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Cardiovascular effects of biological versus conventional synthetic disease-modifying antirheumatic drug therapy in treatment-naïve, early rheumatoid arthritis. | LitMetric

AI Article Synopsis

  • - The study aimed to assess whether cardiovascular disease (CVD) in patients with early rheumatoid arthritis (ERA) could be improved with disease-modifying antirheumatic drugs (DMARDs), comparing the combination of etanercept (ETN) and methotrexate (MTX) against an MTX-only strategy.
  • - In the trial with 81 ERA patients, baseline measurements indicated significantly lower aortic distensibility and left ventricular mass, as well as increased myocardial extracellular volume compared to matched controls, with improvements in aortic distensibility observed over the first year.
  • - Findings suggest that the use of DMARD therapy, while showing vascular and myocardial improvements in ERA patients, did not depend on the specific DMARD

Article Abstract

Objectives: To determine whether patients with early rheumatoid arthritis (ERA) have cardiovascular disease (CVD) that is modifiable with disease-modifying antirheumatic drug (DMARD) therapy, comparing first-line etanercept (ETN) + methotrexate (MTX) with MTX strategy.

Methods: Patients from a phase IV ERA trial randomised to ETN+MTX or MTX strategy±month 6 escalation to ETN+MTX, and with no CVD and maximum one traditional risk factor underwent cardiovascular magnetic resonance (CMR) at baseline, years 1 and 2. Thirty matched controls underwent CMR. Primary outcome measure was aortic distensibility (AD) between controls and ERA, and baseline to year 1 AD change in ERA. Secondary analyses between and within ERA groups performed. Additional outcome measures included left ventricular (LV) mass and myocardial extracellular volume (ECV).

Results: Eighty-one patients recruited. In ERA versus controls, respectively, baseline (geometric mean, 95% CI) AD was significantly lower (3.0×10 mm Hg (2.7-3.3) vs 4.4×10 mm Hg (3.7-5.2), p<0.001); LV mass significantly lower (78.2 g (74.0-82.7), n=81 vs 92.9 g (84.8-101.7), n=30, p<0.01); and ECV increased (27.1% (26.4-27.9), n=78 vs 24.9% (23.8-26.1), n=30, p<0.01). Across all patients, AD improved significantly from baseline to year 1 (3.0×10 mm Hg (2.7-3.4) to 3.6×10 mm Hg (3.1-4.1), respectively, p<0.01), maintained at year 2. The improvement in AD did not differ between the two treatment arms and disease activity state (Disease Activity Score with 28 joint count)-erythrocyte sedimentation rate-defined responders versus non-responders.

Conclusion: We report the first evidence of vascular and myocardial abnormalities in an ERA randomised controlled trial cohort and show improvement with DMARD therapy. The type of DMARD (first-line tumour necrosis factor-inhibitors or MTX) and clinical response to therapy did not affect CVD markers.

Trial Registration Number: ISRCTN: ISRCTN89222125; ClinicalTrials.gov: NCT01295151.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7569379PMC
http://dx.doi.org/10.1136/annrheumdis-2020-217653DOI Listing

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