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Previous Volume 357:443-453 August 2, 2007 Number 5 Next

	Full Text PDF PDA Full Text PowerPoint Slide Set Supplementary Material Perspective by Hunter, D. J. Editorial by Drazen, J. M. Editorial by Rosenzweig, A. Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited E-mail When Letters Appear PubMed Citation

ABSTRACT

Background Modern genotyping platforms permit a systematic search for inherited components of complex diseases. We performed a joint analysis of two genomewide association studies of coronary artery disease.

Methods We first identified chromosomal loci that were strongly associated with coronary artery disease in the Wellcome Trust Case Control Consortium (WTCCC) study (which involved 1926 case subjects with coronary artery disease and 2938 controls) and looked for replication in the German MI [Myocardial Infarction] Family Study (which involved 875 case subjects with myocardial infarction and 1644 controls). Data on other single-nucleotide polymorphisms (SNPs) that were significantly associated with coronary artery disease in either study (P<0.001) were then combined to identify additional loci with a high probability of true association. Genotyping in both studies was performed with the use of the GeneChip Human Mapping 500K Array Set (Affymetrix).

Results Of thousands of chromosomal loci studied, the same locus had the strongest association with coronary artery disease in both the WTCCC and the German studies: chromosome 9p21.3 (SNP, rs1333049) (P=1.80x10^–14 and P=3.40x10^–6, respectively). Overall, the WTCCC study revealed nine loci that were strongly associated with coronary artery disease (P<1.2x10^–5 and less than a 50% chance of being falsely positive). In addition to chromosome 9p21.3, two of these loci were successfully replicated (adjusted P<0.05) in the German study: chromosome 6q25.1 (rs6922269) and chromosome 2q36.3 (rs2943634). The combined analysis of the two studies identified four additional loci significantly associated with coronary artery disease (P<1.3x10^–6) and a high probability (>80%) of a true association: chromosomes 1p13.3 (rs599839), 1q41 (rs17465637), 10q11.21 (rs501120), and 15q22.33 (rs17228212).

Conclusions We identified several genetic loci that, individually and in aggregate, substantially affect the risk of development of coronary artery disease.

Source Information

From the University of Leicester, Leicester (N.J.S., M.M., R.J.D., P.B., S.E.S., H.P., M.D.T., J.R.T.); University of Leeds, Leeds (A.S.H., J.H.B., M.M.I., A.J.B., S.G.B.); University of Cambridge and National Health Service Blood and Transplant, Cambridge (W.O.); and the Wellcome Trust Sanger Institute, Hinxton (P.D.) — all in the United Kingdom; Universität zu Lübeck, Lübeck (J.E., B.M., I.R.K., S.S., F.P., W.L., I.B., A.Z., H.S.); Universität Regensburg, Regensburg (C.H., M.F., A.B.); GSF–Nationales Forschungszentrum für Umwelt und Gesundheit, Neuherberg (T.M., H.-E.W., T.M.S., C.G.); Technische Universität München, Munich (T.M.); Ludwig Maximilians University, Munich (H.-E.W., C.G.); and Johannes Gutenberg University Mainz, Mainz (S.B.) — all in Germany; and INSERM, UMR S525, Université Pierre et Marie Curie, Paris (D.-A.T., F.C.).

This article (10.1056/NEJMoa072366) was published at www.nejm.org on July 18, 2007.

Address reprint requests to Dr. Samani at the Department of Cardiovascular Sciences, University of Leicester, Glenfield Hospital, Leicester LE3 9QP, United Kingdom, or at njs{at}le.ac.uk or to Dr. Schunkert at Medizinische Klinik II, Universität zu Lübeck, 23538 Lübeck, Germany, or at heribert.schunkert{at}innere2.uni-luebeck.de.

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