TY - JOUR
T1 - Galectin 3 and incident atrial fibrillation in the community
AU - Ho, Jennifer E.
AU - Yin, Xiaoyan
AU - Levy, Daniel
AU - Vasan, Ramachandran S.
AU - Magnani, Jared W.
AU - Ellinor, Patrick T.
AU - McManus, David D.
AU - Lubitz, Steven A.
AU - Larson, Martin G.
AU - Benjamin, Emelia J.
N1 - Funding Information:
This work was partially supported by the National Heart, Lung, and Blood Institute's Framingham Heart Study ( N01-HC-25195 ). Dr Ho is supported by a grant from the National Institutes of Health ( 1 K23-HL116780 ) and a Department of Medicine Career Investment Award, Boston University School of Medicine. Dr Benjamin is supported by grants from the National Institutes of Health ( 2R01HL092577 , 1R01 HL102214 , 1RC1HL101056 , 6R01-NS 17950 ). Dr McManus receives partial salary support provided by National Institutes of Health grants 1U01HL105268-01 and KL2RR031981 .
PY - 2014/5
Y1 - 2014/5
N2 - 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.
AB - 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.
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U2 - 10.1016/j.ahj.2014.02.009
DO - 10.1016/j.ahj.2014.02.009
M3 - Article
C2 - 24766984
AN - SCOPUS:84899539214
SN - 0002-8703
VL - 167
SP - 729-734.e1
JO - American Heart Journal
JF - American Heart Journal
IS - 5
ER -