TY - JOUR
T1 - The relationship of body mass and fat distribution with incident hypertension
T2 - Observations from the dallas heart study
AU - Chandra, Alvin
AU - Neeland, Ian J
AU - Berry, Jarett D
AU - Ayers, Colby R.
AU - Rohatgi, Anand K
AU - Das, Sandeep R
AU - Khera, Amit
AU - McGuire, Darren K
AU - de Lemos, James A
AU - Turer, Aslan T
N1 - Funding Information:
Dr. Berry has been on the Speakers’ Bureau for Merck & Co. Dr. Rohatgi has received grant support from Merck & Co.; and consulting income from Aegerion. Dr. McGuire has received consulting income from F. Hoffmann LaRoche, Genentech, Sanofi-Aventis, Daiichi Sankyo, and Novo Nordisk; and has been on a trial executive committee for Eisai; and on data monitoring committees for Orexigen Therapeutics and Takeda Pharmaceuticals. Dr. de Lemos has received grant support from Roche Diagnostics and Abbott Diagnostics ; and consulting income from Novo Nordisk, AstraZeneca, and Janssen Pharmaceuticals. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Publisher Copyright:
© 2014 by the American College of Cardiology Foundation.
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2014
Y1 - 2014
N2 - BACKGROUND Obesity has been linked to the development of hypertension, but whether total adiposity or site-specific fat accumulation underpins this relationship is unclear. OBJECTIVES This study sought to determine the relationship between adipose tissue distribution and incident hypertension. METHODS Normotensive participants enrolled in the Dallas Heart Study were followed for a median of 7 years for the development of hypertension (systolic blood pressure [SBP] ≥140 mm Hg, diastolic blood pressure ≥90 mm Hg, or initiation of blood pressure medications). Visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) was quantified by magnetic resonance imaging and proton-spectroscopic imaging, and lower body fat (LBF) was imaged by dual-energy x-ray absorptiometry. Multivariable relative risk regression was performed to test the association between individual fat depots and incident hypertension, adjusting for age, sex, race/ethnicity, diabetes, smoking, SBP, and body mass index (BMI). RESULTS Among 903 participants (median age, 40 years; 57% women; 60% nonwhite; median BMI 27.5 kg/m2), 230 (25%) developed incident hypertension. In multivariable analyses, higher BMI was significantly associated with incident hypertension (relative risk: 1.24; 95% confidence interval: 1.12 to 1.36, per 1-SD increase). However, when VAT, SAT, and LBF were added to the model, only VAT remained independently associated with incident hypertension (relative risk: 1.22; 95% confidence interval: 1.06 to 1.39, per 1-SD increase). CONCLUSIONS Increased visceral adiposity, but not total or subcutaneous adiposity, was robustly associated with incident hypertension. Additional studies will be needed to elucidate the mechanisms behind this association. (J Am Coll Cardiol 2014;64:997-1002)
AB - BACKGROUND Obesity has been linked to the development of hypertension, but whether total adiposity or site-specific fat accumulation underpins this relationship is unclear. OBJECTIVES This study sought to determine the relationship between adipose tissue distribution and incident hypertension. METHODS Normotensive participants enrolled in the Dallas Heart Study were followed for a median of 7 years for the development of hypertension (systolic blood pressure [SBP] ≥140 mm Hg, diastolic blood pressure ≥90 mm Hg, or initiation of blood pressure medications). Visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) was quantified by magnetic resonance imaging and proton-spectroscopic imaging, and lower body fat (LBF) was imaged by dual-energy x-ray absorptiometry. Multivariable relative risk regression was performed to test the association between individual fat depots and incident hypertension, adjusting for age, sex, race/ethnicity, diabetes, smoking, SBP, and body mass index (BMI). RESULTS Among 903 participants (median age, 40 years; 57% women; 60% nonwhite; median BMI 27.5 kg/m2), 230 (25%) developed incident hypertension. In multivariable analyses, higher BMI was significantly associated with incident hypertension (relative risk: 1.24; 95% confidence interval: 1.12 to 1.36, per 1-SD increase). However, when VAT, SAT, and LBF were added to the model, only VAT remained independently associated with incident hypertension (relative risk: 1.22; 95% confidence interval: 1.06 to 1.39, per 1-SD increase). CONCLUSIONS Increased visceral adiposity, but not total or subcutaneous adiposity, was robustly associated with incident hypertension. Additional studies will be needed to elucidate the mechanisms behind this association. (J Am Coll Cardiol 2014;64:997-1002)
KW - Body fat distribution
KW - Hypertension
KW - Obesity
KW - Visceral fat
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U2 - 10.1016/j.jacc.2014.05.057
DO - 10.1016/j.jacc.2014.05.057
M3 - Article
C2 - 25190234
AN - SCOPUS:84908178972
SN - 0735-1097
VL - 64
SP - 997
EP - 1002
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 10
ER -