Reumatologia. 2025 Nov 11;63(5):304-312. doi: 10.5114/reum/203546. eCollection 2025.
ABSTRACT
INTRODUCTION: Biologic treatments have demonstrated increasing benefits for cardiovascular health in patients with rheumatoid arthritis (RA), including reductions in myocardial infarction risk factors, atherosclerosis progression, and the incidence of heart failure. This study aimed to compare treatment options: one combination of tumor necrosis factor inhibitors (adalimumab, etanercept) with methotrexate (MTX) and second treatment with anti-interleukin-6 (tocilizumab) - to determine whether cardiovascular effects are driven primarily by disease activity reduction or through distinct effects based on the mechanism of action. Moreover, we aimed to assess the influence of treatment on heart structure.
MATERIAL AND METHODS: This study included 120 RA patients on various therapies (etanercept, adalimumab, tocilizumab, and MTX) and compared them to 22 healthy controls. All participants underwent echocardiographic assessment to measure left ventricle (LV) mass, LV mass index, and LV hypertrophy type. Resting electrocardiograms were also conducted.
RESULTS: All patients showed normal LV function (ejection fraction > 50%). Patients treated with MTX exhibited larger right ventricular (28.1 mm vs. 21.1 mm, p < 0.05) and left atrial (37.5 mm vs. 31.1 mm, p < 0.01) dimensions compared to those on adalimumab. Additionally, MTX-treated patients had a higher LV mass index (106.8 vs. 90.9, p < 0.05) and the highest incidence of LV hypertrophy (56%), predominantly of the concentric type. Electrocardiographic findings showed a prolonged PR interval in patients on tocilizumab, while those on etanercept displayed a shortened PR interval. Disease activity was significantly lower in biologic-treated patients than in those receiving MTX.
CONCLUSIONS: Biologics, irrespective of their specific mechanisms, significantly reduce disease activity, which positively influences LV mass and reduces the incidence of LV hypertrophy. Additionally, biologics do not adversely affect cardiac electrical function.
PMID:41347103 | PMC:PMC12673476 | DOI:10.5114/reum/203546