title: Prasugrel reduces agonists' inducible platelet activation and leukocyte-platelet interaction more efficiently than clopidogrel.
abstract: OBJECTIVE
  The antiplatelet effects of clopidogrel and prasugrel have mainly been compared using different platelet reactivity tests. Further, data on the impact of both drugs on thrombin-inducible platelet activation are scarce. We therefore investigated the influence of clopidogrel and prasugrel on different flow cytometric parameters of platelet activation as well as on platelet function assessed by leukocyte-platelet interaction.
  
  
  METHODS
  Baseline, ADP and thrombin receptor-activating peptide (TRAP)-6 inducible P-selectin expression, activation of glycoprotein (GP) IIb/IIIa and monocyte-platelet aggregate (MPA) formation were determined by flow cytometry in 84 clopidogrel- and 21 prasugrel-treated patients undergoing percutaneous coronary intervention with stent implantation.
  
  
  RESULTS
  Baseline expressions of P-selectin and activated GPIIb/IIIa did not differ significantly between clopidogrel- and prasugrel-treated patients (both P > 0.2). After activation with ADP or TRAP-6, patients with clopidogrel therapy exhibited significantly higher platelet surface expressions of P-selectin and activated GPIIb/IIIa than prasugrel-treated patients (all P ≤ 0.001). Further, high P-selectin and high GPIIb/IIIa were significantly more frequent in clopidogrel-treated patients than in patients on prasugrel therapy (all P = 0.01). Likewise, the formation of MPA without addition of agonists did not differ significantly between patients receiving clopidogrel and patients on prasugrel therapy (P = 0.2). After activation with ADP or TRAP-6, clopidogrel-treated patients showed a significantly more pronounced formation of MPA than patients-receiving prasugrel (both P = 0.02).
  
  
  CONCLUSIONS
  Prasugrel reduces ADP and TRAP-6 inducible platelet activation, and leukocyte-platelet interaction more efficiently than clopidogrel.
authors: Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
authors: Thomas
authors: T
authors: Gremmel
authors: Roza Badr
authors: RB
authors: Eslam
authors: Renate
authors: R
authors: Koppensteiner
authors: Irene M
authors: IM
authors: Lang
authors: Simon
authors: S
authors: Panzer
mesh_terms: D000368:Aged; D001792:Blood Platelets / Q000187:drug effects* / Q000502:physiology; D002450:Cell Communication / Q000187:drug effects*; D000077144:Clopidogrel; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects* / Q000502:physiology; D019007:P-Selectin / Q000032:analysis; D010446:Peptide Fragments / Q000494:pharmacology; D010879:Piperazines / Q000494:pharmacology*; D015539:Platelet Activation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000502:physiology; D000068799:Prasugrel Hydrochloride; D013876:Thiophenes / Q000494:pharmacology*; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000494:pharmacology
chemical_list: D019007:P-Selectin; D010446:Peptide Fragments; D010879:Piperazines; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D013876:Thiophenes; C082835:thrombin receptor peptide (42-47); D000077144:Clopidogrel; D000068799:Prasugrel Hydrochloride; D013988:Ticlopidine
keywords: Clopidogrel; monocyte-platelet aggregates; platelet activation; prasugrel