Background The risk of cardiovascular disease (CVD) is increased in RA patients. We have previously reported a rapid increase in risk of acute coronary syndromes (ACS) following RA diagnosis. Despite known variation in time-to-risk patterns for different subtypes of CVD, indicating differences in underlying mechanisms, most studies on CV risk factors in RA so far have focused on composite CVD-outcomes.
Objectives To investigate risk factors specifically for ACS in patients with new-onset RA.
Methods We performed a case-control study nested in a cohort of patients with incident RA included in the Epidemiological Investigation of Rheumatoid Arthritis (EIRA) study. Cases with ACS, defined as a hospitalization or cause-of-death listing ACS following RA diagnosis, were identified in the national Patient Register and Cause of Death Register. Up to 5 controls, free of ACS, per case were selected from the same RA cohort matched on sex, year of RA diagnosis and EIRA center. Information on exposures of interest was collected as follows: I) Serology (antibodies towards citrullinated peptides [ACPA], rheumatoid factor [RF]) and shared epitope alleles (SE) was retrieved from the EIRA-study. II) Clinical disease activity data (DAS-28 and its components [CRP, ESR, Joint status, Global Health [GH] patient assessment] were abstracted from medical charts and supplemented with information from Swedish Rheumatology Quality Register (SRQ). III) Information on other risk factors and pharmacotherapies was collected from medical charts, from the Patient Register, and from the national Prescribed Drug Register. IV) Net days of sick leave and disability pension during the first year following RA-diagnosis was obtained from the social insurance agency. Area under the curve (AUC) measures of disease activity per year and for complete follow-up following RA diagnosis was estimated by taking the average of all reported values per time-period. Odds ratios were adjusted for matching factors and age.
Results 93 cases and 440 controls with information were included. Baseline smoking, high BMI and history of MI, as well as high clinical disease activity (AUC of ESR, DAS28 and GH) and functional measures (net days of sick leave) during the first year after RA onset were all associated with ACS risk; by contrast, neither treatment (methotrexate or other DMARDs), nor serology (RF/ACPA), nor SE were associated with ACS. The above pattern remained when AUC measures during complete follow-up (average 5.3 yrs) were assessed.
Conclusions Disease activity and perceived health already during the first year following RA onset are strong drivers of ACS risk whereas RF, ACPA and SE are not.
Disclosure of Interest None declared