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Search: (WFRF:(Trompet Stella)) > (2015-2019) > Genetic Risk Predic...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00006061naa a2200805 4500
001oai:lup.lub.lu.se:bfa7eeb8-7800-4294-87e3-afc319bc831a
003SwePub
008170317s2017 | |||||||||||000 ||eng|
0247 a https://lup.lub.lu.se/record/bfa7eeb8-7800-4294-87e3-afc319bc831a2 URI
0247 a https://doi.org/10.1161/CIRCULATIONAHA.116.0241432 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
1001 a Lubitz, Steven Au Boston University4 aut
2451 0a Genetic Risk Prediction of Atrial Fibrillation
264 1c 2017
520 a BACKGROUND—: Atrial fibrillation (AF) has a substantial genetic basis. Identification of individuals at greatest AF risk could minimize the incidence of cardioembolic stroke. METHODS—: To determine whether genetic data can stratify risk for development of AF, we examined associations between AF genetic risk scores and incident AF in five prospective studies comprising 18,919 individuals of European ancestry. We examined associations between AF genetic risk scores and ischemic stroke in a separate study of 509 ischemic stroke cases (202 cardioembolic [40%]) and 3,028 referents. Scores were based on 11 to 719 common variants (≥5%) associated with AF at P-values ranging from <1x10 to <1x10 in a prior independent genetic association study. RESULTS—: Incident AF occurred in 1,032 (5.5%) individuals. AF genetic risk scores were associated with new-onset AF after adjusting for clinical risk factors. The pooled hazard ratio for incident AF for the highest versus lowest quartile of genetic risk scores ranged from 1.28 (719 variants; 95%CI, 1.13-1.46; P=1.5x10) to 1.67 (25 variants; 95%CI, 1.47-1.90; P=9.3x10). Discrimination of combined clinical and genetic risk scores varied across studies and scores (maximum C statistic, 0.629-0.811; maximum ΔC statistic from clinical score alone, 0.009-0.017). AF genetic risk was associated with stroke in age- and sex-adjusted models. For example, individuals in the highest versus lowest quartile of a 127-variant score had a 2.49-fold increased odds of cardioembolic stroke (95%CI, 1.39-4.58; P=2.7x10). The effect persisted after excluding individuals (n=70) with known AF (odds ratio, 2.25; 95%CI, 1.20-4.40; P=0.01). CONCLUSIONS—: Comprehensive AF genetic risk scores were associated with incident AF beyond associations for clinical AF risk factors, though offered small improvements in discrimination. AF genetic risk was also associated with cardioembolic stroke in age- and sex-adjusted analyses. Efforts are warranted to determine whether AF genetic risk may improve identification of subclinical AF or help distinguish between stroke mechanisms.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Medicinsk genetik0 (SwePub)301072 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Medical Genetics0 (SwePub)301072 hsv//eng
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Neurologi0 (SwePub)302072 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Neurology0 (SwePub)302072 hsv//eng
7001 a Yin, Xiaoyan4 aut
7001 a Lin, Henry J.4 aut
7001 a Kolek, Matthew4 aut
7001 a Smith, Gustav G.u Lund University,Lunds universitet,Kardiologi,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Cardiology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Skåne University Hospital4 aut0 (Swepub:lu)med-gvs
7001 a Trompet, Stella4 aut
7001 a Rienstra, Michiel4 aut
7001 a Rost, Natalia S.4 aut
7001 a Teixeira, Pedro L.4 aut
7001 a Almgren, Peteru Lund University,Lunds universitet,Translationell muskelforskning,Forskargrupper vid Lunds universitet,Translational Muscle Research,Lund University Research Groups,Skåne University Hospital4 aut0 (Swepub:lu)endo-pal
7001 a Anderson, Christopher D.4 aut
7001 a Chen, Lin Y.4 aut
7001 a Engström, Gunnaru Lund University,Lunds universitet,Kardiovaskulär forskning - epidemiologi,Forskargrupper vid Lunds universitet,Cardiovascular Research - Epidemiology,Lund University Research Groups,Skåne University Hospital4 aut0 (Swepub:lu)smi-gen
7001 a Ford, Ian4 aut
7001 a Furie, Karen L.4 aut
7001 a Guo, Xiuqing4 aut
7001 a Larson, Martin G.4 aut
7001 a Lunetta, Kathryn L.4 aut
7001 a Macfarlane, Peter W4 aut
7001 a Psaty, Bruce M.4 aut
7001 a Soliman, Elsayed Z4 aut
7001 a Sotoodehnia, Nona4 aut
7001 a Stott, David J.4 aut
7001 a Taylor, Kent D4 aut
7001 a Weng, Lu Chen4 aut
7001 a Yao, Jie4 aut
7001 a Geelhoed, Bastiaan4 aut
7001 a Verweij, Niek4 aut
7001 a Siland, Joylene E.4 aut
7001 a Kathiresan, Sekar4 aut
7001 a Roselli, Carolina4 aut
7001 a Roden, Dan M4 aut
7001 a van der Harst, Pim4 aut
7001 a Darbar, Dawood4 aut
7001 a Jukema, J. Wouter4 aut
7001 a Melander, Olleu Lund University,Lunds universitet,Kardiovaskulär forskning - hypertoni,Forskargrupper vid Lunds universitet,Cardiovascular Research - Hypertension,Lund University Research Groups,Skåne University Hospital4 aut0 (Swepub:lu)endo-ome
7001 a Rosand, Jonathan4 aut
7001 a Rotter, Jerome I.4 aut
7001 a Heckbert, Susan R4 aut
7001 a Ellinor, Patrick T4 aut
7001 a Alonso, Alvaro4 aut
7001 a Benjamin, Emelia J4 aut
7102 a Boston Universityb Kardiologi4 org
7102 a on behalf of the AFGen Consortium
7730 t Circulationg 135:14, s. 1311-1320q 135:14<1311-1320x 0009-7322
8564 u http://dx.doi.org/10.1161/CIRCULATIONAHA.116.024143y FULLTEXT
8564 8u https://lup.lub.lu.se/record/bfa7eeb8-7800-4294-87e3-afc319bc831a
8564 8u https://doi.org/10.1161/CIRCULATIONAHA.116.024143

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