Impact of obesity on left ventricular mass and function in subjects with chronic volume overload.

Abstract

Previous studies evaluated the effect of obesity on left ventricular (LV) mass and systolic function in healthy subjects and in patients with coexistent chronic LV pressure overload due to hypertension, but no data exist regarding subjects with underlying volume overload. This study assessed the impact of overweight-obesity on LV mass and systolic function in patients with coexistent chronic LV volume overload. In 885 subjects with degenerative aortic regurgitation, a common cause of LV volume overload, LV mass, ejection fraction, and myocardial contractility were determined by echocardiography. LV mass was greater in overweight (193.5 +/- 54.2 g) and further increased in obese subjects (208.4 +/- 63.6 g) in comparison with normal-weight patients (177.7 +/- 54.9 g) (p < 0.0001), and these differences were still evident after adjustment for LV workload, gender, and body size. Despite no differences in ejection fraction, LV myocardial contractility was lower in overweight (92.6 +/- 14.8%) and obese subjects (91.7 +/- 14.4%) than normal-weight individuals (95.6 +/- 16.0%) (p = 0.0058). The magnitudes of these effects were not different from those found in age-, gender-, and body size-matched controls, suggesting additive interaction, rather than synergistic, between overweight-obesity and the underlying condition of volume overload. Multivariate analysis showed that BMI independently predicted LV mass and that the negative effect on LV myocardial contractility was mediated by LV hypertrophy. Overweight and obesity are associated with LV hypertrophy and contractile impairment in patients with underlying chronic LV volume overload.