Background It is known that some factors of the fibrinolytic pathway, such as fibrinogen, D-dimer, have been associated with an increased risk of coronary events and stroke. Many publications demonstrated an increase of early development of atherosclerosis in patients with rheumatic diseases. The data have been focused on carotid arterial atherosclerotic alterations, such as intima-media thickness and plaque formation.

Objectives The aim of our study was to assess the procoagulation state and its assotiation with inflammation in female patients with rheumatoid arthritis (RA) and early atherosclerosis.

Methods The study included 37 female patients with rheumatoid arthritis (ACR, 1987), mean age 45,0 (33,0; 51,0) years old, disease duration 9,0 (3,0; 14,0) years, disease activity (DAS28=5,37 (4,69; 5,86) points. Twenty-eight healthy women of the same age formed the control group.

The levels of platelet cells (PLT), activated partial thromboplastin time (APTP), fibrinogen were determined with coagulation analyser, while D-Dimer, LA, IgG/IgM antibodies to cardiolipin (aCL), β2-glycoprotein-1 (aβ2-GP1), high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), were determined with ELISA.

The presence of carotid atherosclerotic alterations was revealed ultrasonographically according to standard procedures.

Results The patients with RA had significantly higher levels of fibrinogen, D-Dimer, LA, aCL IgG, aβ2-GP1 IgG/IgM, hs-CRP, IL-6 and TNF-α than in the control group (Table 1).

The atherosclerotic alterations were found in 48,65% patients with RA, 28,57% in the control group.

We reveled positive correlation between PLT and DAS28 (r=0,626, p=0,005), aCL IgM (r=0,513, p=0,029), D-Dimer and hs-CRP (r=0,747, p=0,003), DAS28 (r=0,819, p=0,0006) in RA patients with carotid atherosclerosis, that reflects association between prothrombotic and inflammatory markers.

Conclusions We demonstrated the presence of prothrombotic state in patients with RA, who had higher levels of inflammatory markers too. Thus, we suggest that inflammation can influence the prothrombotic state in patients with RA, induce endothelial dysfunction and, as a result, early development of atherosclerosis.

Disclosure of Interest None declared