作者: Thomas Hoefer , Paul C. Armstrong , Michaela Finsterbusch , Melissa V. Chan , Nicholas S. Kirkby
DOI: 10.1161/ATVBAHA.115.306219
关键词: Prasugrel 、 Aspirin 、 Prasugrel Hydrochloride 、 Pharmacology 、 Platelet activation 、 Antiplatelet drug 、 Platelet 、 Platelet aggregation inhibitor 、 P2Y12 、 Chemistry
摘要: Objective—Reduced antiplatelet drug efficacy occurs in conditions of increased platelet turnover, associated with proportions drug-free, that is, uninhibited, platelets. Here, we detail mechanisms by which drug-free platelets promote aggregation the face standard therapy. Approach and Results—To model therapy, were treated vitro aspirin, P2Y12 receptor blocker prasugrel active metabolite, or aspirin plus metabolite. Different uninhibited then introduced. Light transmission aggregometry analysis demonstrated clear positive associations between percentage response to a range agonists. Using differential labeling coupled advanced flow cytometry confocal imaging found aggregates formed mixtures aspirin-inhibited together characterized in...