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Relative contribution of cardiovascular risk factors and rheumatoid arthritis clinical manifestations to atherosclerosis

✍ Scribed by Inmaculada del Rincón; Gregory L. Freeman; Roy W. Haas; Daniel H. O'Leary; Agustín Escalante


Publisher
John Wiley and Sons
Year
2005
Tongue
English
Weight
130 KB
Volume
52
Category
Article
ISSN
0004-3591

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✦ Synopsis


Abstract

Objective

To estimate the contribution of cardiovascular (CV) risk factors and rheumatoid arthritis (RA) disease manifestations to atherosclerosis in RA.

Methods

We used high‐resolution carotid ultrasound to measure the carotid intima‐media thickness (IMT) and plaque in 631 RA patients. Using R^2^ measures from multivariable models, we estimated the contribution of demographic characteristics (age, sex, and ethnic group), CV risk factors (diabetes mellitus, hypercholesterolemia, cigarette smoking, hypertension, and body mass index, and RA manifestations (joint tenderness, swelling, and deformity, nodules, erythrocyte sedimentation rate [ESR], C‐reactive protein, rheumatoid factor, the HLA–DRB1 shared epitope, and cumulative glucocorticoid dose) to each of the outcomes. Estimates were obtained in the full sample, and within strata defined by age, sex, and ethnic group. We tested for interaction between CV risk factors and RA manifestations.

Results

The contribution of demographic factors, CV risk factors, and RA manifestations to IMT and plaque R^2^ varied depending on the patients' age stratum. Demographic features explained 11–16% of IMT variance, CV risk factors explained 4%–12%, and RA manifestations explained 1–6%. The greatest contribution of RA manifestations occurred in the youngest age group, while that of CV risk factors occurred in the older age groups. Results for carotid plaque were similar. There was a significant interaction between the number of CV risk factors present and the ESR, suggesting that the ESR's effect on IMT varied according to the number of CV risk factors.

Conclusion

Both established CV risk factors and manifestations of RA inflammation contribute significantly to carotid atherosclerosis in RA, and may modify one another's effects. These findings may have implications regarding the prevention of atherosclerosis in RA.


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