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Eastern Regional Meeting - 2008 Program & Abstracts

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Relation of Obstructive Coronary Atherosclerosis to Disease Activity in Rheumatoid Arthritis

C. Assal, J. Shirani, B. Martin, A. Armstrong, M. Diehl, D. Torretti, J. Blankenship, Cardiology, Geisinger Medical Center, Danville, PA
Purpose of Study: The high prevalence of coronary artery disease (CAD) among adults with rheumatoid arthritis (RA) is attributed to systemic inflammation. Little information is available regarding the correlation of the extent of CAD to clinical markers of RA disease activity. This study examines the relationship of the severity of angiographic CAD to clinical and biochemical markers of RA disease activity.

Methods Used: Between 2001 and 2006, 75 adults (age 66+10, % 47 women) with RA underwent coronary angiography. Obstructive CAD was defined as the presence of =70% stenosis in =1 major epicardial coronary artery. RA disease activity was determined by clinical (duration of disease, number of tender or swollen joints, pharmacotherapy) and laboratory (erythrocyte sedimentation rate, C-reactive protein) data.

Summary of Results: Overall, 46 patients (60%) had obstructive CAD. An inverse relationship was noted between the number of tender joints and the presence of obstructive CAD, such that those with more than 6 tender joints [n=26 (35%)] were less likely to have obstructive CAD (50% vs. 67%, p = 0.0086). No significant association was present between obstructive CAD and number of swollen joints, erythrocyte sedimentation rate, C-reactive protein, duration of RA, prednisone use, methotrexate therapy or American college of Rheumatology functional class. However, patients receiving anti-tumor necrosis factor (anti-TNF) therapy [n= 23 (31%)] were more likely to have obstructive CAD (80% vs. 42%, p = 0.025). This was despite older age of those not receiving anti-TNF therapy (68+10 vs. 63+9 years, p=0.03). Other risk factors had similar distribution in both groups. However, patients receiving anti-TNF therapy had more severe RA disease activity by clinical criteria.

Conclusions: In this small cohort, clinical markers of RA disease activity were not predictive of presence of obstructive CAD. The observed association between the use of biologic agents and the presence of obstructive CAD can be explained by more severe RA in those receiving anti-TNF therapy.

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