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Association analyses based on false discovery rate implicate new loci for coronary artery disease

Association analyses based on false discovery rate implicate new loci for coronary artery disease

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  • Christopher P. Nelson
  • Anuj Goel
  • Adam S. Butterworth
  • Stavroula Kanoni
  • Tom R Webb
  • Eirini Marouli
  • Lingyao Zeng
  • Ioanna Ntalla
  • Florence Y Lai
  • Jemma C. Hopewell
  • Olga Giannakopoulou
  • Tao Jiang
  • Stephen E. Hamby
  • Emanuele Di Angelantonio
  • Themistocles L. Assimes
  • Erwin P. Bottinger
  • John C. Chambers
  • Robert Clarke
  • Colin N A Palmer
  • Richard M. Cubbon
  • Patrick T. Ellinor
  • Raili Ermel
  • Evangelos Evangelou
  • Paul W. Franks
  • Christopher Grace
  • Dongfeng Gu
  • Aroon D. Hingorani
  • Joanna M. M. Howson
  • Erik Ingelsson
  • Adnan Kastrati
  • Thorsten Kessler
  • Theodosios Kyriakou
  • Terho Lehtimäki
  • Xiangfeng Lu
  • Yingchang Lu
  • Winfried März
  • Ruth McPherson
  • Andres Metspalu
  • Mar Pujades-Rodriguez
  • Arno Ruusalepp
  • Eric E. Schadt
  • Amand F Schmidt
  • Michael J Sweeting
  • Pierre A. Zalloua
  • Kamal AlGhalayini
  • Bernard D. Keavney
  • Jaspal S. Kooner
  • Ruth J. F. Loos
  • Riyaz S Patel
  • Martin K Rutter
  • Maciej Tomaszewski
  • Ioanna Tzoulaki
  • Eleftheria Zeggini
  • Jeanette Erdmann
  • George Dedoussis
  • Johan L. M. Björkegren
  • Heribert Schunkert
  • Martin Farrall
  • John Danesh
  • Nilesh J. Samani
  • Hugh Watkins (Lead / Corresponding author)
  • Panos Deloukas
  • EPIC-CVD Consortium, CARDIoGRAMplusC4D, The UK Biobank CardioMetabolic Consortium CHD working group

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Original languageEnglish
Pages (from-to)1385-1391
Number of pages6
JournalNature Genetics
Issue number9
Early online date17 Jul 2017
StatePublished - Sep 2017


Genome-wide association studies (GWAS) in coronary artery disease (CAD) had identified 66 loci at 'genome-wide significance' (P < 5 × 10(-8)) at the time of this analysis, but a much larger number of putative loci at a false discovery rate (FDR) of 5% (refs. 1,2,3,4). Here we leverage an interim release of UK Biobank (UKBB) data to evaluate the validity of the FDR approach. We tested a CAD phenotype inclusive of angina (SOFT; ncases = 10,801) as well as a stricter definition without angina (HARD; ncases = 6,482) and selected cases with the former phenotype to conduct a meta-analysis using the two most recent CAD GWAS. This approach identified 13 new loci at genome-wide significance, 12 of which were on our previous list of loci meeting the 5% FDR threshold, thus providing strong support that the remaining loci identified by FDR represent genuine signals. The 304 independent variants associated at 5% FDR in this study explain 21.2% of CAD heritability and identify 243 loci that implicate pathways in blood vessel morphogenesis as well as lipid metabolism, nitric oxide signaling and inflammation.



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