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Olle Melander

Principal investigator

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Large-scale association analysis identifies 13 new susceptibility loci for coronary artery disease

Author

  • Heribert Schunkert
  • Inke R. Koenig
  • Sekar Kathiresan
  • Muredach P. Reilly
  • Themistocles L. Assimes
  • Hilma Holm
  • Michael Preuss
  • Alexandre F. R. Stewart
  • Maja Barbalic
  • Christian Gieger
  • Devin Absher
  • Zouhair Aherrahrou
  • Hooman Allayee
  • David Altshuler
  • Sonia S. Anand
  • Karl Andersen
  • Jeffrey L. Anderson
  • Diego Ardissino
  • Stephen G. Ball
  • Anthony J. Balmforth
  • Timothy A. Barnes
  • Diane M. Becker
  • Lewis C. Becker
  • Klaus Berger
  • Joshua C. Bis
  • S. Matthijs Boekholdt
  • Eric Boerwinkle
  • Peter S. Braund
  • Morris J. Brown
  • Mary Susan Burnett
  • Ian Buysschaert
  • John F. Carlquist
  • Li Chen
  • Sven Cichon
  • Veryan Codd
  • Robert W. Davies
  • George Dedoussis
  • Abbas Dehghan
  • Serkalem Demissie
  • Joseph M. Devaney
  • Patrick Diemert
  • Ron Do
  • Angela Doering
  • Sandra Eifert
  • Nour Eddine El Mokhtari
  • Stephen G. Ellis
  • Roberto Elosua
  • James C. Engert
  • Stephen E. Epstein
  • Ulf de Faire
  • Marcus Fischer
  • Aaron R. Folsom
  • Jennifer Freyer
  • Bruna Gigante
  • Domenico Girelli
  • Solveig Gretarsdottir
  • Vilmundur Gudnason
  • Jeffrey R. Gulcher
  • Eran Halperin
  • Naomi Hammond
  • Stanley L. Hazen
  • Albert Hofman
  • Benjamin D. Horne
  • Thomas Illig
  • Carlos Iribarren
  • Gregory T. Jones
  • J. Wouter Jukema
  • Michael A. Kaiser
  • Lee M. Kaplan
  • John J. P. Kastelein
  • Kay-Tee Khaw
  • Joshua W. Knowles
  • Genovefa Kolovou
  • Augustine Kong
  • Reijo Laaksonen
  • Diether Lambrechts
  • Karin Leander
  • Guillaume Lettre
  • Mingyao Li
  • Wolfgang Lieb
  • Christina Loley
  • Andrew J. Lotery
  • Pier M. Mannucci
  • Seraya Maouche
  • Nicola Martinelli
  • Pascal P. McKeown
  • Christa Meisinger
  • Thomas Meitinger
  • Olle Melander
  • Pier Angelica Merlini
  • Vincent Mooser
  • Thomas Morgan
  • Thomas W. Muehleisen
  • Joseph B. Muhlestein
  • Thomas Muenzel
  • Kiran Musunuru
  • Janja nahrstaedt
  • Christopher P. Nelson
  • Markus M. Noethen
  • Oliviero Olivieri
  • Riyaz S. Patel
  • Chris C. Patterson
  • Annette Peters
  • Flora Peyvandi
  • Liming Qu
  • Arshed A. Quyyumi
  • Daniel J. Rader
  • Loukianos S. Rallidis
  • Catherine Rice
  • Frits R. Rosendaal
  • Diana Rubin
  • Veikko Salomaa
  • M. Lourdes Sampietro
  • Manj S. Sandhu
  • Eric Schadt
  • Arne Schaefer
  • Arne Schillert
  • Stefan Schreiber
  • Juergen Schrezenmeir
  • Stephen M. Schwartz
  • David S. Siscovick
  • Mohan Sivananthan
  • Suthesh Sivapalaratnam
  • Albert Smith
  • Tamara B. Smith
  • Jaapjan D. Snoep
  • Nicole Soranzo
  • John A. Spertus
  • Klaus Stark
  • Kathy Stirrups
  • Monika Stoll
  • W. H. Wilson Tang
  • Stephanie Tennstedt
  • Gudmundur Thorgeirsson
  • Gudmar Thorleifsson
  • Maciej Tomaszewski
  • Andre G. Uitterlinden
  • Andre M. van Rij
  • Benjamin F. Voight
  • Nick J. Wareham
  • George A. Wells
  • H-Erich Wichmann
  • Philipp S. Wild
  • Christina Willenborg
  • Jaqueline C. M. Witteman
  • Benjamin J. Wright
  • Shu Ye
  • Tanja Zeller
  • Andreas Ziegler
  • Francois Cambien
  • Alison H. Goodall
  • L. Adrienne Cupples
  • Thomas Quertermous
  • Winfried Maerz
  • Christian Hengstenberg
  • Stefan Blankenberg
  • Willem H. Ouwehand
  • Alistair S. Hall
  • Panos Deloukas
  • John R. Thompson
  • Kari Stefansson
  • Robert Roberts
  • Unnur Thorsteinsdottir
  • Christopher J. O'Donnell
  • Ruth McPherson
  • Jeanette Erdmann
  • Nilesh J. Samani

Summary, in English

We performed a meta-analysis of 14 genome-wide association studies of coronary artery disease (CAD) comprising 22,233 individuals with CAD (cases) and 64,762 controls of European descent followed by genotyping of top association signals in 56,682 additional individuals. This analysis identified 13 loci newly associated with CAD at P < 5 x 10(-8) and confirmed the association of 10 of 12 previously reported CAD loci. The 13 new loci showed risk allele frequencies ranging from 0.13 to 0.91 and were associated with a 6% to 17% increase in the risk of CAD per allele. Notably, only three of the new loci showed significant association with traditional CAD risk factors and the majority lie in gene regions not previously implicated in the pathogenesis of CAD. Finally, five of the new CAD risk loci appear to have pleiotropic effects, showing strong association with various other human diseases or traits.

Department/s

  • Cardiovascular Research - Hypertension
  • EXODIAB: Excellence in Diabetes Research in Sweden
  • EpiHealth: Epidemiology for Health

Publishing year

2011

Language

English

Pages

153-333

Publication/Series

Nature Genetics

Volume

43

Issue

4

Document type

Journal article

Publisher

Nature Publishing Group

Topic

  • Cardiac and Cardiovascular Systems

Status

Published

Research group

  • Cardiovascular Research - Hypertension

ISBN/ISSN/Other

  • ISSN: 1546-1718