Platelet Aggregation in Direct Oral Factor Xa Inhibitors-treated Patients With Atrial Fibrillation: A Pilot Study.

ABSTRACT

BACKGROUND: Activated factor X (factor Xa) plays an important role in regulation of platelets. The aim of this study was to test the effect of direct oral factor Xa inhibitors-rivaroxaban and apixaban-on platelet aggregation in patients with nonvalvular atrial fibrillation. PATIENTS AND METHODS: This single-center pilot study enrolled 21 factor Xa inhibitors-treated (9 rivaroxaban-treated and 12 apixaban-treated) patients with nonvalvular atrial fibrillation. The trough and peak samples of these patients were tested for adenosine diphosphate (ADP)-induced, epinephrine-induced, and collagen-induced platelet aggregation with light transmission aggregometry, and with factor Xa-calibrated anti-Xa chromogenic analysis. RESULTS: The detected trough anti-Xa activity was 57.5 ± 43.4 µg/L. There was a significant increase in peak anti-Xa activity to 175.9 ± 119.6 µg/L (P < 0.001) observed. The platelet aggregation was reduced with reduced inductor concentration. However, no significant changes in ADP-induced, or in epinephrine-induced, or in collagen-induced platelet aggregation were seen comparing trough and peak sample. There were no significant differences in anti-Xa activity or in platelet aggregation comparing rivaroxaban-treated and apixaban-treated patients. CONCLUSIONS: This study showed that factor Xa inhibition does not affect ADP-induced, epinephrine-induced, and collagen-induced platelet aggregation.