title: Pharmacodynamic effect of prasugrel 5 mg vs clopidogrel 150 mg in elderly patients with high on-clopidogrel platelet reactivity.
abstract: BACKGROUND
  Elderly patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI) frequently exhibit high platelet reactivity (HPR) while on clopidogrel. In the elderly cohort, either prasugrel is not recommended or, if used, halving of the dose has been suggested. We aimed to test the hypothesis that in elderly patients exhibiting HPR after standard treatment with clopidogrel, prasugrel-reduced dose (5 mg) could be more effective than high-dose (150 mg) clopidogrel.
  
  
  METHODS
  Consecutive elderly (≥75 years old) patients with ACS undergoing PCI and loaded with clopidogrel were considered for platelet reactivity (PR) assessment at 24 hours after PCI with the VerifyNow assay (Accumetrics Inc, San Diego, CA), measured in P2Y12 reaction units (PRU). Of 63 screened patients, 30 (47.6%) were found with HPR (defined as PRU ≥230) and 27 of them participated in a prospective, randomized, single-center, single-blind, investigator-initiated, crossover study of platelet inhibition by prasugrel 5 mg/d vs clopidogrel 150 mg/d, with a 15-day treatment period.
  
  
  RESULTS
  The primary end point of PR at the end of the 2 study periods was lower in patients receiving low-dose prasugrel than those receiving high-dose clopidogrel (least squares estimates 190.8 [95% CI 161.5-220.1] and 240.8 [95% CI 211.0-270.6], respectively; P = .008). The secondary end point of HPR rate at the end of treatment periods was lower for prasugrel (8/24; 33.3%) compared with clopidogrel (16/24; 66.7%), P = .02.
  
  
  CONCLUSIONS
  In elderly patients with ACS undergoing PCI and exhibiting HPR after standard clopidogrel treatment, prasugrel 5 mg/d is significantly more efficacious than clopidogrel 150 mg/d in reducing PR and HPR rate.
authors.affiliation: Department of Cardiology, Patras University Hospital, Rion, Patras, Greece. dalex@med.upatras.gr
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Alexopoulos
authors.forename: Ioanna
authors.initials: I
authors.lastname: Xanthopoulou
authors.forename: Theodora-Eleni
authors.initials: TE
authors.lastname: Plakomyti
authors.forename: Konstantinos C
authors.initials: KC
authors.lastname: Theodoropoulos
authors.forename: Eleni
authors.initials: E
authors.lastname: Mavronasiou
authors.forename: Anastasia
authors.initials: A
authors.lastname: Damelou
authors.forename: George
authors.initials: G
authors.lastname: Hahalis
authors.forename: Periklis
authors.initials: P
authors.lastname: Davlouros
mesh_terms: D054058:Acute Coronary Syndrome / Q000188:drug therapy* / Q000601:surgery; D000368:Aged; D000077144:Clopidogrel; D005260:Female; D006801:Humans; D008297:Male; D062645:Percutaneous Coronary Intervention / Q000379:methods*; D010879:Piperazines / Q000009:adverse effects / Q000494:pharmacology*; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects / Q000494:pharmacology*; D010979:Platelet Function Tests; D000068799:Prasugrel Hydrochloride; D011446:Prospective Studies; D013876:Thiophenes / Q000009:adverse effects / Q000494:pharmacology*; D013988:Ticlopidine / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000494:pharmacology; D016896:Treatment Outcome
chemical_list: D010879:Piperazines; D010975:Platelet Aggregation Inhibitors; D013876:Thiophenes; D000077144:Clopidogrel; D000068799:Prasugrel Hydrochloride; D013988:Ticlopidine