FRI0072 The impact of anti-tnf-therapy on endothelial function in patients with rheumatoid arthritis, psoriatic arthritis or ankylosing spondylitis
Authors: K. Heinz, P. Oelzner, T. Eidner, K. Goetze, A. Saemann, G. Wolf, T. Neumann
Journal: Annals of the Rheumatic Diseases (2018)

<h3>Background</h3> Increased mortality in chronic rheumatic diseases is mostly attributed to cardiovascular events (CVE). Assessment of endothelial dysfunction can help to identify patients at risk for major CVE. Studies have shown that the underlying endothelial dysfunction in rheumatoid arthritis is closely associated with inflammation. Only limited information is available whether the blockade of TNFα can restore endothelial function. <h3>Objectives</h3> To investigate parameters of endothelial function bevor and after initiation of immunosuppressive therapie (anti-TNF-therapy or methotrexate) in patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA) or ankylosing spondylitis in an open-label, prospective study. <h3>Methods</h3> Patients with active RA, PsA or SpA were eligible for inclusion with active disease and when new treatment with sDMARD (methotrexate) or bDMARD (anti-TNF-therapy) was started. Study visits were performed at baseline, at 3 and at 12 months. Clinical disease activity and inflammation marker were obtained. Systemic Coronary Risc Evaluation (SCORE) and measurement of intima media thickness (IMT) were performed to assess baseline cardiovascular (CV) risk. Endothelial function was measured as arterial dilatation (artFID), arterial constriction (artFIC) and venous dilatation (venFID) in response to flicker light by dynamic vessel analysis (DVA; IMEDOS) and by peripheral arterial tonometry (EndoPAT) as reactive hyperemia index (RHI). For the primary endpoint, we analysed the endothelial function before and during treatment (month 12). Secondary endpoints were ACR20/50 response for RA and PsA and ASAS20 response for SpA. A comparison was made for changes in endothelial function in responder and non-responder to immunosuppressive treatment. <h3>Results</h3> 62 patients (37 RA, 13 PsA, 14 SpA) were included (mean age 51.3±14.9 years, 46.8% females). The mean ten-year risk of fatal cardiovascular disease (SCORE) was estimated with 2.2% (95%CI: 1.5–3.0). Mean IMT was 0.59±0.13 mm. Treatment was initiated with etanercept (n=21), certolizumab (n=10), infliximab (n=2), adalimumab (n=13), golimumab (n=4) or methotrexat (n=12). Response to treatment after 3 (n=57) and 12 months (n=32) measured by ACR20/50 (RA and PsA) and ASAS20 (SpA) was found in 33.3/16.7% and 57.2% (month 3) and 29.2/20.8% and 50.0% (month 12). ArtFID increased (3.1%±2.8% to 4.0±3.2%; p&lt;0.05), while artFIC and venFID remained unchanged (−0.3±1.6% to −0.2±2.1%; p=0.613, 3.7±3.0% to 3.9%±2.2%; p=0.383). RHI did not change (1.9%±0.5% to 1.8±0.5%; p=0.166). There were no differences in changes of endothelial function between responder and non-responder to immunosuppressive therapy or between anti-TNF-therapy and methotrexate. <h3>Conclusions</h3> Our data indicate, that patients with active RA, PsA or SpA are at risk for cardiovascular events. Immunosuppressive treatment can improve endothelial function at retinal arteries but has no effect on reactive hyperemia index at peripheral arteries. The effect of immunosuppressive treatment on parameters of endothelial function was not different in responders or non-responders and did not depend on whether the patients were treated with anti-TNF-therapy or methotrexate. <h3>Acknowledgements</h3> The study was funded be a grant from Pfizer Pharma GmbH (WS 1541087). <h3>Disclosure of Interest</h3> None declared