Key result
Ticagrelor, ruciromab, and PGE1, but not aspirin, suppressed platelet coagulation activity and phosphatidylserine exposure both in vitro and in patients with acute coronary syndrome.
Why the study?
Activated platelets accelerate fibrin formation and thrombin generation via phosphatidylserine exposure, prompting investigation into how antiplatelet drugs impact these reactions and phosphatidylserine exposure.
Do antiplatelet drugs (ticagrelor, ASA, ruciromab, PGE1) reduce platelet-dependent coagulation reactions and phosphatidylserine exposure in human platelets?
Population
Washed human platelets and blood from acute coronary syndrome patients and medication-free donors
Comparison
ASA, ticagrelor, ASA plus ticagrelor, ruciromab, or PGE1 vs untreated platelets
Design
In vitro and ex vivo comparative laboratory study
Authors
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May differentiate ticagrelor from aspirin on platelet procoagulant activity in ACS; leaves open outcome implications.
Do antiplatelet drugs (ticagrelor, ASA, ruciromab, PGE1) reduce platelet-dependent coagulation reactions and phosphatidylserine exposure in human platelets?
Ticagrelor, ruciromab, and PGE1, but not aspirin, suppress platelet coagulation activity and phosphatidylserine exposure both in vitro and in patients with acute coronary syndrome.
Muravlev et al. (2023) studied Acute coronary syndrome. Antiplatelet drugs (ticagrelor, aspirin, ruciromab, PGE1) vs. Untreated platelets / donors free of medications was evaluated on Fibrin formation, thrombin generation, and phosphatidylserine exposure. Ticagrelor, ruciromab, and PGE1, but not aspirin, suppressed platelet coagulation activity and phosphatidylserine exposure both in vitro and in patients with acute coronary syndrome.
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