Why the study?
Does the extent of platelet disaggregation vary depending on the agonist and the type of dual antiplatelet therapy in patients undergoing PCI?
Does the extent of platelet disaggregation vary depending on the agonist and the type of dual antiplatelet therapy in patients undergoing PCI?
Pathways of platelet activation not inhibited by standard antiplatelet therapy allow persisting platelet aggregation, which may contribute to adverse ischemic events.
Answers are grounded in this paper and cite their sources.
Variable disaggregation signals incomplete DAPT inhibition by some pathways; leaves open whether agonist-specific testing refines ischemic risk assessment.
Disaggregation as the difference between maximal and final platelet aggregation by light transmission aggregometry indicates the stability of platelet aggregates. We evaluated the extent of disaggregation after platelet stimulation with adenosine diphosphate (ADP), arachidonic acid (AA), collagen, epinephrine, and thrombin receptor-activating peptide (TRAP)-6 in 323 patients on dual antiplatelet therapy with daily aspirin and clopidogrel (group 1), prasugrel (group 2), or ticagrelor (group 3) therapy. All patients in group 1 underwent elective angioplasty and stenting, whereas all patients included in groups 2 and 3 suffered from acute coronary syndromes (STEMI or NSTEMI) and underwent urgent PCI. Significant differences between maximal and final platelet aggregation were observed with all agonists throughout the groups (all p<0.001). Disaggregation was highest using AA (clopidogrel 36.5%; prasugrel/ticagrelor 100%) and ADP (clopidogrel 21.7%; prasugrel/ticagrelor 100%). In contrast, low disaggregation was observed after platelet stimulation with collagen and TRAP-6 in clopidogrel-treated patients, and after platelet stimulation with collagen and epinephrine in prasugrel- and ticagrelor-treated patients. In conclusion, pathways of platelet activation that are not inhibited by standard antiplatelet therapy allow persisting platelet aggregation and may at least in part be responsible for adverse ischemic events.
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Wadowski et al. (2017) studied this question.
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