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Conde, L.* ; Bevan, S.* ; Sitzer, M.* ; Klopp, N. ; Illig, T. ; Thiery, J.* ; Seissler, J.* ; Baumert, J.J. ; Raitakari, O.* ; Kähönen, M.* ; Lyytikäinen, L.-P.* ; Laaksonen, R.* ; Viikari, J.* ; Lehtimäki, T.* ; Koernig, W.* ; Halperin, E.* ; Markus, H.S.*

Novel associations for coronary artery disease derived from genome wide association studies are not associated with increased carotid intima-media thickness, suggesting they do not act via early atherosclerosis or vessel remodeling.

Atherosclerosis 219, 684-689 (2011)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
Background: Recent genome-wide association studies (GWAS) have identified associations with myocardial infarction and coronary artery disease (CAD), but the mechanisms underlying these associations remain largely unclear. Carotid intima-media thickness (IMT) is a measure of early arterial remodeling and arteriosclerosis. Therefore, if CAD associated SNPs are also associated with carotid IMT; it suggests that they are acting via the early stages of the atherosclerotic process. Methods: In three large community based independent populations (CAPS, KORA and Young Finns) of European ancestry in which common carotid IMT had been measured (total 4961 individuals), we determined whether SNPs that have been associated with CAD in GWAS studies are also associated with carotid IMT. Associations with plaque were not examined. Results We identified 11 SNPs and one haplotype previously associated with CAD. None of these were associated with common carotid IMT. Conclusions: We found no evidence that SNPs associated with CAD on GWAS are also associated with carotid IMT. This suggests these genetic associations are not acting via early vessel remodeling or early arteriosclerosis.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Coronary artery disease; Atherosclerosis; Genetics; Myocardial infarction; Intima-media thickness; Genome wide association
ISSN (print) / ISBN 0021-9150
e-ISSN 1879-1484
Journal Atherosclerosis
Quellenangaben Volume: 219, Issue: 2, Pages: 684-689 Article Number: , Supplement: ,
Publisher Elsevier
Publishing Place Amsterdam
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Research Unit Molecular Epidemiology (AME)
Institute of Epidemiology (EPI)