JACC：半乳凝素3与心力衰竭和死亡风险相关

近日，来自国立卫生研究所的研究者报道说，一种名为半乳凝素3（galectin-3）的蛋白质可以判断人们是否处于高风险的心力衰竭阶段，相关研究报告刊登在了国际杂志Journal of the American College of Cardiology上。

当心脏没有足够的能量血液供应时就会发生心力衰竭，近来研究表明，半乳凝素3和心肌纤维化明显相关，心肌纤维化在心衰发展过程中扮演着重要角色。心衰往往伴随着死亡或者终生残疾的风险，因此检测血液中半乳凝素3的水平或许为识别个体是否处于会患心力衰竭提供帮助。早期疾病的发现对于治疗非常有用。

研究者在1996-1998年期间检测3353个参与者的血液中半乳凝素3的水平，平均检测年龄为59岁，在接年来的11年终，166个参与者发生了第一次心衰事件，其中25%的人群血液中半乳凝素水平较高（每毫升15.4-52.1纳克），这些人群每年发生心衰的比例为1000人中有12人发生；而对于血液中半乳凝素水平较低（每毫升3.9-12纳克）的参与者来说，每年发生心衰的比例为每1000人中发生3例。

治疗心脏纤维化的药物-螺内酯（Spironolactone）和其它相关的药物也可以改善心力衰竭病人的症状，研究者后期将会深入研究，来确定是否这些药物对于血液半乳凝素3较高的正常人具有效用。

编译自：Protein Linked to Increased Risk of Heart Failure and Death in Older Adults

doi:10.1016/j.jacc.2012.04.053
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Galectin-3, a Marker of Cardiac Fibrosis, Predicts Incident Heart Failure in the Community

Jennifer E. Ho, MD⁎, †, ‡, Chunyu Liu, PhD⁎, Asya Lyass, PhD⁎, §, Paul Courchesne, MBA⁎, Michael J. Pencina, PhD⁎, §, Ramachandran S. Vasan, MD⁎, ∥, Martin G. Larson, ScD⁎, §, Daniel Levy, MD⁎, †, ,

Objectives The aim of this study was to examine the relation of galectin-3 (Gal-3), a marker of cardiac fibrosis, with incident heart failure (HF) in the community. Background 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. Methods 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. Results Gal-3 was associated with increased left ventricular mass in age-adjusted and sex-adjusted analyses (p = 0.001); this association was attenuated in multivariate analyses (p = 0.06). A total of 166 participants developed incident HF and 468 died during a mean follow-up period of 8.1 years. Gal-3 was associated with risk for incident HF (hazard ratio [HR]: 1.28 per 1 SD increase in log Gal-3; 95% confidence interval [CI]: 1.14 to 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 to 1.47; p = 0.02). Gal-3 was also associated with risk for all-cause mortality (multivariable-adjusted HR: 1.15; 95% CI: 1.04 to 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 net reclassification improvement. Conclusions Higher concentration of Gal-3, a marker of cardiac fibrosis, is associated with increased risk for 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.