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Ann Rheum Dis doi:10.1136/annrheumdis-2013-205058
  • Clinical and epidemiological research
  • Extended report

Systemic inflammation and cardiovascular risk factors predict rapid progression of atherosclerosis in rheumatoid arthritis

  1. Agustín Escalante1
  1. 1Division of Rheumatology and Clinical Immunology, Department of Medicine, The University of Texas Health Science Center at San Antonio, Texas, USA
  2. 2Division of Cardiology, Department of Medicine, The University of Texas Health Science Center at San Antonio, Texas, USA
  3. 3Ultrasound Reading Center, Tufts Medical Center, Boston, Massachusetts, USA
  4. 4Brooke Army Medical Center, Fort Sam Houston, Texas, USA
  1. Correspondence to Dr Inmaculada del Rincón, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA; delrincon{at}uthscsa.edu
  • Received 12 December 2013
  • Revised 19 April 2014
  • Accepted 1 May 2014
  • Published Online First 20 May 2014

Abstract

Objective To estimate atherosclerosis progression and identify influencing factors in rheumatoid arthritis (RA).

Methods We used carotid ultrasound to measure intima-media thickness (IMT) in RA patients, and ascertained cardiovascular (CV) risk factors, inflammation markers and medications. A second ultrasound was performed approximately 3 years later. We calculated the progression rate by subtracting the baseline from the follow-up IMT, divided by the time between the two scans. We used logistic regression to identify baseline factors predictive of rapid progression. We tested for interactions of erythrocyte sedimentation rate (ESR) with CV risk factors and medication use.

Results Results were available for 487 RA patients. The mean (SD) common carotid IMT at baseline was 0.571 mm (0.151). After a mean of 2.8 years, the IMT increased by 0.050 mm (0.055), p≤0.001, a progression rate of 0.018 mm/year (95% CI 0.016 to 0.020). Baseline factors associated with rapid progression included the number of CV risk factors (OR 1.27 per risk factor, 95% CI 1.01 to 1.61), and the ESR (OR 1.12 per 10 mm/h, 95% CI 1.02 to 1.23). The ESR×CV risk factor and ESR×medication product terms were significant, suggesting these variables modify the association between the ESR and IMT progression.

Conclusions Systemic inflammation and CV risk factors were associated with rapid IMT progression. CV risk factors may modify the role of systemic inflammation in determining IMT progression over time. Methotrexate and antitumour necrosis factor agents may influence IMT progression by reducing the effect of the systemic inflammation on the IMT.