Inflammation as a Mediator of the Association Between Race and Atrial Fibrillation: Results from the Health, Aging, and Body Composition Study.
BACKGROUND
Despite a lower prevalence of established atrial fibrillation (AF) risk factors, Whites exhibit substantially higher rates of this arrhythmia compared to 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.


OBJECTIVE
We sought to determine the degree to which racial differences in AF risk are explained by differences in inflammation and adiposity.


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, Aging, and Body Composition (Health ABC) Study. Participants were prospectively followed for the diagnosis of AF using study ECGs 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 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% CI 1.30 to 1.84, p < 0.001). Abdominal adiposity was not associated with AF when added to the adjusted model. Among the studied biomarkers, adiponectin, TNF-α, TNF-α 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 race-AF association.


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 pro-inflammatory cardiovascular comorbidities.
Electrophysiology Section, Division of Cardiology, Department of Medicine, University of California, San Francisco ; Knight Cardiovascular Institute, Oregon Health & Science University, Portland.
Thomas A
TA
Dewland
Department of Epidemiology and Biostatistics, University of California, San Francisco.
Eric
E
Vittinghoff
Laboratory of Epidemiology and Population Sciences, National Institute on Aging, Bethesda, Maryland.
Tamara B
TB
Harris
Department of Medicine, Section of Cardiovascular Medicine, Boston University School of Medicine, Boston, Massachusetts.
Jared W
JW
Magnani
Division of Public Health Sciences, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Yongmei
Y
Liu
Department of Biostatistical Sciences, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Fang-Chi
FC
Hsu
Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, Tennessee.
Suzanne
S
Satterfield
Department of Epidemiology, University of Pittsburgh, Pittsburgh, Pennsylvania.
Christina
C
Wassel
Electrophysiology Section, Division of Cardiology, Department of Medicine, University of California, San Francisco.
Gregory M
GM
Marcus
atrial fibrillation; inflammation; race