Published Online
on November 17, 2003

A more recent version of this article appeared on December 16, 2003

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Submitted on July 28, 2003
Revised on September 19, 2003
Accepted on September 22, 2003

Inflammation as a Risk Factor for Atrial Fibrillation

Ronnier J. Aviles MD, David O. Martin MD, MPH, Carolyn Apperson-Hansen MS, Penny L. Houghtaling MS, Pentti Rautaharju MD, Richard A. Kronmal PhD, Russell P. Tracy PhD, David R. Van Wagoner PhD, Bruce M. Psaty MD, PhD, Michael S. Lauer MD, and Mina K. Chung MD^*

From the Department of Cardiovascular Medicine (R.J.A., D.O.M., D.R.V.W., M.S.L., M.K.C.), Department of Biostatistics (C.A.-H., P.L.H.), The Cleveland Clinic Foundation, Cleveland, Ohio; Cardiovascular Health Research Unit (B.M.P.), University of Washington, Seattle, Wash; Wake Forest University School of Medicine (P.R.), Winston-Salem, NC; Department of Pathology and Biochemistry, (R.P.T.), University of Vermont, Colchester, Vt; and the CHS Coordinating Center (R.A.K.), Seattle, Wash. Dr Aviles is now with the Cardiovascular Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.

^* To whom correspondence should be addressed. E-mail: chungm{at}ccf.org.

Background--The presence of systemic inflammation determined by elevations in C-reactive protein (CRP) has been associated with persistence of atrial fibrillation (AF). The relationship between CRP and prediction of AF has not been studied in a large population-based cohort.

Methods and Results--CRP measurement and cardiovascular assessment were performed at baseline in 5806 subjects enrolled in the Cardiovascular Health Study. Patients were followed up for a mean of 6.9±1.6 (median 7.8) years. AF was identified by self-reported history and ECGs at baseline and by ECGs and hospital discharge diagnoses at follow-up. Univariate and multivariate analyses were used to assess CRP as a predictor of baseline and future development of AF. At baseline, 315 subjects (5%) had AF. Compared with subjects in the first CRP quartile (<0.97 mg/L), subjects in the fourth quartile (>3.41 mg/L) had more AF (7.4% versus 3.7%, adjusted OR 1.8, 95% CI 1.2 to 2.5; P=0.002). Of 5491 subjects without AF at baseline, 897 (16%) developed AF during follow-up. Baseline CRP predicted higher risk for developing future AF (fourth versus first quartile adjusted hazard ratio 1.31, 95% CI 1.08 to 1.58; P=0.005). When treated as a continuous variable, elevated CRP predicted increased risk for developing future AF (adjusted hazard ratio for 1-SD increase, 1.24; 95% CI 1.11 to 1.40; P<0.001).

Conclusions--CRP is not only associated with the presence of AF but may also predict patients at increased risk for future development of AF.

Key words: atrial flutter • fibrillation • inflammation • arrhythmia

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