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. 2019 Sep 27;50(11):3004–3012. doi: 10.1161/STROKEAHA.119.026545

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© 2019 American Heart Association, Inc.

Stroke is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 2. — Cross-sectional analyses of the genetic factor XI (FXI) score for clinical end points and ischemic stroke subtypes. A, Association of the FXI genetic score with 4 primary safety and efficacy outcomes (United Kingdom Biobank [UKB], external genetics consortia). After correcting for testing 4 primary outcomes (Bonferroni threshold=0.05/4=0.01), we observe significant associations of the FXI genetic score, expressed as a 30% relative increase in activated partial thromboplastin time (aPTT), with venous thromboembolism (odds ratio [OR]=0.1 [0.07–0.14], P=3.03×10⁻⁴³) and ischemic stroke (OR=0.47 [0.36–0.61]; P=1.5×10⁻⁸) and (B) cross-sectional analysis of CCS ischemic stroke subgroups from the MEGASTROKE dataset. Integration of MEGASTROKE¹² effect sizes for 2 common FXI SNPs (rs4253417, rs1593) by fixed-effect meta-analysis showed significant risk reduction for the cardioembolic stroke subtype (OR=0.16 [0.09–0.28]; P=2.08×10⁻¹⁰).