Regular Article Lack of association between the P2Y 12 receptor gene polymorphism and platelet response to clopidogrel in patients with coronary artery disease Dominick J. Angiolillo a, T , Antonio Fernandez-Ortiz b , Esther Bernardo b , Celia Ramı ´rez b , Ugo Cavallari c , Elisabetta Trabetti c ,ManelSabate´ b , Pilar Jimenez-Quevedo b , Rosana Herna ´ndez b , Raul Moreno b , Javier Escaned b , Fernando Alfonso b , Camino Ban ˜uelos b , Marco A. Costa a , Theodore A. Bass a , Pier Franco Pignatti c , Carlos Macaya b a Division of Cardiology, University of Florida-Shands Jacksonville, 655 West 8th Street, Jacksonville, FL 32209, United States b Cardiovascular Institute, San Carlos University Hospital, Madrid, Spain c Department of Mother and Child and Biology—Genetics, University of Verona, Verona, Italy Received 5 January 2005; received in revised form 25 February 2005; accepted 4 March 2005 Available online 20 April 2005 Abstract Introduction: Clopidogrel inhibits the ADP subtype P2Y 12 receptor. Recently, poly- morphisms of this receptor have been associated with different degrees of platelet aggregation in healthy volunteers and have been suggested to modulate clopidogrel response. However, the role of gene sequence variations of the P2Y 12 receptor in patients treated with clopidogrel has not yet been assessed. Materials and methods: The T744C polymorphism of the P2Y 12 receptor gene was assessed in 119 patients: 36 undergoing coronary stenting receiving a 300 mg loading dose (Group A) and 83 on long-term clopidogrel (75 mg/day) treatment (Group B). Patients were divided into 2 subgroups according to the presence or absence of the C allele: carriers (CT heterozygotes and CC homozygotes) and non-carriers (TT homozygotes). Platelet aggregation, assessed by light transmittance aggregometry following ADP, collagen, TRAP and epinephrine stimuli, and platelet activation (GP IIb/IIIa activation and P-selectin expression), assessed by whole blood flow 0049-3848/$ - see front matter D 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.thromres.2005.03.001 T Corresponding author. Tel.: +1 904 2443933; fax: +1 904 2443102. E-mail address: dominick.angiolillo@jax.ufl.edu (D.J. Angiolillo). KEYWORDS Clopidogrel; Polymorphism; Platelet function Thrombosis Research (2005) 116, 491 — 497 intl.elsevierhealth.com/journals/thre