title: Efficacy of Change to New P2Y12 Receptor Antagonists in Patients High on Treatment Platelet Reactivity Undergoing Percutaneous Coronary Intervention.
abstract: Selective intensification of platelet inhibition may improve high on treatment platelet reactivity (HPR). We evaluated the efficacy of dual-antiplatelet therapy, including clopidogrel (CPG), compared to new P2Y12-receptor antagonists in patients with HPR undergoing percutaneous coronary intervention, regarding the outcome of composite major adverse cardiac events (MACEs, including death, acute coronary syndrome [ACS], and stent restenosis). The presence of HPR (71 of 181 patients) almost doubled the risk of MACEs. The new antiplatelet agent reduced MACEs (45.8%, 26%, and 16.7% for CPG, prasugrel, and ticagrelor [TGL]; RR 0.36; 0.13-0.98, P = .03, TGL), specifically in patients with ACS. Failure to reduce HPR after the antiplatelet change and diabetes were independent predictors for MACEs. The HPR was early and effectively reduced after changing the antiplatelet therapy, but the intensity of this reduction did not significantly decrease the risk of MACEs. These findings support the benefit of HPR-guided intensification of platelet inhibition. Whether the intensity of this reduction improves the patient's clinical outcomes deserves further investigation.
authors.affiliation: Servicio de Hemodinamia, Departamento de Cardiologíay, Centro Médico Nacional "20 de Noviembre" ISSSTE, Mexico City, Mexico rogelio_robledo@hotmail.com.
authors.forename: Rogelio
authors.initials: R
authors.lastname: Robledo-Nolasco
authors.affiliation: Servicio de Hemodinamia, Departamento de Cardiologíay, Centro Médico Nacional "20 de Noviembre" ISSSTE, Mexico City, Mexico.
authors.forename: A
authors.initials: A
authors.lastname: Godínez-Montes de Oca
authors.affiliation: Servicio de Hemodinamia, Departamento de Cardiologíay, Centro Médico Nacional "20 de Noviembre" ISSSTE, Mexico City, Mexico.
authors.forename: J F
authors.initials: JF
authors.lastname: Zaballa-Contreras
authors.affiliation: División de Investigación Biomédica y Clínica, Centro Médico Nacional "20 de Noviembre" ISSSTE, Mexico City, Mexico Clinical Research Unit, Hospital General de Ticomán and Mexican Group for Basic and Clinical Research in Internal Medicine, Mexico City, Mexico.
authors.forename: J A
authors.initials: JA
authors.lastname: Suárez-Cuenca
authors.affiliation: División de Investigación Biomédica y Clínica, Centro Médico Nacional "20 de Noviembre" ISSSTE, Mexico City, Mexico.
authors.forename: P
authors.initials: P
authors.lastname: Mondragón-Terán
authors.affiliation: Clinical Research Unit, Hospital General de Ticomán and Mexican Group for Basic and Clinical Research in Internal Medicine, Mexico City, Mexico.
authors.forename: A F
authors.initials: AF
authors.lastname: Rubio-Guerra
authors.affiliation: Servicio de Hemodinamia, Departamento de Cardiologíay, Centro Médico Nacional "20 de Noviembre" ISSSTE, Mexico City, Mexico.
authors.forename: M A
authors.initials: MA
authors.lastname: Meléndez-Alcántara
mesh_terms: D000368:Aged; D000077144:Clopidogrel; D005260:Female; D006331:Heart Diseases / Q000517:prevention & control*; D006801:Humans; D008297:Male; D008875:Middle Aged; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects*; D000068799:Prasugrel Hydrochloride / Q000008:administration & dosage*; D058925:Receptors, Purinergic P2Y12; D013988:Ticlopidine / Q000008:administration & dosage / Q000031:analogs & derivatives*
chemical_list: C548576:P2RY12 protein, human; D058925:Receptors, Purinergic P2Y12; D000077144:Clopidogrel; D000068799:Prasugrel Hydrochloride; D013988:Ticlopidine
keywords: acute coronary syndromes; antiplatelet drugs; in vitro platelet function; platelet function; platelet inhibitors; thrombosis prophylaxis