Background: Rheumatoid arthritis (RA) patients are at higher risk of accelerated atherosclerosis. Aims: To assess endothelial dysfunction in RA to find a possiblemechanistic pathway that will explain the clinical phenomenon. Methods: 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. Results: Forty four RA patients (54.42611.14 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. Conclusions: Our study confirmed the feasibility of exploiting endothelial function in clinical practice as an early predictor of atherosclerosis in RA patients. [ABSTRACT FROM AUTHOR]