Key result
Rivaroxaban did not significantly influence platelet reactivity or von Willebrand factor compared to off-treatment values, with a trend toward reduced P-selectin (p=0.06).
Why the study?
Rivaroxaban may have a different bleeding risk profile than warfarin, but the underlying mechanisms and its effect on primary hemostasis are poorly understood.
Does rivaroxaban influence primary hemostasis (platelet function, P-selectin, and VWF) in patients with venous thrombosis?
Observational
Does rivaroxaban influence primary hemostasis (platelet function, P-selectin, and VWF) in patients with venous thrombosis?
p-value: p=0.06
Rivaroxaban does not significantly alter primary hemostasis parameters such as platelet reactivity or vWF activity, suggesting its distinct bleeding profile is not driven by these mechanisms.
No effect on platelet reactivity or vWF in this cohort; leaves open alternative mechanisms for rivaroxaban's bleeding profile.
Factor Xa inhibitors are safe and effective alternatives to warfarin, but several studies indicate that rivaroxaban may cause a different risk profile for bleeding. For instance, while the risk of major bleeding in general may be lower with rivaroxaban than for warfarin, the risk of gastrointestinal bleeding or abnormal uterine bleeding may be higher. The underlying mechanisms for these differences are not known, and the effect of rivaroxaban on primary hemostasis is poorly understood. The aim of this study was to investigate the effect of rivaroxaban on platelet function, P-selectin and von Willebrand factor (VWF) antigen and activity. Patients with venous thrombosis assigned to 3 months of treatment due to temporary risk factors were included. Blood was collected both during (on-treatment) and 4–6 weeks after end of treatment (without treatment). The platelet reactivity was assessed by light transmission aggregometry. P-selectin was measured by an enzyme-linked immunosorbent assay and vWF antigen and activity by latex immunoagglutination assays. Platelet reactivity during on-treatment (trough- and peak concentration) was similar to values without treatment. There was a trend toward a reduction of P-selectin during rivaroxaban treatment (peak concentration) compared to value without treatment (p = 0.06). There were no differences in vWF antigen and activity between the different time-points. We found no difference in platelet reactivity or vWF antigen/activity during rivaroxaban treatment compared with values without treatment. Apart from possibly causing a reduction of P-selectin, rivaroxaban seems not to influence primary hemostasis.
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Schultz et al. (2018) conducted an observational in Venous thrombosis. Rivaroxaban vs. Without treatment (4-6 weeks after end of treatment) was evaluated on Platelet reactivity, P-selectin, and von Willebrand factor (VWF) antigen and activity (p=0.06). Rivaroxaban did not significantly influence platelet reactivity or von Willebrand factor compared to off-treatment values, with a trend toward reduced P-selectin (p=0.06).
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