title: Reduced arterial elasticity in rheumatoid arthritis and the relationship to vascular disease risk factors and inflammation.
abstract: OBJECTIVE
  Rheumatoid arthritis (RA) is associated with increased rates of cardiovascular disease. Reduced small artery elasticity (SAE) and large artery elasticity (LAE) and increased systemic vascular resistance (SVR) have been found in other high-risk groups. In the present study, we sought to determine whether arterial elasticity was reduced and SVR was increased in RA patients compared with controls matched for coronary artery disease (CAD) status, and to relate the results to vascular disease risk factors, including measures of inflammation.
  
  
  METHODS
  Arterial elasticity was assessed by pulse wave analysis in RA patients with (n = 15) and without (n = 38) CAD, and in controls matched 1:1 for age, sex, and CAD status. Vascular risk factors, including high-sensitivity C-reactive protein (hsCRP), soluble vascular cell adhesion molecule 1 (sVCAM-1), and serum amyloid A (SAA) levels, were assessed.
  
  
  RESULTS
  SAE and LAE were significantly lower and SVR was significantly higher in RA patients than in controls. RA patients also had higher levels of hsCRP, SAA, and sVCAM-1. SAE and LAE values were inversely correlated with markers of inflammation. Associations of SAE and LAE with RA were independent of conventional risk factors, but were dependent on markers of inflammation.
  
  
  CONCLUSIONS
  Vascular function is abnormal in RA, with reduced SAE and LAE and increased SVR relative to controls. Arterial elasticity is inversely associated with measures of inflammation. These measures may be clinically useful in the detection and monitoring of vascular disease in RA.
authors.affiliation: St. Vincent's Hospital, Fitzroy, Victoria, Australia.
authors.forename: Melinda
authors.initials: M
authors.lastname: Wong
authors.forename: Ling
authors.initials: L
authors.lastname: Toh
authors.forename: Andrew
authors.initials: A
authors.lastname: Wilson
authors.forename: Kevin
authors.initials: K
authors.lastname: Rowley
authors.forename: Connie
authors.initials: C
authors.lastname: Karschimkus
authors.forename: David
authors.initials: D
authors.lastname: Prior
authors.forename: Evange
authors.initials: E
authors.lastname: Romas
authors.forename: Laurence
authors.initials: L
authors.lastname: Clemens
authors.forename: George
authors.initials: G
authors.lastname: Dragicevic
authors.forename: Harry
authors.initials: H
authors.lastname: Harianto
authors.forename: Ian
authors.initials: I
authors.lastname: Wicks
authors.forename: Geoff
authors.initials: G
authors.lastname: McColl
authors.forename: James
authors.initials: J
authors.lastname: Best
authors.forename: Alicia
authors.initials: A
authors.lastname: Jenkins
mesh_terms: D000368:Aged; D001172:Arthritis, Rheumatoid / Q000453:epidemiology* / Q000276:immunology / Q000473:pathology*; D015415:Biomarkers; D003324:Coronary Artery Disease / Q000453:epidemiology* / Q000276:immunology / Q000473:pathology*; D003430:Cross-Sectional Studies; D004548:Elasticity; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D014655:Vascular Resistance; D014657:Vasculitis / Q000453:epidemiology / Q000276:immunology / Q000473:pathology
chemical_list: D015415:Biomarkers