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Published on: June 15, 2020
Impact of obesity on left ventricular mass and function in subjects with chronic volume overload
Piercarlo Ballo1, Andrea Motto, Sergio Mondillo
1Cardiology Operative Unit, S. Andrea Hospital, La Spezia, Italy. pcballo@tin.it
Insights
Overweight and obesity increase left ventricular (LV) mass and impair contractility in patients with volume overload. These conditions lead to LV hypertrophy and reduced heart muscle function.
Area of Science:
- Cardiology
- Obesity Medicine
- Echocardiography
Background:
- Previous research explored obesity's impact on left ventricular (LV) function in pressure overload conditions.
- Limited data exist on how overweight and obesity affect LV mass and function in patients with chronic LV volume overload.
Purpose of the Study:
- To assess the impact of overweight and obesity on LV mass and systolic function in patients with chronic LV volume overload.
Main Methods:
- Echocardiography was used to determine LV mass, ejection fraction, and myocardial contractility in 885 subjects with degenerative aortic regurgitation.
- Body Mass Index (BMI) was analyzed for its independent predictive value on LV mass and contractility.
Main Results:
- LV mass was significantly greater in overweight and obese individuals compared to normal-weight patients, even after adjusting for workload, gender, and body size.
- Despite similar ejection fractions, LV myocardial contractility was reduced in overweight and obese subjects.
- Multivariate analysis confirmed BMI as an independent predictor of LV mass, with LV hypertrophy mediating the negative effect on contractility.
Conclusions:
- Overweight and obesity are linked to LV hypertrophy and impaired cardiac contractility in patients with chronic LV volume overload.
- The effects of overweight-obesity appear additive rather than synergistic with the underlying volume overload condition.
Objective:
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.
Research Methods And Procedures:
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.
Results:
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.
Discussion:
Overweight and obesity are associated with LV hypertrophy and contractile impairment in patients with underlying chronic LV volume overload.
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