Thrombin Receptor Agonist Peptide–Induced Platelet Aggregation Is Reduced in Patients Receiving Dabigatran
Author(s) -
František Neháj,
Juraj Sokol,
Michal Mokáň,
Jela Ivanková,
Maros Mokan
Publication year - 2017
Publication title -
clinical and applied thrombosis/hemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.643
H-Index - 53
eISSN - 1938-2723
pISSN - 1076-0296
DOI - 10.1177/1076029617713871
Subject(s) - dabigatran , medicine , platelet , agonist , thrombin , coagulation , direct thrombin inhibitor , thrombin receptor , pharmacology , platelet activation , atrial fibrillation , thrombin time , anesthesia , cardiology , receptor , warfarin , partial thromboplastin time
The availability of direct oral anticoagulants has caused a paradigm shift in thrombosis management. The direct thrombin inhibitor dabigatran seems to obstruct tenase complex by inhibiting thrombin generated in the initial phase and feed back to the amplification phase of cell-based coagulation reactions. However, it is still not fully understood if and how dabigatran impact platelet function. This observational study aimed to assess in vitro platelet function in patients with atrial fibrillation receiving dabigatran. Platelet aggregability was tested with platelet-rich plasma using platelet aggregometry (PACKS-4 aggregometer). Blood samples were stimulated with thrombin receptor agonist peptide (TRAP; 32 μmol/L).
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