Clinical InvestigationElectrophysiologyPlasma resistin, adiponectin, and risk of incident atrial fibrillation: The Framingham Offspring Study
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.
References (37)
- et al.
Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: population-based estimates
Am J Cardiol
(1998) - et al.
The natural history of atrial fibrillation: Incidence, risk factors, and prognosis in the Manitoba follow-up study
Am J Med
(1995) - et al.
Overweight and obesity as risk factors for atrial fibrillation or flutter: the Danish diet, cancer, and health study
Am J Med
(2005) - et al.
The role of resistin as a regulator of inflammation: Implications for various human pathologies
Clin Immunol
(2009) - et al.
Role of resistin in cardiac contractility and hypertrophy
J Mol Cell Cardiol
(2008) - et al.
Resistin, adiponectin, and risk of heart failure the Framingham Offspring study
J Am Coll Cardiol
(2009) - et al.
Paradoxical decrease of an adipose-specific protein, adiponectin, in obesity
Biochem Biophys Res Commun
(1999) - et al.
Adiponectin and development of type 2 diabetes in the Pima Indian population
Lancet
(2002) - et al.
The Framingham Offspring study. Design and preliminary data
Prev Med
(1975) - et al.
Development of a risk score for atrial fibrillation (Framingham Heart study): a community-based cohort study
Lancet
(2009)
Role of inflammation in initiation and perpetuation of atrial fibrillation: a systematic review of the published data
J Am Coll Cardiol
Pioglitazone, a peroxisome proliferator-activated receptor-gamma activator, attenuates atrial fibrosis and atrial fibrillation promotion in rabbits with congestive heart failure
Heart Rhythm
Secular trends in incidence of atrial fibrillation in Olmsted County, Minnesota, 1980 to 2000, and implications on the projections for future prevalence
Circulation
Independent risk factors for atrial fibrillation in a population-based cohort. The Framingham Heart study
JAMA
Incidence of and risk factors for atrial fibrillation in older adults
Circulation
Obesity and the risk of new-onset atrial fibrillation
JAMA
C-reactive protein elevation in patients with atrial arrhythmias: inflammatory mechanisms and persistence of atrial fibrillation
Circulation
Inflammation as a risk factor for atrial fibrillation
Circulation
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/).
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Contributed equally to the manuscript.