Assessment of Preclinical Atherosclerosis in Patients with Ankylosing Spondylitis

Objective. Epidemiological studies recently confirmed the increased risk of vascular morbidity and mortality during ankylosing spondylitis (AS). Increase of intima-media thickness (IMT) of the common carotid artery is a useful and noninvasive marker of preclinical atherosclerosis. The aim of our study was to compare IMT in patients with AS with matched controls and to determine risk factors of atherosclerosis related to AS. Methods. We performed a prospective study of 60 consecutive patients meeting modified New York criteria for AS, compared to 60 controls matched for age and sex. Disease-specific measures were determined. Measurement of IMT was performed by the same radiologist using the same machine and probe in right and left common carotid arteries, and the average of the 2 measurements was considered. Results. In total 48 male and 12 female patients were recruited, and 60 corresponding controls; mean age was 36 +/- 11 years. We found significantly increased IMT in the AS group (0.51 +/- 0.12 mm) compared with controls (0.39 +/- 0.09 mm; p = 0.001). After adjustment for confounding factors, increased IMT was still present (p = 0.003). Age at onset of AS (p = 0.001), Bath AS Disease Activity Index (p = 0.002), AS Disease Activity Score (ASDAS) erythrocyte sedimentation rate (ESR; p = 0.047), ASDAS C-reactive protein (CRP; p = 0.012), Bath AS Functional Index (p = 0.008), global spine visual analog scale for pain (p = 0.000), Schober index (p = 0.039), Bath AS Metrology Index (p = 0.028), modified Stoke Ankylosing Spondylitis Spine Score (p = 0.035), and high ESR (p = 0.001) and CRP (p = 0.000) were correlated with high IMT in patients with AS. Otherwise, status of arthritis (p = 0.442), enthesitis (p = 0.482), and HLA-B27 (p = 0.528) seemed to have no effect on IMT. Conclusion. AS is associated with an increased risk of atherosclerosis independent of traditional risk factors. Disease activity, functional and mobility limitations, structural damage, and inflammation are the most incriminated risk factors. (First Release Jan 15 2012; J Rheumatol 2012;39:322-6; doi:10.3899/jrheum.110792)