@article{10902/34437,
year = {2024},
url = {https://hdl.handle.net/10902/34437},
abstract = {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.},
organization = {Funding: This study was supported by Pfizer through an investigator-initiated grant award (grant ID number 68633259) to GAK. The sponsors were not involved in the study design, study-related procedures, data collection, data analysis or interpretation, manuscript drafting or manuscript submission. Acknowledgements: We thank ATACC-RA consortium member Cynthia Crowson, PhD for her contributions. We also acknowledge all patients and health personnel involved. Preliminary results were presented at the EULAR 2023 Congress: Karpouzas G, Ormseth S, Van Riel P, et al. POS0034 Biologic use influences the impact of inflammation on cardiovascular risk in rheumatoid arthritis Ann Rheum Dis. 2023;82:225.},
publisher = {BMJ Publishing Group},
publisher = {RMD open, 2024, 10, e004546},
title = {Biological use influences the impact of inflammation on risk of major adverse cardiovascular events in rheumatoid arthritis},
author = {Karpouzas, George Athanasios and Ormeseth, Sarah R. and Van Riel, Piel Leonardus Cornelis Maria and González-Gay Mantecón, Miguel Ángel and Corrales Martínez, Alfonso and Rantapää-Dahlqvist, Solbritt and Sfikakis, Petros P. and Dessein, Patrick and Tsang, Linda and Hitchon, Carol and El-Gabalawy, Hani and Pascual-Ramos, Virginia and Contreras-Yáñez, Irazú and Colunga-Pedraza, Iris, J. and Galarza-Delgado, Dionicio Angel and Azpiri-López, José Ramón and Semb, Anne Grete and Misra, Durga Prasanna and Hauge, Ellen-Margrethe and Kitas, George},
}