Metabolic syndrome and incidence of atrial fibrillation among blacks and whites in the Atherosclerosis Risk in Communities (ARIC) Study

Alanna M. Chamberlain, Sunil K. Agarwal, Marietta Ambrose, Aaron R. Folsom, Elsayed Z. Soliman, Alvaro Alonso

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106 Scopus citations


Background: The metabolic syndrome (MetSyn) has been implicated in the development of atrial fibrillation (AF); however, knowledge of this association among blacks is limited. Methods: We determined the risk of incident AF through December 2005 in relation to baseline (1987-1989) MetSyn status in 15,094 participants of the Atherosclerosis Risk in Communities study. Results: Over a mean follow-up of 15.4 years, 1,238 incident AF events were identified. The hazard ratio (HR) for AF among individuals with, compared to those without, the MetSyn was 1.67 (95% CI 1.49-1.87), and associations did not differ by race (P for interaction = .73). The population attributable risk of AF from the MetSyn was 22%. The multivariable-adjusted HRs (95% CI) for each MetSyn component were 1.95 (1.72-2.21) (elevated blood pressure), 1.40 (1.23-1.59) (elevated waist circumference), 1.20 (1.06-1.37) (low high-density lipoprotein cholesterol), 1.16 (1.03-1.31) (impaired fasting glucose), and 0.95 (0.84-1.09) (elevated triglycerides). A monotonically increasing risk of AF with increasing number of MetSyn components was observed, with an HR of 4.40 (95% CI 3.25-5.94) for those with all 5 MetSyn components compared to those with 0 components. Conclusion: In this large cohort, the MetSyn and most of its components were associated with a higher risk of AF in both blacks and whites. Given the high prevalence of the MetSyn, strategies to prevent its development or to control individual components may reduce the burden of AF.

Original languageEnglish (US)
Pages (from-to)850-856
Number of pages7
JournalAmerican Heart Journal
Issue number5
StatePublished - May 2010

Bibliographical note

Funding Information:
The Atherosclerosis Risk in Communities Study is carried out as a collaborative study supported by NHLBI contracts N01-HC-55015, N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021, and N01-HC-55022. This study was also supported by grants RC1HL099452 from NHLBI and 09SDG2280087 from the American Heart Association. A.M.C. was supported by NHLBI grant T32-HL-007779. The authors are solely responsible for the design and conduct of this study, all study analyses, the drafting and editing of the article, and its final contents.

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