Galectin-3 and incidence of atrial fibrillation: The Atherosclerosis Risk in Communities (ARIC) study

Oluwaseun E. Fashanu, Faye L. Norby, David Aguilar, Christie M. Ballantyne, Ron C. Hoogeveen, Lin Y. Chen, Elsayed Z. Soliman, Alvaro Alonso, Aaron R. Folsom

Research output: Contribution to journalArticlepeer-review

16 Scopus citations

Abstract

Background Galectin-3, a β-galactoside binding lectin involved in important regulatory roles in adhesion, inflammation, immunity, and fibrosis, may be relevant to atrial fibrillation (AF) etiology. Methods We included 8,436 participants free of AF at baseline (1996-1998) and with measures of plasma galectin-3 from the Atherosclerosis Risk in Communities study. We ascertained incident AF through 2013 from study visit electrocardiograms, hospitalizations, and death certificates. Multivariable Cox proportional hazards models, adjusted for AF risk factors plus incident heart failure (HF) and coronary heart disease (CHD), were used to estimate hazard ratios for the association between galectin-3 and incident AF. Results The mean age (SD) of participants was 62.6 (5.6) years, and the sample was comprised of 58.7% women and 21.2% blacks. During a median follow-up of 15.7 years, 1,185 incident cases of AF were observed. After adjusting for AF risk factors, participants with galectin-3 levels ≥90th percentile (19.5 ng/mL) had a significantly higher risk of incident AF when compared with the lowest quartile (4.4-11.9 ng/mL), with hazard ratios (95% CI) of 1.40 (1.04-1.89) for the 90th-<95th percentile and 1.51 (1.11-2.06) for the 95th-100th percentile. This association was attenuated and no longer statistically significant after accounting for incident CHD and HF as time-dependent variables. Conclusions Elevated plasma galectin-3 is associated with increased risk of incident AF. Galectin-3 may increase AF risk via pathways involving CHD and HF.

Original languageEnglish (US)
Pages (from-to)19-25
Number of pages7
JournalAmerican Heart Journal
Volume192
DOIs
StatePublished - Oct 2017

Bibliographical note

Funding Information:
Dr Ballantyne has received research grant to institution from Abbott Diagnostics and consults with Abbott. The other authors report no conflicts.

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