title: Retinal vascular calibre is altered in patients with rheumatoid arthritis: a biomarker of disease activity and cardiovascular risk?
abstract: OBJECTIVE
  Alterations in retinal vascular calibre, particularly wider venular calibre, have been independently associated with elevated markers of inflammation and cardiovascular risk in the general population. We hypothesized that retinal vascular calibre would be altered in patients with RA, who are known to have both elevated cardiovascular risk and chronic, systemic inflammation.
  
  
  METHODS
  Retinal vascular calibre was measured from digital retinal photographs using computerized methods in 51 RA patients and 51 age- and gender-matched controls. Retinal vascular calibre was compared between RA and control patients with adjustment for relevant variables including cardiovascular risk factors and companion vessel calibre. The relationship between retinal venular calibre and inflammation was assessed by comparing controls and RA patients with high and lower disease activity.
  
  
  RESULTS
  Retinal venular calibre [mean (s.d.)] was significantly wider in RA patients than in controls [235.9 (24.6) vs. 211.6 (21.0) µm, P < 0.001]. After adjustment for all relevant variables, mean venular calibre remained 20.3 µm (95% CI 10.4, 30.3) wider in RA patients compared with controls. Retinal venular calibre [mean (s.d.)] also increased with increasing levels of systemic inflammation: 211.6 (21.0) µm in controls, 232.3 (22.4) µm in RA patients with moderate or lower disease activity and 255.5 (28.3) µm in RA patients with high disease activity (P for trend < 0.0001).
  
  
  CONCLUSIONS
  This study demonstrates that RA patients have dilated retinal venular calibre, reflecting systemic inflammation and possibly increased cardiovascular risk. Longitudinal studies correlating retinal vascular calibre with subsequent cardiovascular events will clarify the clinical utility of this test in patients with RA.
authors.affiliation: Department of Medicine (RMH/WH), University of Melbourne, 4th Floor Clinical Sciences Building, Royal Melbourne Hospital, Parkville Vic 3050, Melbourne, Australia. svd@unimelb.edu.au
authors.forename: Sharon
authors.initials: S
authors.lastname: Van Doornum
authors.forename: Gemma
authors.initials: G
authors.lastname: Strickland
authors.forename: Ryo
authors.initials: R
authors.lastname: Kawasaki
authors.forename: Jing
authors.initials: J
authors.lastname: Xie
authors.forename: Ian P
authors.initials: IP
authors.lastname: Wicks
authors.forename: Lauren A B
authors.initials: LA
authors.lastname: Hodgson
authors.forename: Tien Y
authors.initials: TY
authors.lastname: Wong
mesh_terms: D000368:Aged; D001172:Arthritis, Rheumatoid / Q000473:pathology* / Q000503:physiopathology*; D015415:Biomarkers; D002318:Cardiovascular Diseases / Q000453:epidemiology*; D016022:Case-Control Studies; D005260:Female; D005451:Fluorescein Angiography; D006801:Humans; D007249:Inflammation / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D012171:Retinal Vessels / Q000473:pathology* / Q000503:physiopathology; D012307:Risk Factors; D012720:Severity of Illness Index; D014699:Venules / Q000473:pathology / Q000503:physiopathology
chemical_list: D015415:Biomarkers