Open Access Open Badges Research article

Progression of coronary artery atherosclerosis in rheumatoid arthritis: comparison with participants from the Multi-Ethnic Study of Atherosclerosis

Cecilia P Chung18, Jon T Giles2, Richard A Kronmal4, Wendy S Post35, Allan C Gelber15, Michelle Petri1, Moyses Szklo5, Robert Detrano6, Matthew J Budoff7, Roger S Blumenthal3, Pamela Ouyang3, David Bush3 and Joan M Bathon2*

Author Affiliations

1 Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA

2 Division of Rheumatology, Columbia University, New York, NY, USA

3 Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA

4 Department of Biostatistics, University of Washington, Seattle, WA, USA

5 Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA

6 Department of Radiological Sciences, University of California at Irvine, Irvine, CA, USA

7 Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA, USA

8 Vanderbilt University School of Medicine, Nashville, USA

For all author emails, please log on.

Arthritis Research & Therapy 2013, 15:R134  doi:10.1186/ar4314

Published: 25 September 2013



In cross-sectional studies, patients with rheumatoid arthritis (RA) have higher coronary artery calcium (CAC) than controls. However, their rate of progression of CAC and the predictors of CAC progression have heretofore remained unknown.


Incidence and progression of CAC were compared in 155 patients with RA and 835 control participants. The association of demographic characteristics, traditional cardiovascular risk factors, RA disease characteristics and selected inflammatory markers with incidence and progression of CAC were evaluated.


The incidence rate of newly detected CAC was 8.2/100 person-years in RA and 7.3/100 person-years in non-RA control subjects [IRR 1.1 (0.7-1.8)]. RA patients who developed newly detectable CAC were older (59±7 vs. 55±6 years old, p=0.03), had higher triglyceride levels (137±86 vs. 97±60 mg/dL, p=0.03), and higher systolic blood pressure (129±17 vs. 117±15 mm Hg, p=0.01) compared to those who did not develop incident CAC. Differences in blood pressure and triglyceride levels remained significant after adjustment for age (p<=0.05). RA patients with any CAC at baseline had a median rate of yearly progression of 21 (7–62) compared to 21 (5–70) Agatston units in controls. No statistical differences between RA progressors and RA non-progressors were observed for inflammatory markers or for RA disease characteristics.


The incidence and progression of CAC did not differ between RA and non-RA participants. In patients with RA, incident CAC was associated with older age, higher triglyceride levels, and higher blood pressure, but not with inflammatory markers or RA disease characteristics.