title: A randomized trial of platelet reactivity monitoring-adjusted clopidogrel therapy versus prasugrel therapy to reduce high on-treatment platelet reactivity.
abstract: BACKGROUND
  Peri-procedural platelet reactivity (PR) inhibition is critical in patients undergoing percutaneous coronary intervention (PCI). High on-treatment PR (HTPR) was associated with recurrent ischemic events in acute coronary syndrome (ACS) patients undergoing PCI. We aimed to compare a strategy of clopidogrel loading dose-adjustment (CDA) according to PR monitoring with standard prasugrel therapy to reduce the rate of patients exhibiting HTPR.
  
  
  METHODS
  We enrolled 177 ACS patients in a prospective multicentre randomized trial comparing CDA according to PR monitoring and prasugrel therapy. The VASP index was used to measure PR and a VASP ≥ 50% defined HTPR. The primary endpoint of the study was the rate of HTPR on discharge.
  
  
  RESULTS
  Baseline characteristics of the CDA group (n = 88) and of the prasugrel group (n = 89) were similar. CDA significantly reduced PR and the rate of HTPR compared to a single LD of clopidogrel (30.9 ± 13.9%; p < 0.0001 and 43 to 2.3%; p < 0.001, respectively). Following CDA the rate of patients with HTPR was significantly lower in the CDA group compared to the prasugrel group on discharge (2.3 vs 15.7%; p = 0.005). In addition fewer patients in the CDA group had a VASP < 16% on discharge (14.7 vs 50.5%; p <0.0001).
  
  
  CONCLUSIONS
  In the present study, PR monitoring was superior to standard prasugrel therapy to reduce the rate of HTPR in ACS patients. In addition such strategy reduced the number of patients with very low PR.
authors.affiliation: Département de cardiologie, Hôpital universitaire nord, Aix-Marseille Univ., Marseille, France; INSERM UMRS 608, UFR de pharmacie, Marseille, France. Electronic address: laurentbonello@yahoo.fr.
authors.forename: Laurent
authors.initials: L
authors.lastname: Bonello
authors.forename: Marc
authors.initials: M
authors.lastname: Laine
authors.forename: Karine
authors.initials: K
authors.lastname: Baumstarck
authors.forename: Jessica
authors.initials: J
authors.lastname: Fernandez
authors.forename: Luc
authors.initials: L
authors.lastname: Maillard
authors.forename: Michael
authors.initials: M
authors.lastname: Peyrol
authors.forename: Jacques
authors.initials: J
authors.lastname: Bessereau
authors.forename: Daniel
authors.initials: D
authors.lastname: Aradi
authors.forename: Elise
authors.initials: E
authors.lastname: Camilleri
authors.forename: François
authors.initials: F
authors.lastname: Roubille
authors.forename: Christophe
authors.initials: C
authors.lastname: Piot
authors.forename: Franck
authors.initials: F
authors.lastname: Paganelli
authors.forename: Laurence
authors.initials: L
authors.lastname: Camoin-Jau
authors.forename: Françoise
authors.initials: F
authors.lastname: Dignat-George
mesh_terms: D000368:Aged; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism; D000077144:Clopidogrel; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D010879:Piperazines / Q000494:pharmacology / Q000627:therapeutic use*; D015539:Platelet Activation / Q000187:drug effects* / Q000502:physiology*; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D000068799:Prasugrel Hydrochloride; D011446:Prospective Studies; D058921:Purinergic P2Y Receptor Antagonists / Q000494:pharmacology / Q000627:therapeutic use*; D016037:Single-Blind Method; D013876:Thiophenes / Q000494:pharmacology / Q000627:therapeutic use*; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D010879:Piperazines; D010975:Platelet Aggregation Inhibitors; D058921:Purinergic P2Y Receptor Antagonists; D013876:Thiophenes; D000077144:Clopidogrel; D000068799:Prasugrel Hydrochloride; D013988:Ticlopidine
keywords: Acute coronary syndrome; Bleeding; Platelet reactivity monitoring; Stent thrombosis; VASP