The incidence of cardiovascular disease (CVD) is increased in RA. This study was designed to evaluate whether a reduction in disease activity influences early markers of CVD.
In a prospective longitudinal study, 58 newly diagnosed RA patients and 58 age- and sex-matched healthy controls (HCs) were included. Endothelial dysfunction was measured by small artery elasticity (SAE) and endothelial cell activation was assessed by measuring soluble vascular cellular activation molecule 1(sVCAM-1) and von Willebrand factor (vWF). Advanced glycation end products (AGEs) were quantified by skin autofluorescence. After 1 year, measurements were repeated in all RA patients.
At entry, SAE was decreased in RA vs HCs [median 3.4 ml/mmHg100 (range 1.2-9.0) vs 6.1 (range 5.0-15.3), P < 0.0001] and sVCAM-1 and vWF were increased: 391 ng/ml (range 256-680) vs 341 (range 223-691) (P = 0.0015) and 120 ng/ml (range 26.5-342) vs 99 (range 22-298) (P = 0.02), respectively. SAE was inversely correlated with the 28-joint DAS (DAS28; r = -0.31, P = 0.016). AGEs were increased by 2.55 arbitrary units (range 1.29-4.65) vs 2.12 (range 1.32-3.82) in HCs (P = 0.003). In multivariate analysis, the presence of RA, age and systolic blood pressure were independently and inversely related to SAE. After 1 year, SAE had significantly improved in RA, from 3.4 (range 1.2-9.0) to 3.8 (range 1.5-10.3) (P = 0.03).
Endothelial dysfunction is present in newly diagnosed RA patients, independently of traditional risk factors and is inversely correlated with disease activity. By reducing disease activity, endothelial dysfunction improves, although not to normal values. Also, a reduction in disease activity targeting traditional risk factors remains important in preventing CVD in RA.