Genetically predicted NT-proBNP levels showed no significant causal association with the risk of ischemic stroke (OR -0.044, 95% CI -0.129 to 0.041, p=0.313).
Observational (n=446,696)
Mendelian Randomization
Yes
Ischemic stroke and its subtypes (n=446,696)
Genetically predicted N-terminal probrain natriuretic peptide (NT-proBNP) levels vs Control
Ischemic stroke — OR -0.044 (-0.129, 0.041), p=0.313
Effect estimate: OR -0.044 (95% CI -0.129, 0.041)
p-value: p=0.313
Mendelian randomization was used to evaluate the potential causal association between N-terminal probrain natriuretic peptide (NT-proBNP) and ischemic stroke based on summary statistics data from large-scale genome-wide association studies. Three single-nucleotide polymorphisms (SNPs) rs198389, rs13107325, and rs11105306 associated with NT-proBNP levels found in large general populations and in patients with acute heart disease were used as instrumental variables. The results of genetic association analysis of each single SNP show that there is no significant association between NT-proBNP levels and ischemic stroke or its subtypes, whereas rs198389 alone has a suggestive association with large-artery atherosclerosis stroke. The MR analysis of three SNPs shows that NT-proBNP levels may reduce the risk of small-vessel occlusion stroke suggestively. This genetic analysis provides insights into the pathophysiology and treatment of ischemic stroke.
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Ming Li
Wuxi People's Hospital
Yi Xu
Jiaqi Wu
Frontiers in Genetics
Columbia University
Beihang University
Capital Medical University
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Li et al. (Tue,) conducted a observational in Ischemic stroke and its subtypes (n=446,696). Genetically predicted N-terminal probrain natriuretic peptide (NT-proBNP) levels vs. Control was evaluated on Ischemic stroke (OR -0.044, 95% CI -0.129, 0.041, p=0.313). Genetically predicted NT-proBNP levels showed no significant causal association with the risk of ischemic stroke (OR -0.044, 95% CI -0.129 to 0.041, p=0.313).
synapsesocial.com/papers/6a12c6b983732aa7db9e4a34 — DOI: https://doi.org/10.3389/fgene.2022.795479