Dr. Askling has received consulting fees, speaking fees, and/or honoraria from Bristol-Myers Squibb and Pfizer (less than $10,000 each).
Treatment with tumor necrosis factor inhibitors and the risk of acute coronary syndromes in early rheumatoid arthritis
Version of Record online: 29 DEC 2011
Copyright © 2012 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 64, Issue 1, pages 42–52, January 2012
How to Cite
Ljung, L., Simard, J. F., Jacobsson, L., Rantapää-Dahlqvist, S., Askling, J. and Anti-Rheumatic Therapy in Sweden (ARTIS) Study Group (2012), Treatment with tumor necrosis factor inhibitors and the risk of acute coronary syndromes in early rheumatoid arthritis. Arthritis & Rheumatism, 64: 42–52. doi: 10.1002/art.30654
- Issue online: 29 DEC 2011
- Version of Record online: 29 DEC 2011
- Accepted manuscript online: 26 AUG 2011 01:19PM EST
- Manuscript Accepted: 23 AUG 2011
- Manuscript Received: 25 JAN 2011
- Swedish Research Council. Grant Numbers: K2010-52X-20307-04-3, K2008-52X-20611-01-3
- Swedish Rheumatism Association
- King Gustav V's 80-Year Foundation
- Västerbotten County Council
- Swedish Heart-Lung Foundation
- Combine Collaboration
Rheumatoid arthritis (RA) is associated with an increased risk of ischemic heart disease, in both early and established RA. Data on the risk of ischemic heart disease in relation to therapy with tumor necrosis factor (TNF) antagonists (anti-TNF) are conflicting in patients with established RA and essentially lacking in those with early RA. In established RA, the risk of myocardial infarction has been linked to the response to anti-TNF therapies. The aim of this study was to determine the risk of acute coronary syndromes (ACS) in patients with early RA in relation to treatment with, and response to, anti-TNF.
A cohort consisting of patients in whom RA was diagnosed between 1999 and 2007 was identified from the Swedish Rheumatology Register (n = 6,000), from which information on disease activity and pharmacologic treatments was extracted. In a cohort study, the risk of first occurrence of an ACS was compared between patients treated with anti-TNF and those without exposure to anti-TNF, using hazard ratios (HRs). In a nested case–control study, the relationship between response to anti-TNF according to the European League Against Rheumatism (EULAR) response criteria and the risk of ACS was investigated.
In the cohort study, treatment with anti-TNF was not related to any statistically significant alteration in the risk of ACS (HR 0.80, 95% confidence interval [95% CI] 0.52–1.24). In the nested case–control study, a good or moderate EULAR treatment response at 3 months and at 6 months was not associated with a risk of ACS (odds ratio [OR] 1.7, 95% CI 0.5–5.1 and OR 1.5, 95% CI 0.3–6.9, respectively), when adjusted for disease activity before treatment start.
In this study of patients treated with anti-TNF within the first years of RA, neither treatment with, nor response to, anti-TNF therapy could be linked to any statistically significant decrease in the risk of ACS.