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Peer-reviewedCC BY-NCJournal of the American Heart Association

Body Mass Index, Valsartan, and Myocardial Remodeling in Early‐Stage Hypertrophic Cardiomyopathy: A Secondary Analysis of the Randomized VANISH Trial

14 more authors
17 affiliations
  1. 1Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School
  2. 2Copenhagen University Hospital
  3. 3University of Pennsylvania Perelman School of Medicine
  4. 4University of Michigan
  5. 5Cleveland Clinic Foundation
  6. 6Heart Institute, University of São Paulo Medical School
  7. 7Boston Children's Hospital
  8. 8Johns Hopkins University School of Medicine
  9. 9Washington University School of Medicine
  10. 10Stanford University School of Medicine
  11. 11Children's Hospital of Philadelphia
  12. 12University of Colorado Anschutz Medical Campus
  13. 13University of Virginia Health System
  14. 14Heart Institute, Cincinnati Children's Hospital Medical Center
  15. 15Vanderbilt University Medical Center
  16. 16University of Pittsburgh School of Medicine and UPMC
  17. 17DC Veterans Administration Medical Center

Abstract

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.

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BibTeX
@article{ostrominski2026body,
  title = {{Body Mass Index, Valsartan, and Myocardial Remodeling in Early‐Stage Hypertrophic Cardiomyopathy: A Secondary Analysis of the Randomized VANISH Trial}},
  author = {John W. Ostrominski and Brian L. Claggett and Michael Jerosch‐Herold and Anna Axelsson Raja and Sharlene M. Day and Mark W. Russell and Kenneth Zahka and Alexandre C. Pereira and Steven D. Colan and Anne M. Murphy and Charles Canter and Richard G. Bach and Matthew T. Wheeler and Joseph W. Rossano and Anjali T. Owens and Luisa Mestroni and Matthew R.G. Taylor and Amit R. Patel and Ivan Wilmot and Jonathan H. Soslow and Jason R. Becker and Neal K. Lakdawala and Henning Bundgaard and Jose D. Vargas and Carolyn Y. Ho and for the Valsartan for Attenuating Disease Evolution in Early Sarcomeric Hypertrophic Cardiomyopathy (VANISH) Investigators},
  journal = {Journal of the American Heart Association},
  year = {2026},
  month = oct,
  doi = {10.1161/jaha.126.050131},
  url = {https://www.ahajournals.org/doi/10.1161/JAHA.126.050131},
  note = {CC BY-NC},
}
RIS
TY  - JOUR
TI  - Body Mass Index, Valsartan, and Myocardial Remodeling in Early‐Stage Hypertrophic Cardiomyopathy: A Secondary Analysis of the Randomized VANISH Trial
AU  - John W. Ostrominski
AU  - Brian L. Claggett
AU  - Michael Jerosch‐Herold
AU  - Anna Axelsson Raja
AU  - Sharlene M. Day
AU  - Mark W. Russell
AU  - Kenneth Zahka
AU  - Alexandre C. Pereira
AU  - Steven D. Colan
AU  - Anne M. Murphy
AU  - Charles Canter
AU  - Richard G. Bach
AU  - Matthew T. Wheeler
AU  - Joseph W. Rossano
AU  - Anjali T. Owens
AU  - Luisa Mestroni
AU  - Matthew R.G. Taylor
AU  - Amit R. Patel
AU  - Ivan Wilmot
AU  - Jonathan H. Soslow
AU  - Jason R. Becker
AU  - Neal K. Lakdawala
AU  - Henning Bundgaard
AU  - Jose D. Vargas
AU  - Carolyn Y. Ho
AU  - for the Valsartan for Attenuating Disease Evolution in Early Sarcomeric Hypertrophic Cardiomyopathy (VANISH) Investigators
PY  - 2026
DA  - 2026/10/20
JO  - Journal of the American Heart Association
DO  - 10.1161/jaha.126.050131
UR  - https://www.ahajournals.org/doi/10.1161/JAHA.126.050131
AB  - 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.
SN  - 2047-9980
ER  -