Search: onr:"swepub:oai:lup.lub.lu.se:b61033fe-1cfc-4a64-a753-7f671f17e625" >
Heritability of Atr...
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Weng, Lu ChenMassachusetts Institute of Technology
(author)
Heritability of Atrial Fibrillation
- Article/chapterEnglish2017
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LIBRIS-ID:oai:lup.lub.lu.se:b61033fe-1cfc-4a64-a753-7f671f17e625
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https://lup.lub.lu.se/record/b61033fe-1cfc-4a64-a753-7f671f17e625URI
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https://doi.org/10.1161/CIRCGENETICS.117.001838DOI
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Language:English
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Summary in:English
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Background - Previous reports have implicated multiple genetic loci associated with AF, but the contributions of genome-wide variation to AF susceptibility have not been quantified. Methods and Results - We assessed the contribution of genome-wide single-nucleotide polymorphism variation to AF risk (single-nucleotide polymorphism heritability, h2 g) using data from 120 286 unrelated individuals of European ancestry (2987 with AF) in the population-based UK Biobank. We ascertained AF based on self-report, medical record billing codes, procedure codes, and death records. We estimated h2 g using a variance components method with variants having a minor allele frequency ≥1%. We evaluated h2 g in age, sex, and genomic strata of interest. The h2 g for AF was 22.1% (95% confidence interval, 15.6%-28.5%) and was similar for early- versus older-onset AF (≤65 versus >65 years of age), as well as for men and women. The proportion of AF variance explained by genetic variation was mainly accounted for by common (minor allele frequency, ≥5%) variants (20.4%; 95% confidence interval, 15.1%-25.6%). Only 6.4% (95% confidence interval, 5.1%-7.7%) of AF variance was attributed to variation within known AF susceptibility, cardiac arrhythmia, and cardiomyopathy gene regions. Conclusions - Genetic variation contributes substantially to AF risk. The risk for AF conferred by genomic variation is similar to that observed for several other cardiovascular diseases. Established AF loci only explain a moderate proportion of disease risk, suggesting that further genetic discovery, with an emphasis on common variation, is warranted to understand the causal genetic basis of AF.
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Choi, Seung HoanMassachusetts Institute of Technology
(author)
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Klarin, DerekMassachusetts Institute of Technology
(author)
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Smith, J. GustavLund University,Lunds universitet,Kardiologi,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Heart Failure and Mechanical Support,Forskargrupper vid Lunds universitet,Molecular Epidemiology and Cardiology,Cardiovascular Epigenetics,Cardiology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Lund University Research Groups,Skåne University Hospital,Broad Institute,Massachusetts Institute of Technology(Swepub:lu)med-gvs
(author)
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Loh, Po RuMassachusetts Institute of Technology,Harvard University
(author)
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Chaffin, MarkMassachusetts Institute of Technology
(author)
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Roselli, CarolinaMassachusetts Institute of Technology
(author)
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Hulme, Olivia L.Massachusetts Institute of Technology
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Lunetta, Kathryn L.Boston University
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Dupuis, JoséeBoston University
(author)
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Benjamin, Emelia J.Boston University
(author)
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Newton-Cheh, ChristopherMassachusetts Institute of Technology
(author)
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Kathiresan, SekarMassachusetts Institute of Technology
(author)
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Ellinor, Patrick T.Massachusetts General Hospital,Massachusetts Institute of Technology
(author)
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Lubitz, Steven A.Massachusetts General Hospital,Massachusetts Institute of Technology
(author)
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Massachusetts Institute of TechnologyKardiologi
(creator_code:org_t)
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In:Circulation: Cardiovascular Genetics10:61942-325X
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Weng, Lu Chen
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Choi, Seung Hoan
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Klarin, Derek
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Smith, J. Gustav
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Loh, Po Ru
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Chaffin, Mark
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Roselli, Carolin ...
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Hulme, Olivia L.
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Dupuis, Josée
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Benjamin, Emelia ...
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