title: Double-blind, randomized, prospective comparison of loading doses of 600 mg clopidogrel versus 60 mg prasugrel in patients with acute ST-segment elevation myocardial infarction scheduled for primary percutaneous intervention: the ETAMI trial (early thienopyridine treatment to improve primary PCI in patients with acute myocardial infarction).
abstract: OBJECTIVE
  This study compared the timing of onset of antiplatelet action after treatment with clopidogrel and prasugrel at first medical contact in patients with ST-segment elevation myocardial infarction (STEMI) scheduled for primary percutaneous coronary intervention (PPCI).
  
  
  BACKGROUND
  Little is known about the timing of onset of antiplatelet action after a pre-percutaneous coronary intervention (PCI) loading dose of clopidogrel or prasugrel in patients with STEMI.
  
  
  METHODS
  This double-blind, prospective study randomized 62 patients with STEMI scheduled for PPCI in the ambulance or the emergency department to 60 mg prasugrel (n = 31) or 600 mg clopidogrel (n = 31). The primary endpoint was the platelet reactivity index (PRI) measured with the vasodilator-stimulated phosphoprotein assay 2 h after intake of the study medication. Secondary endpoints were PRI after 4 h, TIMI (Thrombolysis In Myocardial Infarction) patency of the infarct-related artery before and after PCI, and clinical events until day 30.
  
  
  RESULTS
  The PRI after 2 h (50.4 ± 32.7% vs. 66.3 ± 22.2%; p = 0.035) and after 4 h (39.1 ± 27.5% vs. 54.5 ± 49.3%; p = 0.038) were significantly lower with prasugrel compared with clopidogrel. In addition, the rate of patients with a PRI <50% tended to be higher with prasugrel compared with clopidogrel after 2 h (46.7% vs. 28.6%; p = 0.15) and after 4 h (63.0% vs. 38.9%; p = 0.06). There were no significant differences in TIMI 2/3 patency before PCI (39.2% vs. 31.0%; p = 0.43) and TIMI 3 patency after PCI (88.5% vs. 89.3%; p = 0.92).
  
  
  CONCLUSIONS
  The pre-PCI administration of prasugrel in patients with STEMI undergoing PPCI was associated with a significant faster platelet inhibition compared with clopidogrel. Therefore, prasugrel should be preferred to clopidogrel in this setting. (ETAMI-Study: Early Thienopyridine Treatment to Improve Primary PCI in Patients With Acute Myocardial Infarction; NCT01327534).
authors.affiliation: Klinikum Ludwigshafen and Institut für Herzinfarkt für Herzinfarktforschung, Ludwigshafen, Germany. Electronic address: zeymeru@klilu.de.
authors.forename: Uwe
authors.initials: U
authors.lastname: Zeymer
authors.affiliation: Charite Campus Benjamin Franklin, Berlin, Germany.
authors.forename: Hans-Christian
authors.initials: HC
authors.lastname: Mochmann
authors.affiliation: Klinikum Ludwigshafen, Ludwigshafen, Germany.
authors.forename: Bernd
authors.initials: B
authors.lastname: Mark
authors.affiliation: Charite Campus Benjamin Franklin, Berlin, Germany.
authors.forename: Hans-Richard
authors.initials: HR
authors.lastname: Arntz
authors.affiliation: Universitätsklinikum Schleswig-Holstein, Lübeck, Germany.
authors.forename: Holger
authors.initials: H
authors.lastname: Thiele
authors.affiliation: Institut für Herzinfartktforschung, Ludwigshafen, Germany.
authors.forename: Frank
authors.initials: F
authors.lastname: Diller
authors.affiliation: Centre Hospitalier Universitaire Pitié-Salpêtriėre, INSERM UMRS 1166, Paris, France.
authors.forename: Gilles
authors.initials: G
authors.lastname: Montalescot
authors.affiliation: Klinikum Ludwigshafen, Ludwigshafen, Germany.
authors.forename: Ralf
authors.initials: R
authors.lastname: Zahn
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000097:blood; D000077144:Clopidogrel; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology; D004311:Double-Blind Method; D004334:Drug Administration Schedule; D005260:Female; D006801:Humans; D008297:Male; D008840:Microfilament Proteins / Q000097:blood; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000175:diagnosis / Q000401:mortality / Q000628:therapy*; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects; D010750:Phosphoproteins / Q000097:blood; D010879:Piperazines / Q000008:administration & dosage* / Q000009:adverse effects; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage* / Q000009:adverse effects; D010979:Platelet Function Tests; D000068799:Prasugrel Hydrochloride; D011446:Prospective Studies; D013876:Thiophenes / Q000008:administration & dosage* / Q000009:adverse effects; D013988:Ticlopidine / Q000008:administration & dosage / Q000009:adverse effects / Q000031:analogs & derivatives*; D013997:Time Factors; D016896:Treatment Outcome; D014654:Vascular Patency / Q000187:drug effects; D000098662:Vasodilator-Stimulated Phosphoprotein
chemical_list: D015415:Biomarkers; D015815:Cell Adhesion Molecules; D008840:Microfilament Proteins; D010750:Phosphoproteins; D010879:Piperazines; D010975:Platelet Aggregation Inhibitors; D013876:Thiophenes; D000098662:Vasodilator-Stimulated Phosphoprotein; D000077144:Clopidogrel; D000068799:Prasugrel Hydrochloride; D013988:Ticlopidine
keywords: ADP receptor inhibitors; clopidogrel; inhibition of platelet aggregation; prasugrel; primary percutaneous coronary intervention