Abstract 19248: Atrial Fibrillation/Flutter Associated with Rheumatoid Arthritis vs. Osteoarthritis and the use of Etoricoxib vs. Diclofenac: Results from the MEDAL Program
Background: The use of non-steroidal anti-inflammatory drugs (NSAIDs) and rheumatoid arthritis (RA) have been associated with atrial fibrillation/flutter (AF) and adverse cardiovascular outcomes in registry studies. The MEDAL program provides a unique opportunity within the context of large randomized controlled trials to explore this relationship.
Methods: MEDAL represents a pooled population from 3 trials; 34,701 patients with osteoarthritis (OA) or RA randomized to receive either a coxib (etoricoxib, 60 or 90 mg daily) or a non-selective NSAID (diclofenac 150 mg daily) had a mean follow up of 18 months. All patients who received at least one dose of study drug were included in the analyses (modified Intent to Treat). AF events occurring on study drug, defined as serious or resulting in drug discontinuation (reported up to 14 days after last date of drug), were counted and unadjusted incidence rates are reported in this post-hoc analysis.
Results: Overall, the rates of AF in the study were low (0.5%). More patients with AF were male, ≥65 years, white race, and had ≥2 coronary risk factors (p<0.01 for all). Patients with OA had a slightly higher mean age than those with RA (64.0 vs. 61.2 years) and a somewhat higher proportion of coronary risk factors. In the pooled treatment group (selective plus non-selective NSAIDs), there was a slightly lowerrate of AF in patients with RA compared with OA (0.4% vs. 0.6%). When stratified by treatment group and type of arthritis, the highest rate of AF occurred in patients receiving etoricoxib 90 mg and having OA (0.7%) (Figure).
Conclusion: Within the MEDAL program, patients with RA did not appear to have a higher unadjusted rate of AF than patients with OA. Furthermore, 90 mg etoricoxib in patients with OA was associated with a higher rate of AF relative to a non-selective NSAID and this relationship may be dose-related. These data suggest greater degrees of COX-2 inhibition may increase the risk of AF, although the absolute risk is small.
- © 2012 by American Heart Association, Inc.