title: Prasugrel versus high dose clopidogrel to overcome early high on clopidogrel platelet reactivity in patients with ST elevation myocardial infarction.
abstract: OBJECTIVE
  There is a paucity of data regarding the early effectiveness of the proposed 600 mg clopidogrel loading dose (LD) on platelet reactivity (PR) in ST elevation myocardial infarction (STEMI) patients. If high on-treatment platelet reactivity (HTPR) is present, prasugrel reloading and subsequent maintenance dose (MD), might offer faster and stronger platelet inhibition than high clopidogrel MD.
  
  
  METHODS
  In 93 STEMI patients treated by primary percutaneous coronary intervention we assessed PR using the VerifyNow P2Y12 platelet function test, 2 h following 600 mg LD of clopidogrel. All the 60 (64.5 %) patients exhibiting HTPR (defined as PR ≥ 235 P2Y12 reaction units), were randomized to 1 of 2 therapeutic strategies: reloading with prasugrel 60 mg/10 mg MD or high (150 mg) clopidogrel MD.
  
  
  RESULTS
  The primary endpoint of PR at 24 h post randomization was lower in the prasugrel compared to the clopidogrel group (51.3, 25.7-77.0 versus 242.4, 215.8-268.9 P2Y12 reaction units, least square estimates, 95 % confidence intervals, p < 0.001). PR at 2 h and 5 days post randomization was lower in the prasugrel compared to the clopidogrel group (117.2, 70.9-163.4 and 101.6, 70.1-133.2 least square mean difference, 95 % confidence intervals, p < 0.001 for both). At all the time points of PR assessment, HTPR rates were lower in prasugrel than in clopidogrel group.
  
  
  CONCLUSIONS
  HTPR is commonly observed early post 600 mg clopidogrel LD in STEMI patients. In this case, prasugrel 60 mg LD/10 mg MD provides faster and stronger platelet inhibition than a high clopidogrel MD regimen.
authors.affiliation: Department of Cardiology, Patras University Hospital, Rion, 26500, Patras, Greece. dalex@med.upatras.gr
authors.forename: D
authors.initials: D
authors.lastname: Alexopoulos
authors.forename: K C
authors.initials: KC
authors.lastname: Theodoropoulos
authors.forename: E F
authors.initials: EF
authors.lastname: Stavrou
authors.forename: I
authors.initials: I
authors.lastname: Xanthopoulou
authors.forename: G
authors.initials: G
authors.lastname: Kassimis
authors.forename: G
authors.initials: G
authors.lastname: Tsigkas
authors.forename: A
authors.initials: A
authors.lastname: Damelou
authors.forename: P
authors.initials: P
authors.lastname: Davlouros
authors.forename: G
authors.initials: G
authors.lastname: Hahalis
authors.forename: A
authors.initials: A
authors.lastname: Athanassiadou
mesh_terms: D000368:Aged; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology; D000077144:Clopidogrel; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology; D010879:Piperazines / Q000008:administration & dosage*; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage*; D000068799:Prasugrel Hydrochloride; D058921:Purinergic P2Y Receptor Antagonists / Q000008:administration & dosage*; D013876:Thiophenes / Q000008:administration & dosage*; D013988:Ticlopidine / Q000031:analogs & derivatives
chemical_list: D010879:Piperazines; D010975:Platelet Aggregation Inhibitors; D058921:Purinergic P2Y Receptor Antagonists; D013876:Thiophenes; D000077144:Clopidogrel; D000068799:Prasugrel Hydrochloride; D013988:Ticlopidine