Oluwaseun E Fashanu1, Faye L Norby1, David Aguilar2, Christie M Ballantyne2, Ron C Hoogeveen2, Lin Y Chen3, Elsayed Z Soliman4, Alvaro Alonso5, Aaron R Folsom6. 1. Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN. 2. Department of Medicine, Baylor College of Medicine and Methodist DeBakey Heart and Vascular Center, Houston, TX. 3. Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, MN. 4. Epidemiological Cardiology Research Center, Wake Forest School of Medicine, Winston Salem, NC. 5. Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA. 6. Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN. Electronic address: folso001@umn.edu.
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.
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.
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