PB0794 - Effects of antiplatelet drugs on platelet procoagulant reactions

Monday, June 24, 2024

13:45 – 14:45 ICT

Room: Exhibition Hall

Presenting Author(s)

Ivan Muravlev, PhD

Researcher
Chazov National Medical Research Center of Cardiology, Russian Ministry of Health
Moscow, Moskva, Russia

Co-Author(s)

AD

Anatoly Dobrovolsky

Head of the lab
Chazov National Medical Research Center of Cardiology, Russian Ministry of Health
Moscow, Moskva, Russia
Olga A. Antonova, PhD

Research Associate
Chazov National Medical Research Center of Cardiology, Russian Ministry of Health
Moscow, Moskva, Russia
SK

Svetlana Khaspekova

Researcher
Chazov National Medical Research Center of Cardiology, Russian Ministry of Health
Moscow, Moskva, Russia
AA

Amina Alieva

Cardiologist
Chazov National Medical Research Center of Cardiology, Russian Ministry of Health
Moscow, Moskva, Russia
DP

Dmitry Pevzner

Head of department
Chazov National Medical Research Center of Cardiology, Russian Ministry of Health
Moscow, Moskva, Russia
AM

Alexey Mazurov

Head of the lab
Chazov National Medical Research Center of Cardiology, Russian Ministry of Health
Moscow, Moskva, Russia

Background: Activated platelets expose phosphatidylserine (PS) serving as a substrate for assembling coagulation complexes. Due to PS exposure platelets are able to accelerate thrombin generation and fibrin formation. Effects of antiplatelet drugs on platelet procoagulant activities are not thoroughly explored, and sometimes contradictory results are reported.

Aims: We investigated effects of antiplatelet drugs on platelet ability to expose PS and to enhance thrombin generation and fibrin formation.

Methods: Blood was collected from healthy volunteers free of medications or after taking acetylsalicylic acid (ASA) and from patients with acute coronary syndrome (ACS) receiving ASA + ticagrelor. PS exposure on platelet surface was evaluated by flow cytometry using annexin V-FITC in washed platelets or in a whole blood. Platelet ability to accelerate thrombin generation and fibrin formation was explored using washed platelets sedimented on the surface of 96-well plates in thrombin generation test (TGT) and plasma recalcification assay [Muravlev et al, Platelets 2023;34:2139365]. PS exposure in washed platelets was stimulated by thrombin or thrombin + collagen and in a whole blood by TRAP or TRAP + collagen. In TGT and recalcification assay platelets were not treated with exogenous agonists or preactivated by collagen.

Results: In in vitro experiments ticagrelor, ruciromab (Russian glycoprotein IIb-IIIa antagonist) and prostaglandin E1, but not ASA were able to decrease PS exposure on platelets surface (both in washed platelets and in a whole blood), thrombin generation (decrease of the peak and the maximal rate) and fibrin formation (increase of the lag phase and decrease of the maximal rate). ASA taken by volunteers decreases the level of PS exposure on platelets in a whole blood. PS exposure was also decreased in ACS patients receiving ASA + ticagrelor.

Conclusion(s): Antiplatelet drugs suppress platelet procoagulant activities. The discrepancy of ASA effects under in vitro conditions and after in vivo uptake needs further investigations.
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