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AHA中国之声丨血清白蛋白与心力衰竭发病:来自流行病学和孟德尔随机化研究的启示
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 编辑:国际循环网 时间:2019/11/20 11:19:32 关键字:心力衰竭 
  编者按:11月16~18日,由美国心脏协会(AHA)主办的2019科学年会在美国费城召开。全球心血管领域专家汇聚一堂,群贤毕至,共襄盛举。中山大学附属第一医院心血管内科庄晓东博士在大会上做了重要成果展示。
 
中山大学附属第一医院 庄晓东博士
 
  研究描述血清白蛋白和心力衰竭之间相关性的性质和程度,并使用孟德尔随机化研究证实其因果关联。
 
  研究假设
 
  血清白蛋白与心力衰竭的发生有因果关系。
 
  研究方法
 
  对动脉粥样硬化风险前瞻性研究中的15 792名非心力衰竭参与者进行研究,测定基线血清白蛋白水平。评估发生心力衰竭的血清白蛋白的危险比(95%置信区间)。八个与血清白蛋白相关且具有全基因组显著差异的单核苷酸多态性被用作工具变量。使用全基因组测序数据的孟德尔随机化方法来估计暴露对结果的因果关系。
 
 
  研究结果
 
  平均随访25.1年,观察到2446例(19.9%)心力衰竭发生。多因素调整后,血清白蛋白与HF发病率呈负相关(HR=0.54,95% CI:0.46~0.64,每增加1 g/dl;HR= 0.71,95% CI:0.63~0.81,Q4比Q1)。孟德尔随机分析未发现血清白蛋白水平与心力衰竭之间有因果关系[比值比(OR)=1.00,95% CI:0.99~1.01,每增加1 g/dl白蛋白;P=0.38],没有证据表明来自单个SNPs的估计(P异质性= 0.21)和多效性效应(多效性=0.83)之间存在异质性。
 
  研究结论
 
  血清白蛋白水平与心力衰竭发病呈线性关系,然而,孟德尔随机分析并不支持血清白蛋白在心力衰竭病因学中的因果作用。
 
  上下滑动查看英文摘要
 
  Abstract 15669: Serum Albumin and Incident Heart Failure: Insights From Epidemiological and Mendelian Randomization Studies.
 
  Abstract
 
  Introduction: To characterize the nature and magnitude of prospective association between serum albumin and incident heart failure (HF), and to investigate any causal relevance to the association using Mendelian randomization.
 
  Hypothesis: Serum albumin is causally associated with incident heart failure.
 
  Methods: Serum albumin levels were measured at baseline in the Atherosclerosis Risk in Communities (ARIC) prospective study of 15,792 participants without HF. Hazard ratios (95% confidence intervals) of serum albumin with incident HF were assessed. Eight single-nucleotide polymorphisms associated with serum albumin at genome-wide significance were used as instrumental variables. Mendelian randomization based on summary-level data was used to estimate the causal influence of the exposure on the outcome.
 
  Results: During a median follow-up of 25.1 years, 2,446 (19.9%) HF were observed. After multiple adjustment, serum albumin was inversely associated with incidence of HF (HR: 0.54, 95% CI: 0.46-0.64, per 1 g/dL increase; HR: 0.71, 95% CI: 0.63-0.81, Q4 vs. Q1). In MR analysis, no causal relationship was detected between serum albumin level and HF (odds ratio [OR]: 1.00, 95% CI: 0.99-1.01, per 1 g/dL increase of albumin; P=0.38) without evidence of heterogeneity between estimates from individual SNPs (Pheterogeneity= 0.21) and pleiotropy effect (Ppleiotropy= 0.83).
 
  Conclusions: The serum albumin level is independently inverse associated with incident HF in a linear pattern. However, MR analyses did not support a causal role of serum albumin in the etiology of HF.
 
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