Key result
In an in vitro model, none of the four haemostatic drugs corrected ticagrelor-induced platelet inhibition, though rFVIIa, fibrinogen, and FXIII improved specific coagulation parameters.
Why the study?
Do haemostatic drugs (rFVIIa, Fib, TXA, FXIII) improve haemostatic capacity in vitro in the presence of ticagrelor?
Do haemostatic drugs (rFVIIa, Fib, TXA, FXIII) improve haemostatic capacity in vitro in the presence of ticagrelor?
In vitro, haemostatic agents like rFVIIa, fibrinogen, and FXIII do not reverse ticagrelor's antiplatelet effect but may improve overall haemostasis by enhancing fibrin formation or reducing fibrinolysis.
Answers are grounded in this paper and cite their sources.
Certain haemostatic agents may enhance clot formation with ticagrelor; hypothesis-generating and should not yet change practice.
Aim Management of ticagrelor-induced bleeding is challenging as platelet transfusion is ineffective. An effective strategy is needed. This study aimed to investigate in vitro the efficacy of four haemostatic drugs (HDs), namely recombinant activated factor VII (rFVIIa), fibrinogen concentrate (Fib), tranexamic acid (TXA) and factor XIII concentrate (FXIII) to improve the haemostatic capacity in the presence of ticagrelor. Methods Blood was spiked with ticagrelor then supplemented by either HD or control. Several assays were performed: ADP-induced platelet aggregation measured by impedance aggregometry, light transmission and two global assays, thrombolastography with the platelet mapping device (TEG-PM) and a platelet-dependent thrombin generation assay (TGA). Results Ticagrelor inhibited ADP-induced platelet aggregation and decreased the clot strength maximum amplitude (MA) in TEG-PM ADP . None of the HDs corrected these parameters. However, rFVIIa shortened the coagulation time R using TEG-PM thrombin and the time to peak prolonged by ticagrelor in TGA. Fib increased MA thrombin and FXIII decreased LY30. TXA had no effects. Conclusions Whereas none of the HDs corrected ticagrelor-induced platelet inhibition, rFVIIa shortened coagulation times, Fib increased clot firmness and FXIII decreased fibrinolysis. Consequently, they may bypass ticagrelor effects by acting on fibrin formation or fibrinolysis. Further studies are needed to confirm these data in vivo .
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Calmette et al. (2017) studied Ticagrelor-induced bleeding. Haemostatic drugs (rFVIIa, fibrinogen concentrate, tranexamic acid, factor XIII concentrate) vs. Control was evaluated on ADP-induced platelet aggregation and clot strength. In an in vitro model, none of the four haemostatic drugs corrected ticagrelor-induced platelet inhibition, though rFVIIa, fibrinogen, and FXIII improved specific coagulation parameters.
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