Sustained improvement of vascular endothelial function during anti‐TNFα treatment in rheumatoid arthritis patients

Abstract

Objectives: Vascular endothelial function and common carotid artery intima–medial thickness (CCA‐IMT) are well‐established surrogate markers for early atherosclerotic disease, which accounts for 30–40% of excess mortality in rheumatoid arthritis (RA) patients. Our aim was to investigate whether long‐term treatment with anti‐tumour necrosis factor (TNF)α agents can modulate endothelial function and CCA‐IMT.

Methods: Twelve patients with RA (mean age 54.8±15 years) on anti‐TNFα treatment (seven adalimumab, five infliximab) due to uncontrolled disease activity, with mean Disease Activity Score (DAS28) 5.7 (range 4.6–6.9) despite disease‐modifying anti‐rheumatic drugs (DMARDs), were studied prospectively. Patients were assessed at baseline and after 3 and 18 months for endothelial‐dependent vasodilatation, assessed by flow‐mediated vasodilatation (FMD), endothelial‐independent vasodilatation and CCA‐IMT. RA disease activity and response to therapy were assessed by the DAS28 index.

Results: After 18 months of treatment, 67% of the patients were responders according to European League Against Rheumatism (EULAR) response criteria. Anti‐TNFα treatment improved FMD (from 7±4.3% to 11.1±3.8%, p = 0.026) whereas CCA‐IMT did not change significantly [from 0.67 (0.4–1) to 0.68 (0.39–1.2) mm; mean change 0.01 (−0.06 to 0.08) mm]. Endothelial‐independent vasodilatation remained stable (20.4±7.3% to 22.9±6.5%, p = 0.4).

Conclusions: In this small cohort of patients with RA and no clinically overt cardiovascular disease (CVD), after 18 months of treatment with anti‐TNFα agents, endothelial function improved significantly while CCA‐IMT remained stable. Longitudinal studies using more patients are needed to determine the clinical significance of these findings in relation to the risk of atherosclerosis.