Background: Atherosclerosis plays a pivotal role in the development of cardiovascular disease (CVD) and controlling atherosclerosis might be important for the management of CVD in rheumatoid arthritis (RA). However, factors associated with change in atherosclerosis are not fully understood in RA, particularly in those receiving targeted therapies. Carotid intima-media thickness (IMT) and plaque are markers of atherosclerosis which can reflect future CVD risk.
Objectives: We examined the factors associated with regression or progression of carotid IMT and plaque in RA patients receiving targeted therapies.
Methods: This prospective cohort study included patients who initiated biologic agents or janus kinase inhibitors in a tertiary care hospital between August 2020 and May 2023. Study participants underwent carotid ultrasonography at baseline and after 1-year treatment. Maximum IMT of plaque-free segments at the common carotid artery (CCA) and the presence and size of plaque were measured. Treatment response was evaluated using EULAR response criteria.
Results: A total of 113 patients who continued the initial treatment for a year and finished follow-up examination were included. At follow-up, maximum CCA IMT regressed in 23 (20.4%) patients, remained stable in 80 patients, and progressed in 10 patients; and 13 (11.5%) had plaque progression. A multivariable analysis revealed that good response (adjusted odds ratio [aOR] 5.82, 95% CI 1.23-27.59), decrease in fat mass index (aOR 5.82, 95% CI 1.02-33.11), and decrease in blood glucose levels (aOR 3.72, 95% CI 1.02-13.56) were associated with maximum CCA IMT regression. Meanwhile, age (aOR 2.33, 95% CI 1.09-4.99; per 10 years), ever smoker (aOR 8.71, 95% CI 1.26-60.36), and no response (aOR 10.74, 95% CI 1.81-63.76) independently predicted plaque progression.
Conclusion: In RA patients receiving targeted therapies, achieving a good response was significantly associated with regression of carotid atherosclerosis. Controlling RA disease activity and modifiable risk factors would be important to reduce CVD risk.
REFERENCES: NIL.
Acknowledgements: NIL.
Disclosure of Interests: None declared.
© The Authors 2025. This abstract is an open access article published in Annals of Rheumatic Diseases under the CC BY-NC-ND license (