Peter Bánovčin1, Ingrid Škorňová, Matej Samoš, Martin Schnierer, Tomáš Bolek, František Kovář, Ján Staško, Peter Kubisz, Marián Mokáň. 1. *Department of Gastroenterology, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Martin, Slovak Republic; †National Centre of Hemostasis and Thrombosis, Department of Hematology and Blood Transfusion, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Martin, Slovak Republic; and ‡Department of Internal Medicine I, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Martin, Slovak Republic.
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.
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.
Authors: Antonio Trani; Pietro Benedetto; Ferdinando Di Leo; Angela Baiano; Andrea Esposito; Danilo Menna; Arianna Allegretti; Pierluigi Antonino Cappiello; Domenico Dell'Edera Journal: J Pharm Health Care Sci Date: 2020-08-03
Authors: Dana Prídavková; Matej Samoš; Tomáš Bolek; Ingrid Škorňová; Jana Žolková; Peter Kubisz; Ján Staško; Marián Mokáň Journal: J Diabetes Res Date: 2019-12-06 Impact factor: 4.011