AB0210 Disease modifying anti-rheumatic drugs slow progression of intima media thickness-preliminary report of a prospective study

Background Atherosclerosis is accelerated in rheumatoid arthritis (RA). Cardiovascular disease has become a major cause of morbidity and mortality in RA. Carotid intima media thickness (CIMT) is considered as a noninvasive surrogate marker of early atherosclerosis. Studies in RA showed an accelerated progression of IMT and plaques in carotid arteries [1]. Recently, we presented the results of a retrospective study showing correlation between continuous treatment with disease modifying anti-rheumatic drugs (DMARDs) and slower progression of IMT in rheumatoid arthritis (RA) [2]. We launched a prospective study to confirm this findings. Here we present preliminary results of this study. Objectives To assess the influence of disease modifying anti-rheumatic drugs (DMARDs) on IMT in RA. Methods 40 RA patients and 20 age- and sex-matched healthy controls were included in the study. The mean follow-up period was 36 months in RA patients and 35 months in controls. IMT of the common carotid artery (CIMT) was determined by B-mode ultrasound imaging twice- during the inclusion visit and after follow-up period. Laboratory tests were performed in all patients and controls. DAS28 was calculated in all RA patients. Results All RA patients were treated continuously with DMARDs: 18 patients with methotrexate in monotherapy, 7 patients with methotrexate plus anti-TNFα, 6 patients with metohotrexate plus rituximab, 6 patients with methotrexate plus leflunomide, 1 patient with anti-TNFα in monotherapy and 2 patients with leflunomide in monotherapy. Mean DAS28 in RA patients at the last visit was 3.57 (13 patients had complete remission, 15 patients had low activity disease- LAD, 8 patients had medium activity disease- MAD and 4 patients had high activity disease- HAD). No significant differences in classical atherosclerosis risk factors between study and control groups were found. Mean increase of CIMT in RA patients was similar to control group (27.7µm per year vs 30.7µm per year, p=0.89). We did not find significant differences in CIMT increase between patients with remission/LAD and patients with MAD/HAD. Conclusions Preliminary results of our prospective study confirm that continuous treatment with DMARDs slow the progression of CIMT. Interestingly, we did not find significant differences in CIMT increase between patients with remission/LAD and patients with MAD/HAD. It may suggest that the beneficial effect of DMARDs on the progression of atherosclerosis is present despi