Author + information
- Received March 19, 2014
- Revision received May 15, 2014
- Accepted May 26, 2014
- Published online September 9, 2014.
- Alvin Chandra, MD∗,
- Ian J. Neeland, MD†,
- Jarett D. Berry, MD, MS†,‡,
- Colby R. Ayers, MS∗,‡,
- Anand Rohatgi, MD, MSCS†,
- Sandeep R. Das, MD, MPH†,
- Amit Khera, MD, MS†,
- Darren K. McGuire, MD, MHSc†,‡,
- James A. de Lemos, MD† and
- Aslan T. Turer, MD, MHS†∗ ()
- ∗Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas
- †Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, Texas
- ‡Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, Texas
- ↵∗Reprint requests and correspondence
: Dr. Aslan Turer, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9047.
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.
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.
- Received March 19, 2014.
- Revision received May 15, 2014.
- Accepted May 26, 2014.
- American College of Cardiology Foundation