abstract details

The summaries are free for public use. ARTHROS will continue to add and archive summaries of articles deemed relevant to ARTHROS by our Faculty.

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


Ann Rheum Dis. 2020 Aug 28;annrheumdis-2020-217653.doi: 10.1136/annrheumdis-2020-217653. Online ahead of print.

Sven Plein 1, Bara Erhayiem 1, Graham Fent 1, Sarah Horton 2, Raluca Bianca Dumitru 3, Jacqueline Andrews 3, John P Greenwood 1, Paul Emery 3 4

Author Information

1 Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, UK.

2 Central Lancashire Moving Well Service, Lancashire and South Cumbria NHS Foundation Trust, Lancashire, UK.

3 Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, UK.

4 NIHR Leeds Biomedical Research Centre, Leeds Teaching Hospitals NHS Trust, Leeds, UK.

5 Dental Translational and Clinical Research Unit, University of Leeds, Leeds, UK.

6 Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, UK maya.buch@manchester.ac.uk.

7 Centre for Musculoskeletal Research, Division of Musculoskeletal & Dermatological Sciences, Faculty of Biology, Medicine & Health, University of Manchester, Manchester, United Kingdom.


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 (3.0×10-3 mm Hg-1 (2.7-3.3) vs 4.4×10-3 mm Hg-1 (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 (3.0×10-3 mm Hg-1 (2.7-3.4) to 3.6×10-3 mm Hg-1 (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.