PB0911 - Platelet reactivity in patients with Atrial Fibrillation and Coronary Artery Disease under IIa antagonists and Xa antagonists

Background: Dabigatran is a direct oral anticoagulant(DOAC). Recently, studies suggest increase of myocardial infarction(MI) among patients using dabigatran, including the landmark trial RE-LY. Ever since, there have been discussions on whether dabigatran increases the risk of MI.

Aims: To investigate the platelet activation in patients with atrial fibrillation(AF) and coronary artery disease(CAD) treated under Factor Xa inhibitor(either Rivaroxaban, Apixaban or Edoxaban) and Factor IIa inhibitor(Dabigatran).

Methods: This prospective, single-centre, crossover study included 40 patients diagnosed with AF and CAD on a steady state level of a NOAC between July 2021 and December 2022. Patients switched medication immediately after inclusion for 2 weeks (i.e. Factor IIa inhibitors)or Factor Xa inhibitors. The primary outcome was P-selectin expression by flow-cytometry analysis. Secondary markers included whole blood aggregometry as measured by Multiplate Analyzer Roche in response to ADP and TRAP and coagulation markers as measured by the TEG6s and T-TAS AR chip. Paired t-tests were used to evaluate the differences in platelet activation under Xa and II inhibitors.

Results: There was no significant difference in the P-selectin activation under Factor Xa inhibitors(M=19.9, SD=9.5) and Factor IIa inhibitors(M=20.6, SD=9.7); t(38)=-0.32, p=0.75). Similarly, no significant difference in Multiplate ADP and TRAP AUC under Factor Xa inhibitors(M=53.5, SD=25.3) and Factor IIa inhibitors(M=53.3, SD=21.8), (M=90.3, SD=25.2) and (M=85.9, SD=26.8) respectively. For T-TAS, Area under the flow curve over 30 minutes was significantly higher under Factor Xa inhibitors compared to Factor IIa inhibitors. Similarly, Occlusion time was significantly longer under Factor IIa inhibitors(M=1063 seconds, SD=447) compared to Factor Xa inhibitors(M= 824 seconds, SD=353);t(36)=-3.4, p=0.0015)

Conclusion(s): There was no difference in platelet activation under Xa inhibitors and IIa inhibitors in patients with AF and stable CAD. The AUC30 was significantly higher in Factor Xa inhibitors and OT as measured by T-TAS AR chip was significantly higher under Factor IIa inhibitors.