endothelial dysfunction in rheumatoid arthritis is improved by anti-tumor necrosis factor- treatment

Rheumatoid arthritis (RA) is associated with excess cardiovascular morbidity and mortality. TNFplays a pivotal role in causing both RA synovial damage and atherosclerosis, also by inducing endothelial dysfunction. The aim of the present study was to assess the occurrence of endothelial dysfunction and the effects of anti-TNF- antagonism on endothelial function in RA. Ten RA women with Disease Activity Score (DAS) 3.7 despite treatment with at least two disease-modifying antirheumatic drugs for 4 months underwent anti-TNF- treatment with infliximab or etanercept. Endothelium-dependent vasodilation was significantly lower than normal (3.8 3.7 % vs. 13.7 5.1, p < 0.05), thus demonstrating the presence of endothelial dysfunction in our RA patient population. Anti-TNFtreatment significantly improved flow-mediated vasodilation, which increased from baseline values of 3.8 3.7 % to 10.9 6.6 % (p <0.05) at day 1, to 13.4 5.4 % (p < 0.05) at week 1, to 12.7 5.3 % (p < 0.05) at week 2 and to 15.5 5.2 % at week 6 (p < 0.05). There was no significant difference between two anti-TNFtreatments regarding mean percentage increase of flow-mediated vasodilation during treatment. RA clinical improvement was demonstrated by a significant decrease in the DAS score (from 6.26 1.6 to 5.26 1.38, p < 0.05) associated to a marked decrease of acute phase reactants serum levels. The present study supports the hypothesis of the pivotal role for TNF- as a mediator of systemic and vascular wall inflammation in RA