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Title: Coronary Artery Disease–Associated Locus on Chromosome 9p21 and Early Markers of Atherosclerosis
Authors: Samani, Nilesh J.
Raitakari, Olli T.
Sipilä, Kalle
Tobin, Martin D.
Schunkert, Heribert
Juonala, Markus
Braund, Peter S.
Erdmann, Jeanette
Viikari, Jorma
Moilanen, Leena
Taittonen, Leena
Jula, Antti
Jokinen, Eero
Laitinen, Tomi
Hutri-Kähönen, Nina
Nieminen, Markku S.
Kesäniemi, Y. Antero
Hall, Alistair S.
Hulkkonen, Janne
Kähönen, Mika
Lehtimäki, Terho
First Published: Sep-2008
Publisher: American Heart Association
Citation: Arteriosclerosis Thrombosis and Vascular Biology, 2008, 28 (9), pp. 1679-1683.
Abstract: Background— Genome-wide association studies have recently identified a locus on chromosome 9p21 that influences risk of coronary artery disease (CAD). The effect of the locus on early markers of atherosclerosis is unknown. We examined its association with carotid intima-media thickness (CIMT) and brachial flow-mediated dilatation (FMD). Methods and Results— We genotyped 2277 individuals, age 24 to 39 years, from the Cardiovascular Risk in Young Finns Study with CIMT and FMD measurements and 1295 individuals, age 46 to 76 years, from the Health 2000 Survey with CIMT for rs1333049, the chromosome 9p21 variant showing the strongest association with CAD. Both mean and maximum CIMT were significantly higher (P<0.001) in the older subjects of the Health 2000 Survey compared with the Young Finns Study. However, there was no association of the rs1333049 genotype with either mean or maximum CIMT at either age (P=0.959 and 0.977 for the 2 phenotypes in the Young Finns Study and P=0.714 and 0.725 in the Health 2000 Survey). Similarly, there was no association of the locus with variation in FMD in the Young Finns cohort (P=0.521). Conclusions— The chromosome 9p21 locus does not influence CAD risk through a mechanism that also affects CIMT or induces early changes in FMD. We examined the association with carotid intima-media thickness and brachial flow mediated dilatation of the recently identified susceptibility locus for coronary artery disease on chromosome 9p21. We found no evidence that the risk variant affects either of these early markers of atherosclerosis, suggesting an alternate mechanism for its effect on risk of CAD.
DOI Link: 10.1161/ATVBAHA.108.170332
ISSN: 1079-5642
Type: Article
Rights: This paper was published as Arteriosclerosis Thrombosis and Vascular Biology, 2008, 28 (9), pp. 1679-1683. It is available from Doi: 10.1161/ATVBAHA.108.170332
Appears in Collections:Published Articles, Dept. of Health Sciences

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