Elsevier

American Heart Journal

Volume 163, Issue 1, January 2012, Pages 119-124.e1
American Heart Journal

Clinical Investigation
Electrophysiology
Plasma resistin, adiponectin, and risk of incident atrial fibrillation: The Framingham Offspring Study

https://doi.org/10.1016/j.ahj.2011.09.029Get rights and content

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.

Section snippets

Participants

For the present analysis, we used a sample of the Framingham Heart Study Offspring cohort. The Offspring cohort was constituted in 1971 with the enrollment of 5,124 offspring (and their spouses) of the Original cohort.23 Between 1999 and 2001, 3,539 participants attended the seventh examination cycle. Of these participants, 150 had prevalent AF and were excluded from the present analysis. Because plasma adipokine measurements started partway through the seventh examination cycle, 722 attendees

Study sample characteristics

The characteristics of the 2,487 attendees (mean age 61 ± 10 years, 54% women) included in the analysis are reported in Table I. Median plasma resistin concentration was 12.7 ng/mL (25th percentile 10.0 ng/mL, 75th percentile 16.4 ng/mL) and median plasma adiponectin concentration was 8.6 μg/mL (25th percentile 5.5μg/mL, 75th percentile 13.2μg/mL). The SDs of the loge resistin and adiponectin were 0.41 ng/mL and 0.62 μg /mL, respectively.

Adipokines and AF risk

Incident AF developed in 206 individuals (8.3%, 96 women)

Discussion

In our community-based sample, we observed that higher plasma concentrations of resistin were related to incident AF during up to 10 years of follow-up, after adjusting for traditional AF risk factors. Numerous prior clinical and preclinical studies have demonstrated a relation between inflammation, largely as assessed by concentrations of CRP and AF.28 Resistin, produced by mononuclear cells both within and outside adipose tissue, contributes both to insulin resistance and is related to

Disclosures

None.

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  • Cited by (0)

    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 (http://www.bumc.bu.edu/evanscenteribr/).

    l

    Contributed equally to the manuscript.

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