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.
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.
This study showed that factor Xa inhibition does not affect ADP-induced, epinephrine-induced, and collagen-induced platelet aggregation.