Key result
Elevated BMI in early-stage HCM linked to ~3.6-fold higher odds of developing LGE.
Why the study?
The prevalence and impact of elevated BMI in early-stage hypertrophic cardiomyopathy were uncertain.
Does elevated body mass index worsen exercise capacity and myocardial remodeling in early-stage hypertrophic cardiomyopathy?
Cohort (n=171)
Does elevated body mass index worsen exercise capacity and myocardial remodeling in early-stage hypertrophic cardiomyopathy?
Odds Ratio: 3.6 (95% CI 1.1–11.9)
p-value: p=0.033
Elevated BMI in early-stage hypertrophic cardiomyopathy is common and associated with worsened functional capacity and adverse myocardial remodeling, identifying a potential therapeutic target.
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“It was a bit surprising that in two years, a relatively short period of time, and in a relatively well patient population, there was a statistically significant change in the composite outcome.”
Elevated BMI in early sarcomeric HCM warrants monitoring; leaves open whether it modifies progression or valsartan response.
Background Obesity is associated with adverse outcomes in overt hypertrophic cardiomyopathy, but the prevalence and impact of elevated body mass index (BMI) in early‐stage hypertrophic cardiomyopathy is uncertain. Methods In this post hoc analysis of the randomized VANISH (Valsartan for Attenuating Disease Evolution in Early Sarcomeric Hypertrophic Cardiomyopathy) trial, participants were categorized according to baseline BMI (nonelevated or elevated [≥85th percentile if age <18 years; ≥25 kg/m 2 if age ≥18 years]). Exercise capacity (peak oxygen uptake [milliliters per kilogram per minute]) and cardiac imaging parameters were evaluated by baseline BMI and 2‐year change in BMI. Results Among 171 (96%) participants (mean age, 23±10 years; 39% female sex; 97% White), 82 (48%) had nonelevated BMI and 89 (52%) had an elevated BMI. After covariate adjustment, higher baseline BMI was associated with lower peak oxygen uptake; lower left ventricular systolic and diastolic function; higher left ventricular mass; and higher atrial, ventricular, and extracellular volumes. Similarly, greater 2‐year increases in BMI were associated with greater declines in peak oxygen uptake and greater increases in left ventricular mass. Participants with elevated BMI were more likely to develop late gadolinium enhancement over 2 years (adjusted odds ratio, 3.6 [95% CI, 1.1–11.9]; P =0.033). Valsartan appeared to modestly attenuate 2‐year increases in body weight versus placebo (adjusted mean difference, −3.1% [95% CI, −6.2 to −0.1%]; P =0.042). Baseline BMI did not appear to modify the effect of valsartan on cardiac remodeling ( P interaction =0.96). Conclusions Elevated BMI was common and associated with greater hypertrophic, eccentric, and fibrotic remodeling in early‐stage hypertrophic cardiomyopathy. Two‐year increases in BMI were associated with greater phenotypic progression. These findings suggest prevention and treatment of elevated BMI may attenuate hypertrophic cardiomyopathy progression. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01912534.
No takes yet. Share an insight, caveat, or question.
Ostrominski et al. (2026) conducted a cohort in Early-stage hypertrophic cardiomyopathy (n=171). Elevated BMI vs. Nonelevated BMI was evaluated on Development of late gadolinium enhancement (OR 3.6, 95% CI 1.1-11.9, p=0.033). Elevated BMI in early-stage hypertrophic cardiomyopathy was associated with a higher likelihood of developing late gadolinium enhancement over 2 years (OR 3.6; 95% CI 1.1-11.9; P=0.033).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: