Galectin-3, a marker of cardiac fibrosis, predicts incident heart failure in the community.

Galectin-3, a marker of cardiac fibrosis, predicts incident heart failure in the community.
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DOI:
10.1016/j.jacc.2012.04.053
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发表时间:
2012-10-02
影响因子:
24
通讯作者:
Levy, Daniel
Levy, Daniel
中科院分区:
医学1区
文献类型:
--
作者:
Ho, Jennifer E.;Liu, Chunyu;Lyass, Asya;Courchesne, Paul;Pencina, Michael J.;Vasan, Ramachandran S.;Larson, Martin G.;Levy, Daniel

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我们试图研究心脏纤维化的标志物Galectin-3(Gal-3)与社区发生的心力衰竭(HF)的关系。Gal-3是一个新出现的心衰预后生物标志物,实验研究表明Gal-3是心脏纤维化的重要介质。Gal-3浓度升高是否先于心力衰竭的发生尚不清楚。在弗雷明翰后代队列中,3353名参与者(平均年龄59岁,53%为女性)测量了GAL-3浓度。用比例风险回归分析Gal-3与心力衰竭发病的关系。在年龄和性别调整的分析中,GAL-3与左心室重量增加相关(P=0.001);这种关联在多变量分析中减弱(P=0.06)。在平均8.1年的随访期内,共有166名参与者发生心力衰竭,其中468人死亡。GAL-3与心力衰竭的发生风险相关(LOG-GAL-3标准差每增加1个标准差,HR 1.28,95%CI 1.14~1.43,P&0.0001),调整临床变量和B型利钠肽后,GAL-3仍具有显著意义(HR 1.23,95%CI 1.04~1.47,P=0.02)。GAL-3与全因死亡风险相关(多变量调整后的HR为1.15,95%CI为1.04~1.28,P=0.01)。将Gal-3添加到临床因素后,c统计量的变化可以忽略不计,净重新分类指数略有改善。心肌纤维化的标志物Gal-3浓度越高,发生心力衰竭的风险和死亡率就越高。未来评估Gal-3在心脏重构中的作用的研究可能会为进一步深入了解Gal-3在心力衰竭的病理生理学中的作用提供依据。
We sought to examine the relation of galectin-3 (Gal-3), a marker of cardiac fibrosis, with incident heart failure (HF) in the community. Gal-3 is an emerging prognostic biomarker in HF, and experimental studies suggest that Gal-3 is an important mediator of cardiac fibrosis. Whether elevated Gal-3 concentrations precede the development of HF is unknown. Gal-3 concentrations were measured in 3,353 participants in the Framingham Offspring Cohort (mean age 59 years, 53% women). The relation of Gal-3 to incident HF was assessed using proportional hazards regression. Gal-3 was associated with increased left ventricular mass in age- and sex-adjusted analyses (P=0.001); this association was attenuated in multivariable analyses (P=0.06). A total of 166 participants developed incident HF and 468 died during a mean follow-up of 8.1 years. Gal-3 was associated with risk of incident HF (HR 1.28 per 1 standard deviation increase in log-Gal-3, 95% CI 1.14–1.43, P<0.0001), and remained significant after adjustment for clinical variables and B-type natriuretic peptide (HR 1.23, 95% CI 1.04–1.47, P=0.02). Gal-3 was also associated with risk of all-cause mortality (multivariable-adjusted HR 1.15, 95% CI 1.04–1.28, P=0.01). The addition of Gal-3 to clinical factors resulted in negligible changes to the c-statistic and minor improvements in the net reclassification index. Higher concentration of Gal-3, a marker of cardiac fibrosis, is associated with increased risk of incident HF and mortality. Future studies evaluating the role of Gal-3 in cardiac remodeling may provide further insights into the role of Gal-3 in the pathophysiology of HF.
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