Why the study?
PMVs are implicated in procoagulant, pro-inflammatory, and pro-atherosclerotic effects, but how different P2Y12 receptor antagonists affect plasma PMV numbers in relation to platelet reactivity during DAPT was unknown.
Does ticagrelor or prasugrel compared to clopidogrel reduce plasma platelet-derived microvesicles and platelet reactivity in men with ACS on DAPT?
Does ticagrelor or prasugrel compared to clopidogrel reduce plasma platelet-derived microvesicles and platelet reactivity in men with ACS on DAPT?
Ticagrelor, but not prasugrel, is associated with lower total platelet-derived microvesicle release compared to clopidogrel, suggesting a pleiotropic effect independent of its anti-aggregatory properties.
Answers are grounded in this paper and cite their sources.
Ticagrelor was associated with lower platelet microvesicle release than clopidogrel in ACS; leaves open pleiotropic effects and requires randomized confirmation before practice change.
Background: Platelet-derived microvesicles (PMVs), shed from platelet surface membranes, constitute the majority of circulating microvesicles and have been implicated in procoagulant, pro-inflammatory and pro-atherosclerotic effects. Our aim was to compare plasma PMVs numbers in relation to platelet reactivity during dual antiplatelet therapy (DAPT) with various P2Y12 adenosine diphosphate (ADP) receptor antagonists. Methods: In pre-discharge men treated with DAPT for an acute coronary syndrome, plasma PMVs were quantified by flow cytometry on the basis of CD62P (P-selectin) and CD42 (glycoprotein Ib) positivity, putative indices of PMVs release from activated and all platelets, respectively. ADP-induced platelet aggregation was measured by multiple-electrode aggregometry. Results: Clinical characteristics were similar in patients on clopidogrel (n=16), prasugrel (n=10) and ticagrelor (n=12). Platelet reactivity was comparably reduced on ticagrelor or prasugrel versus clopidogrel (p<0.01). Compared to clopidogrel-treated patients, CD42 + /CD62P + PMVs counts were 3-4-fold lower in subjects receiving ticagrelor (p=0.001) or prasugrel (p<0.05), while CD42 + PMVs were significantly reduced on ticagrelor (by about 6-fold, p<0.001), but not prasugrel (p=0.3). CD42 + /CD62P + PMVs numbers correlated positively to the ADP-induced aggregation on clopidogrel (p<0.01) or prasugrel (p<0.05), which was absent in ticagrelor users (p=0.8). CD42 + PMVs counts were unrelated to platelet reactivity (p>0.5). Conclusions: Higher antiplatelet potency of prasugrel and ticagrelor versus clopidogrel is associated with decreased plasma CD42 + /CD62P + PMVs numbers. However, in contrast to thienopyridines, the association of reduced CD42 + /CD62P + PMVs counts with ticagrelor use appears independent of its anti-aggregatory effect. Despite similar platelet-inhibitory activity of ticagrelor and prasugrel, only the treatment with ticagrelor seems associated with lower total PMVs release. Our preliminary findings may suggest a novel pleiotropic effect of ticagrelor extending beyond pure anti-aggregatory properties of the drug.
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Chyrchel et al. (2019) studied this question.
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