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Visceral and Subcutaneous Adiposity and Brachial Artery Vasodilator Function
Authors:Nisha I. Parikh  Michelle J. Keyes  Martin G. Larson  Karla M. Pou  Naomi M. Hamburg  Joseph A. Vita  Christopher J. O'Donnell  Ramachandran S. Vasan  Gary F. Mitchell  Udo Hoffmann  Caroline S. Fox  Emelia J. Benjamin
Affiliation:1. National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, Massachusetts, USA;2. Present address: Beth Israel Deaconess Medical Center, Harvard Medical School, Brookline, Massachusetts, USA;3. Mathematics and Statistics, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA;4. Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA;5. Cardiology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA;6. Department of Cardiology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA;7. National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA;8. Preventive Medicine Section, Boston University School of Medicine, Boston, Massachusetts, USA;9. Cardiovascular Engineering Inc., Holliston, Massachusetts, USA;10. Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA;11. The last two authors contributed equally to this work.
Abstract:Endothelial dysfunction may link obesity to cardiovascular disease (CVD). We tested the hypothesis that visceral abdominal tissue (VAT) as compared with subcutaneous adipose tissue (SAT) is more related to endothelium‐dependent vasodilation. Among Framingham Offspring and Third Generation cohorts (n = 3,020, mean age 50 years, 47% women), we used multivariable linear regression adjusted for CVD and its risk factors to relate computed tomography (CT)‐assessed VAT and SAT, BMI, and waist circumference (WC), with brachial artery measures. In multivariable‐adjusted models, BMI, WC, VAT, and SAT were positively related to baseline artery diameter and baseline mean flow velocity (all P < 0.001), but not hyperemic mean flow velocity. In multivariable‐adjusted models, BMI (P = 0.002), WC (P = 0.001), and VAT (P = 0.01), but not SAT (P = 0.24) were inversely associated with percentage of flow‐mediated dilation (FMD%). However, there was little incremental increase in the proportion of variability explained by VAT (R2 = 0.266) as compared to SAT (R2 = 0.265), above and beyond traditional risk factors. VAT, but not SAT was associated with FMD% after adjusting for clinical covariates. Nevertheless, the differential association with VAT as compared to SAT was minimal.
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