Key result
A 10% drop in body weight is linked to a ~3% reduction in height-indexed LV mass.
Why the study?
Effects of weight change on cardiac structure have not been extensively investigated in large community-based populations despite obesity being an independent risk factor for incident heart failure.
Does weight loss decrease progressive left ventricular remodeling in a community-based population?
Cohort (n=2,351)
Yes
Does weight loss decrease progressive left ventricular remodeling in a community-based population?
Mean Difference: -2.76 (95% CI -3.42–-2.1)
p-value: p=< 0.0001
Weight loss is associated with significant beneficial effects on cardiac remodeling (decreased LV mass) without a threshold effect, suggesting any degree of weight loss may benefit the heart.
Weight loss may reduce LV mass in community cohorts; extends observational remodeling data but leaves causal effects open for RCTs.
Obesity (body mass index, BMI > 30 kg/m2) is an independent risk factor for incident heart failure (HF). Effects of weight change on cardiac structure have not been extensively investigated in large community-based populations. We hypothesized that weight loss and gain in the Multi-Ethnic Study of Atherosclerosis (MESA) would coincide with changes in left ventricular (LV) mass -- key features in the progression to obesity-related HF. To investigate the association of longitudinal changes in weight on ventricular remodeling, we investigated 2,351 patients in MESA who underwent two serial cardiac magnetic resonance imaging (CMR) examinations at initial enrollment (2002) and at follow-up (2011) with available obesity status. Canonical parameters of LV structure and function (height-indexed LV mass, LV volumes, and LV ejection fraction) were measured. MESA participants were classified by obesity status (normal weight: 18.5-25 kg/m2; overweight/obese ≥ 25 kg/m2). We constructed splines for linear and logistic models using generalized additive models to assess the form of the continuous relationship between indexed LV mass changes and weight change qualitatively. Next, we constructed multivariable linear models, adjusted for confounders involved in the pathogenesis of LV hypertrophy that could be altered by weight change, including: glycemic status, hypertension, waist-to-hip ratio, body-mass-index, and biomarkers of inflammation. Finally, the multivariable linear model was adjusted for age, gender, race, income, educational status, smoking, Exam 1 BMI, and height-indexed LV mass at Exam 1. Of the overall cohort studied, 257 individuals (11%) experienced ≥10% weight loss (median 10.2 kilograms) and 194 (8%) had ≥10% weight gain (median 10.0 kilograms). After adjustment for hypertension, diabetes, age, race, and other clinical risk factors, every 10% decrease in weight was associated with a fully covariate-adjusted 3% additional decrease in height-indexed left ventricular mass. Every 10% loss in body weight increased the odds of a 10% or greater drop in left ventricular mass by 50%. Finally, regression models suggested linear decreases in left ventricular mass regression with increasing weight loss, suggesting no threshold effect for weight loss on cardiac remodeling. Weight loss is associated with significant beneficial effects on cardiac remodeling, even after adjustment for baseline obesity-related cardiometabolic risk. There is no threshold for the weight change needed before benefits on cardiac occur, suggesting that any degree of weight loss may be beneficial to the heart.
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Abbasi et al. (2014) conducted a cohort in Left ventricular remodeling (n=2,351). Weight loss vs. Baseline weight / no weight loss was evaluated on Percent change in height-indexed LV mass (MD -2.76, 95% CI -3.42 to -2.1, p=< 0.0001). Every 10% decrease in body weight was associated with a 2.76% decrease in height-indexed left ventricular mass and increased the odds of a 10% or greater drop in LV mass by 50%.
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