Data in Brief (Apr 2018)

Data on genetic associations of carotid atherosclerosis markers in Mexican American and European American rheumatoid arthritis subjects

  • Rector Arya,
  • Agustin Escalante,
  • Vidya S. Farook,
  • Jose F. Restrepo,
  • Daniel F. Battafarano,
  • Marcio Almeida,
  • Mark Z. Kos,
  • Marcel J. Fourcaudot,
  • Srinivas Mummidi,
  • Satish Kumar,
  • Joanne E. Curran,
  • Christopher P. Jenkinson,
  • John Blangero,
  • Ravindranath Duggirala,
  • Inmaculada del Rincon

Journal volume & issue
Vol. 17
pp. 820 – 829

Abstract

Read online

Carotid Intima-media thickness (CIMT) and plaque are well established markers of subclinical atherosclerosis and are widely used for identifying subclinical atherosclerotic disease. We performed association analyses using Metabochip array to identify genetic variants that influence variation in CIMT and plaque, measured using B-mode ultrasonography, in rheumatoid arthritis (RA) patients. Data on genetic associations of common variants associated with both CIMT and plaque in RA subjects involving Mexican Americans (MA) and European Americans (EA) populations are presented in this article. Strong associations were observed after adjusting for covariate effects including baseline clinical characteristics and statin use. Susceptibility loci and genes and/or nearest genes associated with CIMT in MAs and EAs with RA are presented. In addition, common susceptibility loci influencing CIMT and plaque in both MAs and EAs have been presented. Polygenic Risk Score (PRS) plots showing complementary evidence for the observed CIMT and plaque association signals are also shown in this article. For further interpretation and details, please see the research article titled “A Genetic Association Study of Carotid Intima-Media Thickness (CIMT) and Plaque in Mexican Americans and European Americans with Rheumatoid Arthritis” which is being published in Atherosclerosis (Arya et al., 2018) [1].(Arya et al., in press) Thus, common variants in several genes exhibited significant associations with CIMT and plaque in both MAs and EAs as presented in this article. These findings may help understand the genetic architecture of subclinical atherosclerosis in RA populations.