Reduced arterial elasticity in rheumatoid arthritis and the relationship to vascular disease risk factors and inflammation

• Published in: Arthritis and rheumatism 2003-01, Vol.48 (1), p.81-89
• Main Authors: Wong, Melinda, Toh, Ling, Wilson, Andrew, Rowley, Kevin, Karschimkus, Connie, Prior, David, Romas, Evange, Clemens, Laurence, Dragicevic, George, Harianto, Harry, Wicks, Ian, McColl, Geoff, Best, James, Jenkins, Alicia
• Format: Article
• Language: English
• Subjects: Aged; Arthritis, Rheumatoid - epidemiology; Arthritis, Rheumatoid - immunology; Arthritis, Rheumatoid - pathology; Biological and medical sciences; Biomarkers; Cardiology. Vascular system; Coronary Artery Disease - epidemiology; Coronary Artery Disease - immunology; Coronary Artery Disease - pathology; Coronary heart disease; Cross-Sectional Studies; Diseases of the osteoarticular system; Elasticity; Female; Heart; Humans; Inflammatory joint diseases; Male; Medical sciences; Middle Aged; Risk Factors; Vascular Resistance; Vasculitis - epidemiology; Vasculitis - immunology; Vasculitis - pathology
• ISSN: 0004-3591; 1529-0131
• DOI: 10.1002/art.10748

Objective Rheumatoid arthritis (RA) is associated with increased rates of cardiovascular disease. Reduced small artery elasticity (SAE) and large artery elasticity (LAE) and increased systemic vascular resistance (SVR) have been found in other high‐risk groups. In the present study, we sought to determine whether arterial elasticity was reduced and SVR was increased in RA patients compared with controls matched for coronary artery disease (CAD) status, and to relate the results to vascular disease risk factors, including measures of inflammation. Methods Arterial elasticity was assessed by pulse wave analysis in RA patients with (n = 15) and without (n = 38) CAD, and in controls matched 1:1 for age, sex, and CAD status. Vascular risk factors, including high‐sensitivity C‐reactive protein (hsCRP), soluble vascular cell adhesion molecule 1 (sVCAM‐1), and serum amyloid A (SAA) levels, were assessed. Results SAE and LAE were significantly lower and SVR was significantly higher in RA patients than in controls. RA patients also had higher levels of hsCRP, SAA, and sVCAM‐1. SAE and LAE values were inversely correlated with markers of inflammation. Associations of SAE and LAE with RA were independent of conventional risk factors, but were dependent on markers of inflammation. Conclusion Vascular function is abnormal in RA, with reduced SAE and LAE and increased SVR relative to controls. Arterial elasticity is inversely associated with measures of inflammation. These measures may be clinically useful in the detection and monitoring of vascular disease in RA.