Abstract 4964: Tnf-αAntagonists Improve Arterial Stiffness in Patients With Inflammatory Arthropathies: Results From a One Year Controlled Study
Introduction: The chronic inflammatory state of rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA) contributes to the accelerated atherosclerosis associated with these diseases.
Hypothesis: We assessed the hypothesis that one year treatment with TNF-α antagonists would improve arterial stiffness in patients with RA, AS and PsA.
Methods: A total of 52 patients with RA, AS or PsA and clinical indication for anti-TNF-α therapy were included. 36 patients started with anti-TNF-α therapy and were compared with a non-treatment group of 16 patients. Aortic pulse wave velocity (aPWV) and augmentation index (AIx) were measured at baseline and after one year (Sphygmocor). Each visit also included blood samples and assessment of disease activity.
Results: Values are given as mean± SD. Age of the patients in the treatment/control group was 46.2±12.2/49.0±14.1 years (p=0.21), 42.9/50.0 % (p=0.63) were females and disease duration was 11.0±9.6/11.6±10.1 years (p=0.56). Patients who started anti-TNF-α therapy had a significant decrease in aPWV (−0.53±0.13 m/s) whereas the patients in the control group had no change (+0.08±0.10 m/s, p=0.001 for between groups changes). Between groups differences for AIx were not observed (change 0.1±6.1 % and 0.2±5.7 %, p=0.95). There was no change in blood pressures, lipid levels or kidney function in any of the groups. A significant reduction in CRP and DAS28 (RA patients) was observed in the treatment group, but we did not find any significant bivariate correlations between the changes in aPWV and CRP (ρ=0.11, p=0.55) or between changes in aPWV and DAS28 in the RA group (ρ= −0.21, p=0.44).
Conclusion: The present study shows for the first time in a comparative design that long term anti-TNF-α therapy improves aPWV in patients with RA, AS and PsA. This finding supports the idea that atherosclerosis is partly driven by inflammation, and that this process is amenable to pharmacologic intervention.