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

被引:38
作者
Plein, Sven [1 ]
Erhayiem, Bara [1 ]
Fent, Graham [1 ]
Horton, Sarah [2 ]
Dumitru, Raluca Bianca [3 ]
Andrews, Jacqueline [3 ]
Greenwood, John P. [1 ]
Emery, Paul [3 ,4 ]
Hensor, Elizabeth M. A. [3 ,4 ]
Baxter, Paul [1 ]
Pavitt, Sue [5 ]
Buch, Maya H. [3 ,4 ,6 ]
机构
[1] Univ Leeds, Leeds Inst Cardiovasc & Metab Med, Leeds, W Yorkshire, England
[2] Lancashire & South Cumbria NHS Fdn Trust, Cent Lancashire Moving Well Serv, Preston, Lancs, England
[3] Univ Leeds, Leeds Inst Rheumat & Musculoskeletal Med, Leeds, W Yorkshire, England
[4] Leeds Teaching Hosp NHS Trust, NIHR Leeds Biomed Res Ctr, Leeds, W Yorkshire, England
[5] Univ Leeds, Dent Translat & Clin Res Unit, Leeds, W Yorkshire, England
[6] Univ Manchester, Fac Biol Med & Hlth, Ctr Musculoskeletal Res, Div Musculoskeletal & Dermatol Sci, Manchester M13 9PL, Lancs, England
关键词
LEFT-VENTRICULAR FUNCTION; MYOCARDIAL FIBROSIS; RISK; INFLAMMATION; METAANALYSIS; EVENTS;
D O I
10.1136/annrheumdis-2020-217653
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 (3.0x10(-3) mm Hg-1 (2.7-3.3) vs 4.4x10(-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 (3.0x10(-3) mm Hg-1 (2.7-3.4) to 3.6x10(-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.
引用
收藏
页码:1414 / 1422
页数:9
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