Plasma resistin, adiponectin, and risk of incident atrial fibrillation: The Framingham Offspring Study - 14/12/11
Résumé |
Background |
We sought to investigate whether higher concentrations of resistin and lower concentrations of adiponectin relate to incident atrial fibrillation (AF) and whether this association is mediated by AF risk factors and inflammation. Resistin and adiponectin are adipokines that have been associated with multiple known risk factors for AF including diabetes, obesity, inflammation, and heart failure.
Methods |
We studied the relations between circulating concentrations of both adipokines and incident AF in participants of the Framingham Offspring Study.
Results |
Participants (n = 2,487) had a mean age of 61 ± 10 years, and 54% were women. During a mean follow-up of 7.6 ± 2.0 years, 206 (8.3%) individuals (96 women) developed incident AF. Plasma resistin concentration was significantly associated with incident AF (multivariable-adjusted hazard ratio [HR] 1.17 per SD [0.41 ng/mL] of natural logarithmically transformed resistin, 95% CI 1.02-1.34, P = .028). The resistin-AF association was attenuated after further adjustment for C-reactive protein (HR per SD increase resistin 1.14, 95% CI 0.99-1.31, P = .073). Adiponectin concentrations were not significantly associated with incident AF (multivariable-adjusted HR of 0.95 per SD [0.62 μg/mL] of logarithmically transformed adiponectin, 95% CI 0.81-1.10, P = .478).
Conclusion |
In our community-based longitudinal study, higher mean concentrations of resistin were associated with incident AF, but the relation was attenuated by adjustment for C-reactive protein. We did not detect a statistically significant association between adiponectin and incident AF. Additional studies are needed to clarify the potential role of adipokines in AF and mechanisms linking adiposity to AF.
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The Framingham Heart Study is supported by National Heart, Lung, and Blood Institute; Framingham Heart Study (NHLBI/NIH contract N01-HC-25195); and the Boston University School of Medicine. Dr Rienstra is supported by a grant from the Netherlands Organization for Scientific Research (Rubicon grant 825.09.020). This work was supported by grants from the National Institutes of Health to Drs Benjamin and Ellinor (1R01HL092577); Dr Benjamin (1RC1HL101056, 1R01HL102214, R01AG028321; and support via 6R01-NS17950) and Dr Ellinor (5R21DA027021, 5RO1HL104156, 1K24HL105780); and Dr Vasan (R01-DK-080739). Dr Magnani is supported by American Heart Association Award 09FTF2190028. This work was partially supported by the Evans Center for Interdisciplinary Biomedical Research ARC on “Atrial Fibrillation” at Boston University (evanscenteribr/). |
Vol 163 - N° 1
P. 119 - janvier 2012 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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