Background: Inflammatory activity, as well as traditional cardiovascular risk factors, is thought to underlie the increased risk of coronary disease in patients with rheumatoid arthritis (RA). We therefore wanted to evaluate whether the level of response to tumour necrosis factor inhibitors (TNFi) in RA are associated with the risk of acute coronary syndrome (ACS).
Method: All patients with RA and no previous ischaemic heart disease who started treatment with a first TNFi during 2001–2010 as registered in the Swedish Biologics Register were identified. Of the patients (n ¼ 6615) at risk for exposure (i.e. EULAR response at 5 3 months), response data was available for 75% (n¼ 4938). For each patient, five matched referents were selected randomly from the Population Register. Follow-up was maximized to 1 and 2 years, respectively. The outcome, incident ACS, was defined as a primary discharge diagnosis of myocardial infarction or unstable angina, or myocardial infarction as the underlying cause of death. Incidence rates were calculated and adjusted Cox proportional hazard regression models were used for risk estimations.
Results: During the first year of follow-up, 33 cases of ACS occurred among the patients. The risk (hazard ratio, HR) of ACS for good responders compared with none responders, fully adjusted, was 0.26 (95% CI 0.08–0.83), and for moderate responders compared with no responders 0.81 (95% CI 0.36–1.79). Compared with the general population no increase in the risk of ACS was observed among good responders (HR 0.74, 95% CI 0.27–2.06). The lower risk of ACS among good responders was also noted during 2 years of follow-up.
Conclusions: Good EULAR response after 5 months of treatment with TNFi in RA patients was associated with a significantly decreased risk of ACS. In patients with good response on therapy, no significant increase in the risk of ACS was detectable in comparison with the risk in the general population during the 2 years after the evaluation.
Informa Healthcare, 2014. Vol. 43, no Suppl. 127 Meeting Abstract OP11/PP156, 8-8 p.