José Luis Ferreiro1, David Vivas2, Jesús María De La Hera3, Ana Lucrecia Marcano4, Leslie Marisol Lugo4, Juan Carlos Gómez-Polo2, Iria Silva5, Antonio Tello-Montoliu6, Francisco Marín6, Inmaculada Roldán7. 1. Heart Diseases Institute, Hospital Universitario de Bellvitge - IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain. Electronic address: jlferreiro@bellvitgehospital.cat. 2. Cardiovascular Institute, Hospital Clínico San Carlos, Madrid, Spain. 3. Department of Cardiology, Hospital Universitario Central de Asturias, Oviedo, Spain; Instituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain. 4. Heart Diseases Institute, Hospital Universitario de Bellvitge - IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain. 5. Department of Cardiology, Hospital Universitario Central de Asturias, Oviedo, Spain. 6. Department of Cardiology, Hospital Clínico Universitario Virgen de la Arrixaca, IMIB-Arrixaca, CIBER-CV, Murcia, Spain. 7. Department of Cardiology, Hospital Universitario La Paz, IDIPAZ, CIBER-CV, Madrid, Spain.
Abstract
INTRODUCTION: There is compelling evidence supporting the association between high on-treatment platelet reactivity (HPR) and low on-treatment platelet reactivity (LPR) to clopidogrel with atherothrombotic and bleeding events, respectively. However, it is uncertain if current cutoff values should be used in prasugrel- or ticagrelor-treated subjects. The objective of this analysis was to evaluate the pharmacodynamic (PD) efficacy of P2Y12 antagonists in a contemporary real-world population. MATERIALS AND METHODS: This PD study included 988 patients with acute coronary syndromes (ACS) undergoing percutaneous coronary intervention (PCI) and receiving dual therapy with aspirin and a P2Y12 inhibitor (clopidogrel, prasugrel or ticagrelor). Platelet function was assessed at day 1 and day 30 post-PCI by VerifyNow P2Y12 assay, multiple electrode aggregometry and vasodilator-stimulated phosphoprotein (VASP) assay. RESULTS: Clopidogrel-treated patients (n = 324) had greater platelet reactivity than those receiving ticagrelor (n = 469) or prasugrel (n = 195) at both time points (p < 0.001 for all comparisons). No difference between ticagrelor and prasugrel was observed at day 1 with the VerifyNow P2Y12 assay (51.5 ± 2.8 vs. 42.7 ± 3.5 PRUs; p = 0.298), whereas ticagrelor achieved greater platelet inhibition at day 30 (48.1 ± 2.5 vs. 89.2 ± 4.2 PRUs; p < 0.001). Similar results were obtained with the VASP assay. Both prasugrel and ticagrelor had markedly lower HPR rates than clopidogrel and very high rates of LPR at both time points. CONCLUSIONS: Prasugrel and ticagrelor displayed more potent and consistent PD effects than clopidogrel in ACS patients undergoing PCI, with a trend towards greater platelet inhibition with ticagrelor during the maintenance phase of therapy compared to prasugrel.
INTRODUCTION: There is compelling evidence supporting the association between high on-treatment platelet reactivity (HPR) and low on-treatment platelet reactivity (LPR) to clopidogrel with atherothrombotic and bleeding events, respectively. However, it is uncertain if current cutoff values should be used in prasugrel- or ticagrelor-treated subjects. The objective of this analysis was to evaluate the pharmacodynamic (PD) efficacy of P2Y12 antagonists in a contemporary real-world population. MATERIALS AND METHODS: This PD study included 988 patients with acute coronary syndromes (ACS) undergoing percutaneous coronary intervention (PCI) and receiving dual therapy with aspirin and a P2Y12 inhibitor (clopidogrel, prasugrel or ticagrelor). Platelet function was assessed at day 1 and day 30 post-PCI by VerifyNow P2Y12 assay, multiple electrode aggregometry and vasodilator-stimulated phosphoprotein (VASP) assay. RESULTS:Clopidogrel-treated patients (n = 324) had greater platelet reactivity than those receiving ticagrelor (n = 469) or prasugrel (n = 195) at both time points (p < 0.001 for all comparisons). No difference between ticagrelor and prasugrel was observed at day 1 with the VerifyNow P2Y12 assay (51.5 ± 2.8 vs. 42.7 ± 3.5 PRUs; p = 0.298), whereas ticagrelor achieved greater platelet inhibition at day 30 (48.1 ± 2.5 vs. 89.2 ± 4.2 PRUs; p < 0.001). Similar results were obtained with the VASP assay. Both prasugrel and ticagrelor had markedly lower HPR rates than clopidogrel and very high rates of LPR at both time points. CONCLUSIONS:Prasugrel and ticagrelor displayed more potent and consistent PD effects than clopidogrel in ACS patients undergoing PCI, with a trend towards greater platelet inhibition with ticagrelor during the maintenance phase of therapy compared to prasugrel.
Authors: David Vivas; Vanessa Roldán; María Asunción Esteve-Pastor; Inmaculada Roldán; Antonio Tello-Montoliu; Juan Miguel Ruiz-Nodar; Juan Cosín-Sales; José María Gámez; Luciano Consuegra; José Luis Ferreiro; Francisco Marín Journal: Rev Esp Cardiol Date: 2020-04-22 Impact factor: 4.753
Authors: Abdullah Al-Abcha; Yasser Radwan; Danielle Blais; Ernest L Mazzaferri; Konstantinos Dean Boudoulas; Essa M Essa; Richard J Gumina Journal: Front Cardiovasc Med Date: 2022-03-23
Authors: David Vivas; Vanessa Roldán; María Asunción Esteve-Pastor; Inmaculada Roldán; Antonio Tello-Montoliu; Juan Miguel Ruiz-Nodar; Juan Cosín-Sales; José María Gámez; Luciano Consuegra; José Luis Ferreiro; Francisco Marín Journal: Rev Esp Cardiol (Engl Ed) Date: 2020-06-19