RT Journal Article
SR Electronic
T1 Subclinical coronary artery calcification and relationship to disease duration in women with rheumatoid arthritis.
JF The Journal of Rheumatology
JO J Rheumatol
FD The Journal of Rheumatology
SP 61
OP 69
VO 35
IS 1
A1 Amy H Kao
A1 Shanthi Krishnaswami
A1 Amylynn Cunningham
A1 Daniel Edmundowicz
A1 Penelope A Morel
A1 Lewis H Kuller
A1 Mary Chester M Wasko
YR 2008
UL http://www.jrheum.org/content/35/1/61.abstract
AB OBJECTIVE: To examine the association between disease duration of rheumatoid arthritis (RA) and the presence and extent of coronary artery calcification (CAC) in women with RA. METHODS: In this cross-sectional study, 185 women with RA duration of at least 2 years and no clinical cardiovascular disease completed electron-beam tomography (EBT) scans and risk factor assessment. Multivariable logistic regression was used to associate RA duration quartiles with subclinical CAC and extent of CAC. RESULTS: Age was similar across the quartiles of RA duration. Patients with RA > 23 years had significant increased odds (unadjusted OR 2.60, 95% CI 1.21 5.53) of having more extensive CAC compared to the referent group, those with RA for 2 7 years. This association remained significant after adjustment for traditional coronary heart disease (CHD) risk factors and RA-related covariates. Patients with intermediate RA duration (8 13 yrs) were more likely to have presence of any CAC (OR 3.03, 95% CI 1.06 8.66) compared to the referent group only after adjusting for age, race, and traditional CHD risk factors. Patients with longer RA duration were more likely to have cumulative joint damage, manifested as prior joint surgery, joint deformity, and greater functional disability. Lower body mass index also was associated with longer RA duration. CONCLUSION: Patients with longstanding RA have more extensive subclinical atherosclerosis or CAC compared to patients of the same age, independent of other CHD risk factors. RA duration may be a surrogate for factors related to the disease process or its treatment that may promote coronary atherogenesis.