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Plasma resistin, adiponectin, and risk of incident atrial fibrillation: The Framingham Offspring Study - 14/12/11

Doi : 10.1016/j.ahj.2011.09.029 
Michiel Rienstra, MD, PhD a, b, c, Jenny X. Sun, PhD d, Steven A. Lubitz, MD, MPH e, David S. Frankel, MD f, Ramachandran S. Vasan, MD c, g, h, i, Daniel Levy, MD c, j, Jared W. Magnani, MD c, i, Lisa M. Sullivan, PhD d, James B. Meigs, MD, MPH c, k, Patrick T. Ellinor, MD, PhD a, e, l, Emelia J. Benjamin, MD, ScM c, g, h, i, l,
a Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, MA 
b Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands 
c National Heart Lung and Blood Institute's and Boston University's Framingham Heart Study, Framingham, MA 
d Department of Biostatistics, Boston University School of Public Health, Boston, MA 
e Cardiac Arrhythmia Service, Massachusetts General Hospital, Harvard Medical School, Boston, MA 
f Cardiovascular Division, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, PA 
g Preventive Medicine Section, Boston University School of Medicine, Boston, MA 
h Department of Epidemiology, Boston University School of Public Health, Boston, MA 
i Cardiology Section, Department of Medicine, Boston University School of Medicine, Boston, MA 
j Center for Population Studies, National Heart, Lung, and Blood Institute, Bethesda, MD 
k General Medicine Division, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA 

Reprint requests: Emelia J. Benjamin, MD, ScM, FACC, FAHA, Framingham Heart Study, 73 Mount Wayte Ave, Suite 2, Framingham, MA 0 1702-5827.

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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Plan


 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/).


© 2012  Mosby, Inc. Tous droits réservés.
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P. 119 - janvier 2012 Retour au numéro
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