Endothelial function in rheumatoid arthritis.

Abstract

Rheumatoid arthritis (RA) patients are at higher risk of accelerated atherosclerosis. To assess endothelial dysfunction in RA to find a possible mechanistic pathway that will explain the clinical phenomenon. A prospective study recruited 44 RA patients with an active long standing (>12 months) disease. All underwent a detailed assessment of disease activity. To estimate the endothelial function the brachial artery method was performed, measuring flow mediated diameter percent (FMD%) change. Clustering analyses (hierarchical and k-means) were performed. Patients were compared to healthy subjects. Forty four RA patients (54.42 ± 11.14 years, females (72.7%)) with co-morbidities (70.5%), not taking tumor necrosis factor-blockers or disease modifying anti rheumatic drugs (63.6%). Only 6 (13.6%) had a normal endothelial function. Hierarchical and k-means clustering techniques showed statistically significant differences among the three clusters concerning disease activity score-28 (DAS-28)- erythrocyte sedimentation rate (ESR) (P = 0.000), DAS-28- C-reactive protein (CRP; P = 0.001), clinical disease activity index (P = 0.002), simplified disease activity index (P = 0.001), ESR (P = 0.000), (CRP) (P = 0.003) and FMD% (P = 0.009). The group with the highest FMD% values exhibited the lowest clinical scores and laboratory parameters. Patients with the lowest FMD% values co-clustered with subjects with positive but low FMD% changes and elevated clinical and laboratory parameters. Our study confirmed the feasibility of exploiting endothelial function in clinical practice as an early predictor of atherosclerosis in RA patients.