The findings led the team to believe a focus on treatment strategy, rather than disease activity, is more indicative of aortic distensibility improvement.
A first-time, randomized, controlled longitudinal study has found that vascular function abnormalities in treatment-naiive rheumatoid arthritis (RA) patients could be reversed with disease-modifying antirheumatic drugs (DMARDs).
In a new study presented this week at the American College of Rheumatology Meeting in Chicago, IL, investigators reported a found association between modified vascular function abnormalities and the introduction of DMARD therapy in patients with RA. The findings led the team to believe a focus on treatment strategy, rather than disease activity, is more indicative of aortic distensibility (AD) improvement.
The study, which serves as a follow-up to the team’s assessment of abnormal cardiac MRI (CMR)-determined aortic stiffness prevalence in early-form RA, also sought out whether tumor necrosis factor inhibitors (TNFi) is more beneficial for patients than first-line methotrexate (MXT) conventional synthetic DMARD (csDMARD) subsequent to TNFi.
Led by Maya Buch, PhD, a Professor of Rheumatology Honorary Consultant, Leeds Institute of Rheumatic and Muscoskeletal Medicine, University of Leeds, investigators recruited a subgroup of patients with early, DMARD-naiive RA without cardiovascular disease from a previous randomized controlled trial. Early RA disease was defined as symptoms being apparent for less than 1 year, and qualified patients were to have disease activity scores (DAS) of at least 3.2.
Among the patient population of 80, mean age was 49.4. The mean systolic blood pressure was 123, and 21% were current smokers. Median erythrocyte sedimentation rate and c-reactive protein level were 31 mm/hr and 8 mg/L, respectively. Mean patient DAS28 were 5.6.
Patients were randomized to either first-line etanercept (ETN) + MXT, or MTX/treat-to-target escalation to triple csDMARD. Patients in the latter group were switched to ETN+MTX at week 24 if they had failed to achieve clinical remission by then. Investigators stopped ETN at week 48, with standard of care therapy maintaining in patients through week 96.
At the end of analysis, investigators reported a significant mean AD reduction from baseline to year 1 (3.59 vs 2.99; P < .01), which was maintained in the second year (3.55 vs 2.99; P = .04). When comparing groups 1 and 2, all responders versus non-responders, and group 1 responders versus non-responders, investigators reported there was no significant numerical difference in change at year 1.
In response to the lacking absence of disease activity effect, investigators conducted a correlation analyses between AUC disease activity and AD at year 1 in the combined groups—which also did not identify an association. A planned exploratory comparison of group 1 ETN responders and group 2 responders not exposed to ETN suggested a 16% difference (P = .30).
Buch and her team concluded that DMARD therapy has significant effect on vascular function abnormalities when introduced to the treatment regimen of patients with early RA.
“Treatment strategy rather than disease activity appeared to influence AD change; if confirmed in a larger trial this would suggest ETN+MTX confers a greater benefit over standard initial MTX/csDMARD,” investigators wrote.