FRI0142 TNF-blocking therapy reduces cardiovascular disease and risk factors in rheumatoid arthritis. (23rd January 2014)

• Record Type: Journal Article
• Authors: van Sijl, A.M.; Visman, I.M.; Peters, M.J.; van Dongen, C.; Smulders, Y.M.; Voskuyl, A.E.; Nurmohamed, M.T.
• Is Part Of: Annals of the rheumatic diseases. Volume 71(2012)Supplement 3
• Page Start: 358
• Page End: 358
• Publication Date: 2014-01-23
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2012-eular.2599
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Background: Patients with rheumatoid arthritis (RA) are at increased risk of cardiovascular (CV) disease. The contribution of inflammation to this increased risk is well recognised. Recent register based studies indicate that suppression of tumour necrosis factor (TNF) lowers CV risk. No register to date has accurately assessed both CV- and RA-related parameters. Methods: The CARRΈ study is a Dutch prospective cohort study of 353 randomly selected RA patients, aged 50-75, with 1381 patient years. The Biologics cohort is an ongoing study of 449 Dutch RA patients, also aged 50-75, with 1201 patient years of follow-up since their allocation to their first TNF-blocking agents adalimumab or etanercept. Fatal and non-fatal CV events (according to the international classification of disease, ICD-9) were documented in both cohorts. Cox-proportional hazard analyses were used to investigate the association between use of TNF-blocking agents and CV disease incidence. Results: Incidence rate ratio of CV events in RA patients with TNF-blocking therapy versus those without TNF-blocking therapy was: 0.36 (95%>confidence interval (CI): 0.18-0.73), incidence rate: 8.3 vs. 23.2 per 1.000 patient years, respectively. Age- and gender adjusted hazard ratio for CV disease incidence: 0.54 (95%>CI: 0.24-1.21) in favour of patients receiving TNF-blocking therapy, although not statistically significantly so. The magnitude of this association remained stable after additional adjustment for CV risk factors, RA-related parameters and concomitant medication use. There was a difference in baseline characteristics between populations and there was no increase in CV risk factors over time in either group. Patients receiving TNF-blocking therapy, as expected, had a substantial improvement in RA-related parameters over time. Conclusions: Our observations confirm the association between strong suppression of inflammation and curbing the CV risk in RA. Surprisingly, this CV risk appeared to be independent of CV risk factors. However, whether the reduced incidence of CV disease is due to allocation of patients with certain disease characteristics (more favourable CV risk profile in patients receiving TNF-blocking therapy) is not yet clear and may indicate channelling bias. Disclosure of Interest: None Declared