Journal article
Atrial fibrillation genetic risk differentiates cardioembolic stroke from other stroke subtypes
Sara L Pulit, Lu-Chen Weng, Patrick F McArdle, Ludovic Trinquart, Seung Hoan Choi, Braxton D Mitchell, Jonathan Rosand, Paul IW de Bakker, Emelia J Benjamin, Patrick T Ellinor, Steven J Kittner, Steven A Lubitz, Christopher D Anderson, Ingrid E Christophersen, Michiel Rienstra, Carolina Roselli, Xiaoyan Yin, Bastiaan Geelhoed, John Barnard, Honghuang Lin Show all
NEUROLOGY-GENETICS | LIPPINCOTT WILLIAMS & WILKINS | Published : 2018
Abstract
Objective: We sought to assess whether genetic risk factors for atrial fibrillation (AF) can explain cardioembolic stroke risk. Methods: We evaluated genetic correlations between a previous genetic study of AF and AF in the presence of cardioembolic stroke using genome-wide genotypes from the Stroke Genetics Network (N = 3,190 AF cases, 3,000 cardioembolic stroke cases, and 28,026 referents). We tested whether a previously validated AF polygenic risk score (PRS) associated with cardioembolic and other stroke subtypes after accounting for AF clinical risk factors. Results: We observed a strong correlation between previously reported genetic risk for AF, AF in the presence of stroke, and cardi..
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Awarded by NIH
Awarded by Veni Fellowship (ZonMW) from the Dutch Organization for Scientific Research (Nederlandse Organisatie voor Wetenschappelijk Onderzoek, NWO)
Awarded by Doris Duke Charitable Foundation Clinical Scientist Development Award
Awarded by American Heart Association Postdoctoral Fellowship
Awarded by American Heart Association
Awarded by Fondation Leducq
Awarded by NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
Funding Acknowledgements
S.L. Pulit, B.D. Mitchell, P.F. McArdle, and S.J. Kittner are supported by the NIH grant R01NS100178. The NINDS-SiGN Consortium is supported by the NIH grants R01NS100178 and U01NS069208. S.L. Pulit is supported by Veni Fellowship 016.186.071 (ZonMW) from the Dutch Organization for Scientific Research (Nederlandse Organisatie voor Wetenschappelijk Onderzoek, NWO). C.D. Anderson is supported in part by K23NS086873, R01NS103924, an American Heart Association Strategically Focused Research Network in Atrial Fibrillation Award, and a Massachusetts General Hospital Center for Genomic Medicine Catalyst Award. S.A. Lubitz is supported by the NIH grant K23HL114724, an American Heart Association Strategically Focused Research Network in Atrial Fibrillation Award, and a Doris Duke Charitable Foundation Clinical Scientist Development Award 2014105. L.-C. Weng is supported by an American Heart Association Postdoctoral Fellowship Award 17POST33660226. Drs. Ellinor and Benjamin are supported by the NIH grants R01HL092577 and R01HL128914 and an American Heart Association Strategically Focused Research Network in Atrial Fibrillation Award. E.J. Benjamin is additionally supported by the NIH grants 1RC1HL101056 and 1R01HL102214. P.T. Ellinor is additionally supported by the NIH grants R01HL104156 and K24HL105780; the National Heart, Lung, and Blood Institute (NHLBI); American Heart Association Established Investigator Award 13EIA14220013; and the Fondation Leducq 14CVD01.