Biological use influences the impact of inflammation on risk of major adverse cardiovascular events in rheumatoid arthritis

Objectives: Chronic inflammation promotes cardiovascular risk in rheumatoid arthritis (RA). Biological disease-modifying antirheumatic drugs (bDMARDs) improve disease activity and cardiovascular disease outcomes. We explored whether bDMARDs influence the impact of disease activity and inflammatory m...

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Detalhes bibliográficos
Autores: Karpouzas, George Athanasios, Ormeseth, Sarah R., Van Riel, Piel Leonardus Cornelis Maria, González-Gay Mantecón, Miguel Ángel, Corrales Martínez, Alfonso, Rantapää-Dahlqvist, Solbritt, Sfikakis, Petros P., Dessein, Patrick, Tsang, Linda, Hitchon, Carol, El-Gabalawy, Hani, Pascual-Ramos, Virginia, Contreras-Yáñez, Irazú, Colunga-Pedraza, Iris, J., Galarza-Delgado, Dionicio Angel, Azpiri-López, José Ramón, Semb, Anne Grete, Misra, Durga Prasanna, Hauge, Ellen-Margrethe, Kitas, George
Tipo de documento: artigo
Data de publicação:2024
País:España
Recursos:Universidad de Cantabria (UC)
Repositório:UCrea Repositorio Abierto de la Universidad de Cantabria
OAI Identifier:oai:repositorio.unican.es:10902/34437
Acesso em linha:https://hdl.handle.net/10902/34437
Access Level:Acceso aberto
Palavra-chave:Arthritis
Rheumatoid
Biological Therapy
Cardiovascular Diseases
Inflammation
Descrição
Resumo:Objectives: Chronic inflammation promotes cardiovascular risk in rheumatoid arthritis (RA). Biological disease-modifying antirheumatic drugs (bDMARDs) improve disease activity and cardiovascular disease outcomes. We explored whether bDMARDs influence the impact of disease activity and inflammatory markers on long-term cardiovascular risk in RA. Methods: We studied 4370 participants without cardiovascular disease in a 10-country observational cohort of patients with RA. Endpoints were (1) major adverse cardiovascular events (MACE) encompassing myocardial infarction, stroke and cardiovascular death; and (2) any ischaemic cardiovascular events (iCVE) including MACE plus revascularisation, angina, transient ischaemic attack and peripheral arterial disease. Results. Over 26?534 patient-years, 239 MACE and 362 iCVE occurred. The interaction between 28-joint Disease Activity Score with C-reactive protein (DAS28-CRP) and bDMARD use was significant for MACE (p=0.017), suggesting the effect of DAS28-CRP on MACE risk differed among bDMARD users (n=515) and non-users (n=3855). DAS28-CRP (per unit increase) is associated with MACE risk in bDMARD non-users (HR 1.21 (95% CI 1.07 to 1.37)) but not users (HR 0.69 (95% CI 0.40 to 1.20)). The interaction between CRP (per log unit increase) and bDMARD use was also significant for MACE (p=0.011). CRP associated with MACE risk in bDMARD non-users (HR 1.16 (95% CI 1.04 to 1.30)), but not users (HR 0.65 (95% CI 0.36 to 1.17)). No interaction was observed between bDMARD use and DAS28-CRP (p=0.167) or CRP (p=0.237) for iCVE risk. Conclusions. RA activity and inflammatory markers associated with risk of MACE in bDMARD non-users but not users suggesting the possibility of biological-specific benefits locally on arterial wall independently of effects on systemic inflammation.

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