4.6 Article

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

期刊

ATHEROSCLEROSIS
卷 219, 期 2, 页码 684-689

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.atherosclerosis.2011.08.031

关键词

Coronary artery disease; Atherosclerosis; Genetics; Myocardial infarction; Intima-media thickness; Genome wide association

资金

  1. European Union [201668]
  2. CAPS
  3. Stiftung Deutsche Schlaganfall-Hilfe (German Stroke Foundation)
  4. Young Finns Study
  5. Academy of Finland [117797, 126925, 121584, 117941]
  6. Social Insurance Institution of Finland
  7. Turku University Foundation
  8. Finnish Cultural Foundation
  9. Yrjo Jahnsson Foundation
  10. Emil Aaltonen Foundation
  11. Tampere University Hospital [9M048]
  12. Turku University Central Hospital
  13. Juho Vainio Foundation
  14. Finnish Foundation for Cardiovascular Research
  15. Tampere Tuberculosis Foundation
  16. Helmholtz Zentrum Munchen, German Research Center for Environmental Health, Neuherberg, Germany
  17. German Federal Ministry of Education and Research (BMBF)
  18. German National Genome Research Network (NGFNPlus) [01G50834]
  19. University of Ulm
  20. Munich Center of Health Sciences (MC Health)
  21. Academy of Finland (AKA) [117941, 117941] Funding Source: Academy of Finland (AKA)

向作者/读者索取更多资源

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. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

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