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

2011; Nature Portfolio; Volume: 43; Issue: 4 Linguagem: Inglês

10.1038/ng.784

1546-1718

Heribert Schunkert, Inke R. König, Sekar Kathiresan, Muredach P. Reilly, Themistocles L. Assimes, Hilma Hólm, Michael Preuß, Alexandre F.R. Stewart, Maja Barbalić, 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 Barnes, Diane M. Becker, Lewis C. Becker, Kenneth I. Berger, Joshua C. Bis, S. Matthijs Boekholdt, Eric Boerwinkle, Peter S. Braund, Matthew A. Brown, Mary Susan Burnett, Ian Buysschaert, John F. Carlquist, Li Chen, Sven Cichon, Veryan Codd, R. 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 Elosúa, James C. Engert, Stephen E. Epstein, Ulf dé Fairé, Marcus Fischer, Aaron R. Folsom, Jennifer Freyer, Bruna Gigante, Domenico Girelli, Sólveig Grétarsdóttir, Vilmundur Guðnason, 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 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 Lotery, Pier Mannuccio Mannucci, Seraya Maouche, Nicola Martinelli, Pascal McKeown, Christa Meisinger, Thomas Meitinger, Olle Melander, Pier Angelica Merlini, Vincent Mooser, Thomas M. Morgan, Hae‐Won Uh, Joseph B. Muhlestein, Thomas Münzel, Yan V. Sun, Janja Nahrstaedt, Christopher P. Nelson, Markus M. Nöthen, Oliviero Olivieri, Riyaz S. Patel, C. C. Patterson, Annette Peters, Flora Peyvandi, Liming Qu, Arshed A. Quyyumi, Daniel J. Rader, Lοukianos S. Rallidis, Catherine M. Rice, Frits R. Rosendaal, Deborah C. Rubin, Veikko Salomaa, M. Lourdes Sampietro, Manj S. Sandhu, Eric E. Schadt, Arne Schäfer, Arne Schillert, Stefan Schreiber, Jürgen Schrezenmeir, Stephen M. Schwartz, David S. Siscovick, Mohan U. Sivananthan, Suthesh Sivapalaratnam, Albert V. Smith, Tamara Smith, Jaapjan D. Snoep, Nicole Soranzo, John A. Spertus, Klaus Stark, Kathy Stirrups, Monika Stoll, W.H. Wilson Tang, Stephanie Tennstedt, Guðmundur Þorgeirsson, Guðmar Þorleifsson, Maciej Tomaszewski, André G. Uitterlinden, André M. van Rij, Benjamin F. Voight, Nicholas J. Wareham, George A. Wells, H-Erich Wichmann, Philipp S. Wild, Christina Willenborg, J. C. M. Witteman, Benjamin J. Wright, Shu Ye, Tanja Zeller, Andreas Ziegler, François Cambien, Alison H. Goodall, L. Adrienne Cupples, Thomas Quertermous, Winfried März, Christian Hengstenberg, Stefan Blankenberg, Willem H. Ouwehand, Alistair S. Hall, Panos Deloukas, John R. Thompson, Kāri Stefánsson, Robert Roberts, Unnur Þorsteinsdóttir, Christopher J. O’Donnell, Ruth McPherson, Jeanette Erdmann,

Genetic Mapping and Diversity in Plants and Animals

Heribert Schunkert and colleagues report a meta-analysis of 14 genome-wide association studies of coronary disease (CAD) followed by replication in additional cohorts. They confirm 10 previously associated loci and identify 13 loci newly associated with CAD. 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 × 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.