title: [Extent of platelet aggregation inhibition and clinical events: new evidence with prasugrel].
abstract: Clopidogrel in combination with aspirin is the recommended standard of care for reducing the occurrence of cardiovascular events in patients presenting with acute coronary syndromes; these protective effects of clopidogrel have been shown both in patients undergoing percutaneous coronary intervention (PCI) and in those treated with medical therapy alone. However, significant shortcomings still exist, including a delayed onset of action in platelet inhibition, individual response variability (with some patients being frankly hyporesponsive), and a prolonged time to recovery of platelet function following cessation of treatment. Among these, clopidogrel hyporesponsiveness seems to be particularly important, as a growing body of evidence suggests that residual platelet reactivity on clopidogrel is associated with a significant increase in the risk of developing adverse clinical events. Prasugrel is a novel, third-generation oral thienopyridine that is a specific, irreversible antagonist of the platelet adenosine 5'-diphosphate P2Y12 receptor. Prasugrel has more potent antiplatelet activity, faster onset of action, and less interpatient variability as compared to clopidogrel. These pharmacodynamic properties led prasugrel to be more effective in preventing ischemic events in patients with acute coronary syndromes undergoing PCI in the setting of the recent TRITON-TIMI 38 study. However, the greater protective effects toward ischemic events were partially counterbalanced by an increased risk of bleeding, particularly in patients with history of transient ischemic attack/stroke, in those with body weight <60 kg and in those older than 74 years. A favorable net clinical benefit of prasugrel compared with clopidogrel has been shown.
authors.affiliation: Clinica Medica I, Cardiologia San Luca, AOU Careggi, Firenze.
authors.forename: Rosanna
authors.initials: R
authors.lastname: Abbate
authors.forename: Filippo
authors.initials: F
authors.lastname: Crea
authors.forename: Stefano
authors.initials: S
authors.lastname: De Servi
authors.forename: Erica
authors.initials: E
authors.lastname: Filippi
authors.forename: Gian Franco
authors.initials: GF
authors.lastname: Gensini
authors.forename: Paolo
authors.initials: P
authors.lastname: Golinos
authors.forename: Stefano
authors.initials: S
authors.lastname: Savonitto
mesh_terms: D054058:Acute Coronary Syndrome / Q000188:drug therapy* / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary; D002986:Clinical Trials as Topic; D000077144:Clopidogrel; D004359:Drug Therapy, Combination; D006801:Humans; D010879:Piperazines / Q000494:pharmacology / Q000627:therapeutic use*; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D000068799:Prasugrel Hydrochloride; 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; D013876:Thiophenes; D000077144:Clopidogrel; D000068799:Prasugrel Hydrochloride; D013988:Ticlopidine