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

Author

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.

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 (3.0×10-3 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.