was evaluated on Hemodynamic data and chest roentgenograms. Weight reduction of 39-84 kg reduced resting cardiac output (7.9 to 6.2 L/min), but exercise left ventricular filling pressure remained abnormal (20 mm Hg), indicating persistent dysfunction.