title: 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.
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.
authors.affiliation: Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, Berkeley, CA, USA.
authors.forename: Lucia
authors.initials: L
authors.lastname: Conde
authors.forename: Steve
authors.initials: S
authors.lastname: Bevan
authors.forename: Matthias
authors.initials: M
authors.lastname: Sitzer
authors.forename: Norman
authors.initials: N
authors.lastname: Klopp
authors.forename: Thomas
authors.initials: T
authors.lastname: Illig
authors.forename: Joachim
authors.initials: J
authors.lastname: Thiery
authors.forename: Joachim
authors.initials: J
authors.lastname: Seissler
authors.forename: Jens
authors.initials: J
authors.lastname: Baumert
authors.forename: Olli
authors.initials: O
authors.lastname: Raitakari
authors.forename: Mika
authors.initials: M
authors.lastname: Kähönen
authors.forename: Leo-Pekka
authors.initials: LP
authors.lastname: Lyytikäinen
authors.forename: Reijo
authors.initials: R
authors.lastname: Laaksonen
authors.forename: Jorma
authors.initials: J
authors.lastname: Viikari
authors.forename: Terho
authors.initials: T
authors.lastname: Lehtimäki
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Koernig
authors.forename: Eran
authors.initials: E
authors.lastname: Halperin
authors.forename: Hugh S
authors.initials: HS
authors.lastname: Markus
mesh_terms: D000328:Adult; D000368:Aged; D002340:Carotid Artery Diseases / Q000000981:diagnostic imaging* / Q000235:genetics*; D017536:Carotid Artery, Common / Q000000981:diagnostic imaging*; D003324:Coronary Artery Disease / Q000235:genetics*; D005060:Europe; D005260:Female; D020022:Genetic Predisposition to Disease; D055106:Genome-Wide Association Study; D006239:Haplotypes; D006801:Humans; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D020641:Polymorphism, Single Nucleotide; D012044:Regression Analysis; D018570:Risk Assessment; D012307:Risk Factors; D017539:Tunica Intima / Q000000981:diagnostic imaging*; D017540:Tunica Media / Q000000981:diagnostic imaging*; D014463:Ultrasonography