Impact of immature platelets on platelet response to ticagrelor and prasugrel in patients with acute coronary syndrome

Abstract

Reticulated platelets show a greater impact on platelet reactivity in response to prasugrel when compared with ticagrelor.

Effects of prasugrel pretreatment on angiographic myocardial perfusion parameters in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention

“…We have also shown a reduction in the proportions of reticulated platelets over time [14]. A recent article by Bernlochner et al [15] went further to compare the effect of reticulated platelets on prasugrel and ticagrelor, showing a greater impact on the former. This phenomenon may partially explain why preprocedural therapy with prasugrel does not translate into better clinical outcomes in our study, when administered in the acute phase of STEMI.…”

Ticagrelor versus prasugrel in patients with high on-clopidogrel treatment platelet reactivity after PCI: The ISAR-ADAPT-PF study

“…The main reason for this discrepant finding is that our assumption was based on available data at the time of the study development, which was in 2011, that had shown a high and consistent level of platelet inhibition with both study drugs. By now, several studies have revealed that factors accounting for the response variability to the novel P2Y 12 receptor inhibitors are manifold [37][38][39][40]. In the present study, only patients with HTPR on clopidogrel were included, a factor that has previously shown to influence the antiplatelet efficacy of prasugrel significantly [38] and might have contributed to a large extent to the observed high distribution of platelet aggregation values in both treatment groups.…”

“…As an active drug, ticagrelor is less dependent on metabolic activation when compared with prasugrel [36], which therefore might lead to a faster and stronger inhibition of platelet aggregation. Moreover, ticagrelor leads to a reversible inhibition of platelet aggregation with continuous presence of active P2Y 12 receptor binding molecules in blood, which makes the pharmacodynamic drug efficacy less dependent on platelet turnover when compared with prasugrel [37]. However, by now, it remains a matter of debate if these drug properties indeed reflect on overall platelet inhibition as assessed by point of care whole blood platelet function assays and prospective randomized studies like the ongoing ISAR-REACT 5 trial [17] are necessary to address the question of pharmacodynamic and clinical efficacy of ticagrelor when compared with prasugrel.…”

Impact of platelet turnover on long‐term adverse cardiovascular outcomes in patients undergoing percutaneous coronary intervention

“…Abbreviations: ACE-I, angiotensin convertase enzyme inhibitor; ARB, angiotensin receptor blocker; DBP, diastolic blood pressure; DES, drug-eluting stent; eGFR, estimated glomerular filtration rate; SBP, systolic blood pressure. 6 Stratz and colleagues investigated the mechanism behind impaired antiplatelet response in relation to platelet turnover and the intrinsic properties of reticulated platelets. 4 Similar results have been reported for clopidogrel and prasugrel.…”

“…1,2 Besides genetic and clinical factors, high platelet turnover negatively affects platelet inhibition by introducing high rates of young, reticulated platelets into the circulatory system. [3][4][5][6][7] Reticulated platelets are larger in size, denser, have greater prothrombotic potency and are less susceptible for inhibition than their older counterparts. 4,8 Comparing established predictors of platelet reactivity, reticulated platelet count (RPC) has been shown to be the strongest independent predictor of platelet response during dual antiplatelet therapy (DAPT).…”