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Pfeufer, A. ; Sanna, S.* ; Arking, D.E.* ; Müller, M. ; Gateva, V.* ; Fuchsberger, C.* ; Ehret, G.B.* ; Orrù, M.* ; Pattaro, C.* ; Köttgen, A.* ; Perz, S. ; Usala, G.* ; Barbalic, M.* ; Li, M.* ; Pütz, B.* ; Scuteri, A.* ; Prineas, R.J.* ; Sinner, M.F.* ; Gieger, C. ; Najjar, S.S.* ; Kao, W.H.L.* ; Mühleisen, T.W.* ; Die, M.* ; Happle, C. ; Möhlenkamp, S.* ; Crisponi, L.* ; Erbel, R.* ; Jöckel, K.-H.* ; Naitza, S.* ; Steinbeck, G.* ; Marroni, F.* ; Hicks, A.A.* ; Lakatta, E.* ; Müller-Myhsok, B.* ; Pramstaller, P.P.* ; Wichmann, H.-E. ; Schlessinger, D.* ; Boerwinkle, E.* ; Meitinger, T. ; Uda, M.* ; Coresh, J.* ; Kääb, S.* ; Abecasis, G.R.* ; Chakravarti, A.*

Common variants at ten loci modulate the QT interval duration in the QTSCD Study.

Nat. Genet. 41, 407-414 (2009)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
The QT interval, a measure of cardiac repolarization, predisposes to ventricular arrhythmias and sudden cardiac death ( SCD) when prolonged or shortened. A common variant in NOS1AP is known to influence repolarization. We analyze genome-wide data from five population-based cohorts (ARIC, KORA, SardiNIA, GenNOVA and HNR) with a total of 15,842 individuals of European ancestry, to confirm the NOS1AP association and identify nine additional loci at P < 5 x 10(-8). Four loci map near the monogenic long-QT syndrome genes KCNQ1, KCNH2, SCN5A and KCNJ2. Two other loci include ATP1B1 and PLN, genes with established electrophysiological function, whereas three map to RNF207, near LITAF and within NDRG4-GINS3-SETD6-CNOT1, respectively, all of which have not previously been implicated in cardiac electrophysiology. These results, together with an accompanying paper from the QTGEN consortium, identify new candidate genes for ventricular arrhythmias and SCD.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords nos1 regulator nos1ap; sudden cardiac death; heart-failure; healthy population; genetic variant; disease; repolarization; risk; association; mutation
ISSN (print) / ISBN 1061-4036
e-ISSN 1546-1718
Journal Nature Genetics
Quellenangaben Volume: 41, Issue: 4, Pages: 407-414 Article Number: , Supplement: ,
Publisher Nature Publishing Group
Publishing Place New York, NY
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Human Genetics (IHG)
Institute of Epidemiology (EPI)
Institute of Biological and Medical Imaging (IBMI)