title: Is a 300 mg clopidogrel loading dose sufficient to inhibit platelet function early after coronary stenting? A platelet function profile study.
abstract: BACKGROUND
  Clopidogrel combined to aspirin reduces the early risk of stent thrombosis and a clopidogrel pre-treatment strategy is associated with a better outcome. However, in clinical practice such pre-treatment strategy is not always feasible and clopidogrel is frequently not administered until the time of intervention. Aim of the study was to compare platelet function profiles in patients undergoing coronary stenting receiving clopidogrel pre-treatment (75 mg x 2 daily at least 48 hours before intervention) compared to that of patients receiving a 300 mg loading dose at intervention time.
  
  
  METHODS
  A total of 50 patients were included in whom patients' platelet aggregation (using light transmittance aggregometry) and platelet activation (P-selectin and PAC-1 expression by whole blood flow cytometry) were assessed following ADP stimuli at baseline, and 4 hours and 24 hours following coronary stenting.
  
  
  RESULTS
  In the overall study population, 16/50 (32%) patients were pre-treated with clopidogrel and 34/50 (68%) received clopidogrel loading dose at intervention time. Platelet aggregation, as well as P-selectin and PAC-1 expression were significantly lower in clopidogrel pre-treated patients at baseline (p<0.001) and at 4 hours (p<0.01), while they were similarly inhibited 24 hours after intervention. In conclusion, platelet reactivity of patients treated with clopidogrel front loading at intervention time remains significantly higher than that of pre-treated patients in the early hours after coronary stenting. A higher loading dose at intervention time may be warranted to overcome the early risk of thrombotic complications.
authors.affiliation: Interventional Cardiology Unit-Cardiovascular Institute, San Carlos University Hospital, Madrid, Spain. dominickjangiolillo@hotmail.com
authors.forename: Dominick J
authors.initials: DJ
authors.lastname: Angiolillo
authors.forename: Antonio
authors.initials: A
authors.lastname: Fernandez-Ortiz
authors.forename: Esther
authors.initials: E
authors.lastname: Bernardo
authors.forename: Celia
authors.initials: C
authors.lastname: Ramírez
authors.forename: Manel
authors.initials: M
authors.lastname: Sabaté
authors.forename: Rosana
authors.initials: R
authors.lastname: Hernández-Antolín
authors.forename: Raul
authors.initials: R
authors.lastname: Moreno
authors.forename: Javier
authors.initials: J
authors.lastname: Escaned
authors.forename: Fernando
authors.initials: F
authors.lastname: Alfonso
authors.forename: Camino
authors.initials: C
authors.lastname: Bañuelos
authors.forename: Carlos
authors.initials: C
authors.lastname: Macaya
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology; D000077144:Clopidogrel; D003331:Coronary Vessels; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D005434:Flow Cytometry; D006801:Humans; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood; D015539:Platelet Activation / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage*; D010976:Platelet Count; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000032:analysis; D011292:Premedication; D015607:Stents / Q000009:adverse effects*; D013927:Thrombosis / Q000517:prevention & control*; D013988:Ticlopidine / Q000008:administration & dosage* / Q000031:analogs & derivatives*; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D019007:P-Selectin; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D014841:von Willebrand Factor; D000244:Adenosine Diphosphate; D005340:Fibrinogen; D000077144:Clopidogrel; D013988:Ticlopidine