Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.


Risk of Acute Coronary Syndromes in Relation to TNF-Inhibition in Early Rheumatoid Arthritis.

Ljung5,  Lotta, Simard3,  Julia F., Jacobsson4,  Lennart T. H., Rantapaa-Dahlqvist1,  Solbritt M., Askling2,  Johan

Umea, Sweden
Clinical Epidemiology Unit
Clinical Epidemiology Unit, Stockholm, Sweden
Malmo University Hospital, Malmo, Sweden
Umea University Hospital

Background:

The risk of ischemic cardiovascular disease (CVD) is increased in rheumatoid arthritis (RA) also in the early course of the disease. In established RA, myocardial infarction (MI) risks have been linked to response to anti-TNF-alpha therapies (anti-TNF).

Objectives:

To study the risk of acute coronary syndromes (ACS) in patients with RA during the first years of disease in relation to treatment with, and response to, TNF-inhibitor treatment.

Methods:

All patients with early RA (disease duration <12 months) diagnosed 1995–2007, was identified from the Swedish RA Register (n=8,746). Data on disease activity, laboratory variables and pharmacological treatment was extracted from the register. Through linkage with the National Patient Register and the Cause of Death Register, co-morbidity and hospitalisation with ACS (ICD-10: I20-I21) were identified. Hazard ratios (HR) comparing the risk of incident ACS among patients exposed or not to anti-TNF were estimated using a propensity-score adjusted Cox proportional hazards regression among patients (n=6,000) included 1999 or later, excluding patients with previous ischemic or congestive heart disease. The relationship between response to anti-TNF and risk for an ACS in the cohort was further analysed by conditional logistic regression using a nested case-control design; 24 cases with ACS (unstable angina or MI) after start of anti-TNF were identified, and 81 matched controls were randomly selected. Patient records were reviewed for ACS validation, disease activity, pharmacological treatment, co-morbidity, CVD risk factors and extra-articular disease. No significant differences between cases and controls were noted at start of anti-TNF regarding inflammatory activity, RA therapy, RF-positivity, or extra-articular disease. There was a tendency of more prevalent CVD among cases (37% vs.16 %, p=0.07).

Results:

In the cohort, 1,271 of the 6,000 patients were exposed to anti-TNF during a follow-up time of 21,677 person-years at risk (pyar) with 4,231 anti-TNF-exposed pyar. The incidence of ACS was 9.1/1000 pyar (n incident ACS=198). HR for ACS associated with anti-TNF after stratification for age, sex and year of entry in the cohort was 0.96 (95%CI 0.61–1.49), and after further adjustment for the propensity score HR was 0.81(95%CI 0.52–1.24). In the nested case-control study EULAR response (good or moderate) at 3 and 6 months after initiation of anti-TNF therapy was achieved in 51% (cases 65 %, controls 47 %, n.s.) and 67% (cases 79 %, controls 64 %, n.s.), of the patients respectively. Comparing cases to controls, a good or moderate EULAR response at 3 or 6 months was not associated with risk of ACS, OR 1.65 (0.54–5.05) and 1.48 (0.32–6.88) respectively, adjusted for disease activity before treatment start. Furthermore, no significant associations between response and risk of ACS were observed after adjustment for previous CVD.

Conclusion:

In this study of patients with early RA, treatment with, or response to, anti-TNF could not be linked to any decrease in the risk of acute coronary events. Whether this is due to factors specific for this cohort or if TNF-inhibition have limited protective abilities is not possible to conclude.

To cite this abstract, please use the following information:
Ljung, Lotta, Simard, Julia F., Jacobsson, Lennart T. H., Rantapaa-Dahlqvist, Solbritt M., Askling, Johan; Risk of Acute Coronary Syndromes in Relation to TNF-Inhibition in Early Rheumatoid Arthritis. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :1054
DOI: 10.1002/art.28821

Abstract Supplement

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