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Am Heart J. 2014 May;167(5):729-34.e1. doi: 10.1016/j.ahj.2014.02.009. Epub 2014 Mar 1.

Galectin 3 and incident atrial fibrillation in the community.

Author information

1
Boston University and the National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, MA; Section of Cardiovascular Medicine, Department of Medicine, Boston University, Boston, MA. Electronic address: jenho@bu.edu.
2
Boston University and the National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, MA.
3
Boston University and the National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, MA; Center for Population Studies of the National Heart, Lung, and Blood Institute, Bethesda, MD.
4
Boston University and the National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, MA; Sections of Cardiology and Preventive Medicine and Epidemiology, Department of Medicine, Boston University School of Medicine, Boston, MA.
5
Boston University and the National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, MA; Section of Cardiovascular Medicine, Department of Medicine, Boston University, Boston, MA.
6
Cardiovascular Research Center and Cardiac Arrhythmia Service, Massachusetts General Hospital, Boston, MA.
7
Boston University and the National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, MA; Division of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, Worcester, MA.
8
Boston University and the National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, MA; Department of Mathematics and Statistics, Boston University, Boston, MA.

Abstract

BACKGROUND:

Galectin 3 (Gal-3) is a potential mediator of cardiac fibrosis, and Gal-3 concentrations predict incident heart failure. The same mechanisms that lead to cardiac fibrosis in heart failure may influence development of atrial fibrosis and atrial fibrillation (AF). We examined the association of Gal-3 and incident AF in the community.

METHODS:

Plasma Gal-3 concentrations were measured in 3,306 participants of the Framingham Offspring cohort who attended the sixth examination cycle (1995-1998, mean age 58 years, 54% women). Cox proportional hazards regression models were used to assess the association of baseline Gal-3 concentrations and incident AF.

RESULTS:

Over a median follow-up period of 10 years, 250 participants developed incident AF. Crude incidence rates of AF by increasing sex-specific Gal-3 quartiles were 3.7%, 5.9%, 9.1%, and 11.5% (log-rank test P < .0001). In age- and sex-adjusted analyses, each 1-SD increase in loge-Gal-3 was associated with a 19% increased hazard of incident AF (hazard ratio 1.19, 95% CI 1.05-1.36, P = .009). This association was not significant after adjustment for traditional clinical AF risk factors (hazard ratio 1.12, 95% CI 0.98-1.28, P = .10).

CONCLUSION:

Higher circulating Gal-3 concentrations were associated with increased risk of developing AF over the subsequent 10 years in age- and sex-adjusted analyses but not after accounting for other traditional clinical AF risk factors. Our results do not support a role for Gal-3 in AF risk prediction. Further studies are needed to evaluate whether Gal-3 plays a role in the development of AF substrate similar to HF.

PMID:
24766984
PMCID:
PMC4007212
DOI:
10.1016/j.ahj.2014.02.009
[Indexed for MEDLINE]
Free PMC Article
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