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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

Authors :
Conde, Lucia
Bevan, Steve
Sitzer, Matthias
Klopp, Norman
Illig, Thomas
Thiery, Joachim
Seissler, Joachim
Baumert, Jens
Raitakari, Olli
Kähönen, Mika
Lyytikäinen, Leo-Pekka
Laaksonen, Reijo
Viikari, Jorma
Lehtimäki, Terho
Koernig, Wolfgang
Halperin, Eran
Markus, Hugh S.
Source :
Atherosclerosis (00219150). Dec2011, Vol. 219 Issue 2, p684-689. 6p.
Publication Year :
2011

Abstract

Abstract: 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. [Copyright &y& Elsevier]

Details

Language :
English
ISSN :
00219150
Volume :
219
Issue :
2
Database :
Academic Search Index
Journal :
Atherosclerosis (00219150)
Publication Type :
Academic Journal
Accession number :
67625199
Full Text :
https://doi.org/10.1016/j.atherosclerosis.2011.08.031