AIMS: The aim of this study was to assess the impact of bivalirudin or unfractionated heparin (UFH) on platelet aggregation in patients, pretreated with a 600 mg loading dose clopidogrel, undergoing elective percutaneous coronary intervention (PCI). METHODS AND RESULTS: Patients (n = 100) were recruited consecutively in the setting of a double-blind, randomized trial. Bivalirudin or UFH was administered during PCI. Blood was drawn immediately before PCI, following administration of bivalirudin or UFH directly after PCI, and 24 h after PCI. Adenosine diphosphate (ADP)-induced platelet aggregation was assessed with light transmission aggregometry (LTA) and multiple electrode aggregometry (MEA). Before PCI, ADP-induced platelet aggregation was similar in UFH and bivalirudinpatients (P = 0.99 for LTA; P = 0.28 for MEA). Administration of bivalirudin during PCI resulted in significant additional suppression of platelet aggregation (P = 0.012 for LTA; P = 0.008 for MEA). Administration of UFH did not have a significant influence on platelet aggregation (P = 0.42 for LTA; P = 0.78 for MEA). Platelet aggregation was again similar in the two groups 24 h after PCI (P > 0.05 for LTA and MEA). CONCLUSION:Bivalirudin, given during PCI in patients pretreated with 600 mg of clopidogrel, is in contrast to UFH associated with further inhibition of platelet aggregation.
RCT Entities:
AIMS: The aim of this study was to assess the impact of bivalirudin or unfractionated heparin (UFH) on platelet aggregation in patients, pretreated with a 600 mg loading dose clopidogrel, undergoing elective percutaneous coronary intervention (PCI). METHODS AND RESULTS:Patients (n = 100) were recruited consecutively in the setting of a double-blind, randomized trial. Bivalirudin or UFH was administered during PCI. Blood was drawn immediately before PCI, following administration of bivalirudin or UFH directly after PCI, and 24 h after PCI. Adenosine diphosphate (ADP)-induced platelet aggregation was assessed with light transmission aggregometry (LTA) and multiple electrode aggregometry (MEA). Before PCI, ADP-induced platelet aggregation was similar in UFH and bivalirudin patients (P = 0.99 for LTA; P = 0.28 for MEA). Administration of bivalirudin during PCI resulted in significant additional suppression of platelet aggregation (P = 0.012 for LTA; P = 0.008 for MEA). Administration of UFH did not have a significant influence on platelet aggregation (P = 0.42 for LTA; P = 0.78 for MEA). Platelet aggregation was again similar in the two groups 24 h after PCI (P > 0.05 for LTA and MEA). CONCLUSION: Bivalirudin, given during PCI in patients pretreated with 600 mg of clopidogrel, is in contrast to UFH associated with further inhibition of platelet aggregation.
Authors: B Steppich; F Dobler; L C Brendel; G Hessling; S L Braun; A L Steinsiek; I Deisenhofer; A Hyseni; M Roest; I Ott Journal: J Thromb Thrombolysis Date: 2017-05 Impact factor: 2.300
Authors: Thomas W Johnson; Andrew D Mumford; Lauren J Scott; Stuart Mundell; Mark Butler; Julian W Strange; Chris A Rogers; Barnaby C Reeves; Andreas Baumbach Journal: PLoS One Date: 2015-12-16 Impact factor: 3.240