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Objective  To investigate the genetic background influencing the development of cardiovascular ( CV ) disease in patients with rheumatoid arthritis ( RA ).    Methods  We performed a genome‐wide association study ( GWAS ) in which, after quality control and imputation, a total of 6,308,944 polymorphisms across the whole genome were analyzed in 2,989  RA  patients of European origin. Data on subclinical atherosclerosis, obtained through assessment of carotid intima‐media thickness ( CIMT ) and presence/absence of carotid plaques by carotid ultrasonography, were available for 1,355 individuals.    Results  A genetic variant of the   RARB   gene (rs116199914) was associated with  CIMT  values at the genome‐wide level of significance (minor allele [G] β coefficient 0.142,  P  = 1.86 × 10 −8 ). Interestingly, rs116199914 overlapped with regulatory elements in tissues related to  CV  pathophysiology and immune cells. In addition, biologic pathway enrichment and predictive protein–protein relationship analyses, including suggestive  GWAS  signals of potential relevance, revealed a functional enrichment of the collagen biosynthesis network related to the presence/absence of carotid plaques (Gene Ontology no. 0032964; false discovery rate–adjusted  P  = 4.01 × 10 −3 ). Furthermore, our data suggest potential influences of the previously described candidate  CV  risk loci   NFKB 1 ,   MSRA  , and   ZC 3 HC 1  ( P  = 8.12 × 10 −4 ,  P  = 5.94 × 10 −4 , and  P  = 2.46 × 10 −4 , respectively).    Conclusion  The present findings strongly suggest that genetic variation within   RARB   contributes to the development of subclinical atherosclerosis in patients with  RA .

arthritis and rheumatology

Identification of a 3′‐Untranslated Genetic Variant of   RARB   Associated With Carotid Intima‐Media Thickness in Rheumatoid Arthritis: A Genome‐Wide Association Study