Author + information
- Received March 31, 2015
- Accepted April 23, 2015
- Published online August 1, 2015.
- Thomas A. Dewland, MD∗,†,
- Eric Vittinghoff, PhD, MPH‡,
- Tamara B. Harris, MD, PhD§,
- Jared W. Magnani, MD, MSc‖,
- Yongmei Liu, MD, PhD¶,
- Fang-Chi Hsu, PhD#,
- Suzanne Satterfield, MD, DrPH∗∗,
- Christina Wassel, PhD††,
- Gregory M. Marcus, MD, MAS∗∗ (, )
- Health ABC Study Investigators
- ∗Electrophysiology Section, Division of Cardiology, Department of Medicine, University of California, San Francisco, California
- †Knight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon
- ‡Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, California
- §Laboratory of Epidemiology and Population Sciences, National Institute on Aging, Bethesda, Maryland
- ‖Department of Medicine, Section of Cardiovascular Medicine, Boston University School of Medicine, Boston, Massachusetts
- ¶Division of Public Health Sciences, Wake Forest School of Medicine, Winston-Salem, North Carolina
- #Department of Biostatistical Sciences, Wake Forest School of Medicine, Winston-Salem, North Carolina
- ∗∗Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, Tennessee
- ††Department of Epidemiology, University of Pittsburgh, Pittsburgh, Pennsylvania
- ↵∗Reprint requests and correspondence:
Dr. Gregory M. Marcus, Electrophysiology Section, Division of Cardiology, Department of Medicine, University of California, San Francisco, 505 Parnassus Avenue, M-1180B, Box 0124, San Francisco, California 94143-0124.
Objectives This study sought to determine the degree to which racial differences in atrial fibrillation (AF) risk are explained by differences in inflammation and adiposity.
Background Despite having a lower prevalence of established AF risk factors, whites exhibit substantially higher rates of this arrhythmia than blacks. The mechanism underlying this observation is not known. Both inflammation and obesity are risk factors for AF, and adipose tissue is a known contributor to systemic inflammation.
Methods Baseline serum inflammatory biomarker concentrations and abdominal adiposity (assessed by computed tomography) were quantified in a subset of black and white participants without prevalent AF in the Health ABC (Health, Aging, and Body Composition) study. Participants were prospectively followed for the diagnosis of AF, using study electrocardiography and Medicare claims data. Cox proportional hazards models were used to determine the adjusted relative hazard of incident AF between races before and after biomarker adjustment.
Results Among 2,768 participants (43% black), 721 participants developed incident AF over a median follow-up of 10.9 years. White race was associated with a heightened adjusted risk of incident AF (HR: 1.55; 95% confidence interval [CI]: 1.30 to 1.84, p < 0.001). Abdominal adiposity was not associated with AF when added to the adjusted model. Among the biomarkers studied, adiponectin, tumor necrosis factor (TNF)-α, TNF-α soluble receptor (SR) I, and TNF-α SR II concentrations were each higher among whites and independently associated with a greater risk of incident AF. Together, these inflammatory cytokines mediated 42% (95% CI: 15% to 119%, p = 0.004) of the adjusted association between race and AF.
Conclusions Systemic inflammatory pathways significantly mediate the heightened risk of AF among whites. The higher level of systemic inflammation and concomitant increased AF risk in whites is not explained by racial differences in abdominal adiposity or the presence of other proinflammatory cardiovascular comorbidities.
This study was supported by American Heart Association grants 12POST11810036 (Dr. Dewland) and 12GRNT11780061 (Dr. Marcus) and the Joseph Drown Foundation (Dr. Marcus). Also supported by U.S. National Institutes of Health Intramural Research Program, National Institute on Aging (NIA) contracts N01-AG-6-2101, N01-AG-6-2103, and N01-AG-6-2106 and NIA grants R01-AG028050 and R03-AG045075; National Institute of Nursing Research grant R01-NR012459; and NIH National Center for Advancing Translational Sciences award UL1TR000454. Dr. Dewland has received education-related travel reimbursement from Medtronic. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received March 31, 2015.
- Accepted April 23, 2015.
- American College of Cardiology Foundation