Objectives: We compared EV concentrations and EV procoagulant activity in plasma of patients after AMI treated with ticagrelor or clopidogrel.
Methods: After percutaneous coronary intervention, 60 patients with first AMI were randomized to ticagrelor or clopidogrel. Flow cytometry was used to determine concentrations of EVs from activated platelets (CD61+, CD62p+), fibrinogen+, phosphatidylserine (PS+), from leukocytes (CD45+), endothelial cells (CD31+,146+) and erythrocytes (CD235a+) in plasma at randomisation, after 72 hours and 6 months of treatment. Fibrin generation test was used to determine EV procoagulant activity.
Results: Concentrations of platelet, fibrinogen+, PS+, leukocyte and erythrocyte EVs increased 6 months after AMI compared to the acute phase of AMI (p≤0.03). Concentrations of platelet EVs were lower on ticagrelor compared to clopidogrel after 6 months (p=0.03). Concentrations of fibrinogen+, PS+ and leukocyte EVs were lower on ticagrelor compared to clopidogrel both after 72 hours and 6 months (p≤0.03). Concentrations of endothelial EVs and
20 EV procoagulant activity did not differ between patient groups and over time (p≥0.17).
Conclusions: Ticagrelor attenuates the increase of EV concentrations in plasma after acute myocardial infarction compared to clopidogrel. The ongoing release of EVs despite antiplatelet therapy might explain recurrent thrombotic events after AMI and worse clinical outcomes on clopidogrel compared to ticagrelor.
- ADP receptors
- antiplatelet drugs
- extracellular vesicles