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首页> 外文期刊>Journal of neurology >Genetic correlations and causal inferences in ischemic stroke
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Genetic correlations and causal inferences in ischemic stroke

机译：缺血性脑卒中遗传相关性和因果推论

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Background and purpose Considerable studies have reported inconsistent relationships between ischemic stroke and a large number of factors. These uncertainties may reflect the susceptibility to confounding in observational studies. We aimed to assess genetic correlations and causal relationships between ischemic stroke and diverse phenotypes. Methods Summary-level data for ischemic stroke (34,217 cases and 406,111 controls) from the MEGASTROKE consortium were used as the outcome. Exposures were derived from two GWAS statistics curated databases. We explored the genetic correlations and causalities between hundreds of traits and ischemic stroke, using linkage disequilibrium score regression and Mendelian randomization (MR), respectively. Multiple sensitivity analyses were also performed. Results Genetic correlation analyses reflected genetic overlaps between ischemic stroke and physical activity, cardiometabolic factors, smoking, and lung function. Applying MR, we found suggestive evidence that genetic predisposition to higher concentration of low-density lipoprotein particles (LDL.P) and cholesterol carried in different sizes of LDL.P (LDL.C) were associated with higher risk of ischemic stroke, particular large artery stroke. The strongest effect was observed for small LDL.P in large artery stroke (OR 1.31, 95% CI 1.09-1.56, p = 0.003). The results were overall robust for sensitivity analyses. We further observed significant positive associations of genetically predicted LDL.P and LDL.C with coronary artery disease and myocardial infarction. Conclusions Shared genetic overlaps might exist between ischemic stroke and physical activity, cardiometabolic factors, smoking, and lung function. We provided suggestive evidence for a potential causal role of LDL.P and LDL.C in ischemic stroke, particularly in large artery stroke. Future researches are required to confirm these findings.
机译：背景和目的具有相当大的研究报告了缺血性卒中与大量因素之间的关系不一致。这些不确定性可能反映了对观察研究中的混淆的敏感性。我们旨在评估缺血性卒中与多种表型之间的遗传相关性和因果关系。方法使用来自兆体团联盟的缺血性卒中（34,217个案例和406,111个控制）的摘要级数据作为结果。曝光从两个GWAS统计策划数据库中得出。我们探讨了数百种性状和缺血性卒中之间的遗传相关性和因果性，分别使用锁定不平衡评分回归和孟德尔随机化（MR）。还进行了多种敏感性分析。结果遗传相关分析反映了缺血性卒中与体育活动，心细素因子，吸烟和肺功能之间的反映遗传重叠。申请MR，我们发现暗示证据表明，遗传易受低密度脂蛋白颗粒（LDL.P）和胆固醇的遗传易感性与不同尺寸的LDL.P（LDL.C）携带的胆固醇与缺血性卒中的风险较高有关，特别是大动脉抚摸。对于大动脉中风（或1.31,95％CI 1.09-1.56，P = 0.003），对小型LDL.p观察到最强的效果。结果对敏感性分析进行了总体稳健。我们进一步观察到遗传预测的LDL.P和LDL.C与冠状动脉疾病和心肌梗死的显着阳性阳性。结论缺血性卒中和体育活动，心脏素质因素，吸烟和肺功能之间可能存在共同的遗传重叠。我们为LDL.P和LDL.C在缺血性卒中中的潜在因果作用提供了暗示证据，特别是在大动脉中风中。未来的研究是确认这些调查结果。

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