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SAT0122 Prediction of Coronary Artery Calcification and Association with Inflammation in Rheumatoid Arthritis: A Follow-Up Study
  1. B. Wahlin1,
  2. T. Meedt1,
  3. F. Jonsson2,
  4. K. Karp3,
  5. M. Henein2,
  6. S. Wållberg-Jonsson1
  1. 1Public Health and Clinical Medicine/Rheumatology
  2. 2Public Health and Clinical Medicine/Medicine
  3. 3Clinical Physiology, Umeå University, Umeå, Sweden

Abstract

Background We previously reported increased prevalence of atherosclerosis in patients with RA (1).

Objectives To evaluate (i) the relation between inflammatory markers, measures of atherosclerosis and potential biomarkers of atherosclerosis at baseline and the presence of coronary artery calcification (CAC) and (ii) the relation between current inflammation and CAC.

Methods Twenty-two RA patients (4m, 18f, mean age 65 years, RA-duration 30-36 years) from an original (baseline; n=39) ultrasound study of atherosclerosis (intima-media-thickness (IMT) and plaque) were included in this follow-up study 12 years after baseline. CAC was assessed by CT and quantified according to Agatston. At the same time, inflammatory markers (ESR, CRP, haptoglobin), clinical disease activity (joint counts, DAS28, HAQ, VAS-scales) and lipids (cholesterol, HDL, LDL, triglycerides) were measured. The effect on CAC of cytokines (IL-6, IL2sR), adhesion molecules (ICAM-1, sE-selectine), hemostatic factors (PAI-1, tPA-ag, vWF, fibrinogen, D-dimer, cardiolipin antibodies), circulating immune complexes and antibodies against modified LDL, all collected at baseline, was also evaluated. Statistical analysis of factors explaining presence of CAC was done by orthogonal projection to latent structures (OPLS) with repeated exclusion of variables without explanatory information.

Results Eight patients had no detectable CAC, 2 patients had CAC 1-10 and 12 had >10 (range 18-1700). The final OPLS model discriminated well between groups with low (0-10) and high CAC (>10), predicting 68% and explaining 88% of the variation. ROC analysis showed 89% sensitivity and 92% specificity distinguishing high CAC from low. The variables in the OPLS model are presented in the figure. Female sex and high level of HDL at baseline were associated to low CAC, but for all other variables in the model higher levels were associated to high CAC. Patients with high CAC significantly differed from those with low regarding ESR (24,3 vs 9,9 mm/h; p<0.01) and swollen joint count (2 vs 0; p<0,05).

Conclusions In patients with long term RA, CAC was predicted by markers of endothelial activation and traditional cardiovascular risk factors, but also current disease activity. These findings highlight the importance of inflammation in the process of atherosclerosis.

References

  1. Wallberg-jonsson S et al. Increased prevalence of atherosclerosis in patients with medium term rheumatoid arthritis. J Rheumatol. December 2001;28(12):2597–602.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.5907

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