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Abstract Number: 1267

Inflammatory Burden Predicts Progression of Carotid Plaque in Rheumatoid Arthritis: A 24-Month Longitudinal Analysis

Churl Hyun Im1, Na Ri Kim1, Jong Wan Kang1, Young Ji Kim1, Kyung Hye Kim1, Eon Jeong Nam1 and Young Mo Kang2, 1Internal Medicine (Rheumatology), Kyungpook National University School of Medicine, Daegu, South Korea, 2Department of Internal Medicine (Rheumatology), Kyungpook National University School of Medicine, Daegu, South Korea

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: Atherosclerosis, Cardiovascular disease, Inflammation, longitudinal studies and rheumatoid arthritis (RA)

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Session Information

Title: Rheumatoid Arthritis - Clinical Aspects II: Clinical Features & Comorbidity/Cardiovascular Disease

Session Type: Abstract Submissions (ACR)

Background/Purpose: Carotid atherosclerosis, which is associated with the increased risk of cardiovascular (CV) disease, is increased in rheumatoid arthritis (RA) patients. In our previous study, an inflammatory burden, measured by area under the curve of erythrocyte sedimentation rate (ESR-AUC), increases the risk of carotid plaque formation in RA, independently with traditional CV risk factors. The aim of this study was to evaluate the role of inflammatory burden in the progression of carotid plaques during 2 years of follow up in a RA patient cohort.

Methods: We measured the intima-media thickness (IMT) and plaques using carotid artery ultrasound at baseline and after 2 years in 279 RA patients, who were enrolled in the Kyungpook National University Hospital Atherosclerosis Risk in Rheumatoid Arthritis (KARRA) cohort. Surveys for traditional CV risk factors were performed using the same questionnaire. Clinical and laboratory variables relevant to RA activity were obtained. To assess inflammatory burden, ESR-AUC during 2 years of follow up (ESR-AUC2), 5 years before baseline enrollment (ESR-AUC5, 140 females, ≥ 40 years old), and summation of these two periods (ESR-AUC7) were calculated.

Results: The study population included 227 females and 52 males RA patients. Mean and maximal common carotid IMT was increased during 2 years of follow up (0.799 ± 0.173 vs. 0.809 ± 0.173 mm; P = 0.010 and 0.918 ± 0.214 vs. 0.936 ± 0.210 mm; P = 0.002, respectively). Frequency and number of carotid plaque were also increased from 34.7% to 46.4% (P < 0.001) and from 0.7 ± 1.3 to 1.0 ± 1.7 (P < 0.001), respectively. Plaque presence at 2 years of follow up was associated with tender joint count (TJC), swollen joint count (SJC), disease activity score (DAS) 28, and ESR level at baseline, after the adjustment with age and gender. ESR-AUC2, ESR-AUC5, and ESR-AUC7 were significantly associated plaque at 2 years (P = 0.035, P = 0.018, and P = 0.025 respectively, after the adjustment with age and gender). After multivariate logistic regression analysis, the factors found to be significantly associated with plaque at 2 years were ESR-AUC5 (P = 0.015) and TJC28 at baseline (P = 0.048). In the second step analysis of 71 patients with newly developed plaque at 2 years (33 patients with no plaque at baseline and 38 patients with increased number of plaques from baseline), the factor significantly associated with plaque progression was ESR-AUC5 (P= 0.038) in multivariate logistic regression analysis.

Conclusion: Our findings indicate that residual inflammatory burden increases the risk of carotid plaque progression during 2 years of follow up in RA.


Disclosure:

C. H. Im,
None;

N. R. Kim,
None;

J. W. Kang,
None;

Y. J. Kim,
None;

K. H. Kim,
None;

E. J. Nam,
None;

Y. M. Kang,
None.

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