Background A growing body of evidence supports that patients with rheumatoid arthritis (RA) have an increased risk of cardiovascular diseases (CVDs). Early detection of vascular lesions in the preclinical phase would be of great benefit for CVD prevention and its prognosis. Several non-invasive methods have been developed and used for early detection of vascular changes in patients with RA.
Objectives The aim of this study was to investigate the carotid arterial stiffness in RA patients without cardiovascular risk factors using echo-tracking ultrasonography and its association with clinical parameters of RA.
Methods This study included 51 female RA patients and 44 female healthy controls without any known traditional CV risk factors. Arterial stiffness index β (β index) is assessed by echo-tracking ultrasonography in the common carotid artery (CCA) and the carotid intima-media thickness (cIMT) were also measured. RA activity was assessed by high sensitivity C-reactive protein (hsCRP), erythrocyte sedimentation rate (ESR) and disease activity score in 28 joints (DAS28). 25-hydroxyvitamin D (25(OH)D) and autoantibodies such as rheumatoid factor (RF) and anti-cyclic citrullinated peptide antibody (anti-CCP) were checked.
Results Compared with the control group, the RA group were significantly higher β index (9.371±2.927 vs 7.397±3.140, p=0.02). However, we did not find any differences in IMT between two groups. In the RA group, β index was significantly correlated with age (r =0.435, p=0.001), disease duration (r=0.373, p=0.007) and RF (r=0.412, p=0.003). Older age and longer disease duration were associated with increased β index in univariable regression analyses (Table 1). Multivariable regression analysis also revealed that the significant predictors of β index were age and disease duration after adjustment for confounding factors (Table 1).
Conclusions RA is associated with preclinical vascular changes, characterized by increased carotid β index values, which have been shown to be related to age and disease duration rather than autoantibodies or disease activity.
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Disclosure of Interest None declared