Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.


Longitudinal Predictors of Progression of Subclinical Carotid Atherosclerosis in Rheumatoid Arthritis.

Giles3,  Jon T., Post5,  Wendy, Blumenthal5,  Roger S., Polak6,  Joseph, Petri1,  Michelle A., Gelber2,  Allan C., Szklo5,  Moyses

Timonium, MD
Baltimore, MD
Johns Hopkins Univ, Baltimore, MD
Johns Hopkins University, Baltimore, MD
Johns Hopkins University
Tufts-New England Medical Center

Background:

Coronary and extra-coronary atherosclerosis are increased in rheumatoid arthritis (RA) relative to controls; however, few longitudinal studies have explored predictors of change in atherosclerosis in RA patients.

Methods:

Men and women with RA enrolled in ESCAPE RA, a cohort study of subclinical cardiovascular (CV) disease in RA, underwent bilateral B-mode ultrasonography of the common (CCA) and internal (ICA) carotid arteries at the first and third study visits, separated by an average of 3.2±0.3 years. Multivariate linear or Poisson regression, as appropriate to the outcome, were used to explore the associations of baseline and cumulative demographic, lifestyle, and RA disease and treatment characteristics with the average yearly change in maximal intima-medial thickness (IMT) of the CCA and ICA, and incident or progressive carotid plaque (defined as newly identified plaque or progression in plaque stenosis). Baseline scans were reanalyzed concurrent with follow-up scans, to control for interpretive drift.

Results:

A total of 158 RA patients [36% male; mean baseline age=59±8 years; median baseline RA duration=8.5 years; median baseline DAS28=3.6] underwent carotid scanning at both time points. CCA-IMT increased over time in 82% of patients (median yearly increase=16 mm; p<0.001) and ICA-IMT increased in 70% of patients (median yearly increase=25 mm; p<0.001). After adjusting for demographics, CV risk factors, and baseline IMT, baseline TNF inhibitor use was associated with a 37% lower rate of CCA-IMT progression vs. non-users (14 vs. 22 mm/year; p=0.026: Figure, Panel A). The adjusted average yearly change in CCA-IMT was significantly higher for patients with earlier RA compared with those with longer duration disease (Figure, Panel B).

Adjusted for age, gender, ethnicity, hypertension, diabetes, hyperlipidemia, exercise, smoking, body surface area, baseline maximum CCA-IMT, RA duration (where appropriate), and TNF inhibitor use (where appropriate).

Figure. Adjusted yearly rate of change in CCA-IMT according to (A) baseline TNF inhibitor use and (B) RA duration.

For ICA-IMT, cumulative prednisone exposure was the only RA feature associated with progression [1.2 mm per year per gram increase in cumulative dose (95% CI 0.1, 2.4)] after adjustment. This rate was significantly lower in patients prescribed statins at baseline. Any plaque was identified in 104 patients (68%), with 13 of these (12%) demonstrating new or progressive plaque during follow-up. After demographic and CV risk factor adjustment, higher average swollen joint count (SJC) and higher average CRP were significantly and independently associated with incident or progressive plaque. Cumulative CRP and SJC were both more strongly associated with plaque progression than cross-sectional levels obtained at the time of scanning. Other RA disease and treatment characteristics were not associated with plaque progression.

Conclusions:

These prospective data provide evidence for systemic inflammation and RA disease activity as a contributor to progression of atherosclerosis in RA patients. Further, they suggest that atherosclerosis progression in RA may be modified favorably by TNF inhibitors and detrimentally by glucocorticoids.

To cite this abstract, please use the following information:
Giles, Jon T., Post, Wendy, Blumenthal, Roger S., Polak, Joseph, Petri, Michelle A., Gelber, Allan C., et al; Longitudinal Predictors of Progression of Subclinical Carotid Atherosclerosis in Rheumatoid Arthritis. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :2162
DOI: 10.1002/art.29926

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