title: Prasugrel monitoring and bleeding in real world patients.
abstract: The aim of this study was to evaluate platelet reactivity and 30-day bleeding events in patients treated with prasugrel 10 mg after acute coronary syndromes. A total of 444 patients with acute coronary syndromes treated with percutaneous coronary intervention and prasugrel 10 mg/day were monitored by measurement of the vasodilator-stimulated phosphoprotein (VASP) index 2 to 4 weeks after hospital discharge. Platelet reactivity was also assessed using the VerifyNow P2Y(12) assay and light transmission aggregometry. Bleeding events (per the Bleeding Academic Research Consortium [BARC] definition) and ischemic events (death, myocardial infarction, and definite stent thrombosis) were collected over 30 days of follow-up. Two thirds of the patients presented with ST-segment elevation myocardial infarctions, 28.8% had diabetes, and 12.4% were aged >75 years. High on-treatment platelet reactivity according to 3 prespecified definitions (VASP index ≥ 50%, platelet reactivity ≥ 235 P2Y(12) reaction units, and residual platelet reactivity ≥ 46.2%) was found in 6.8%, 3.4%, and 3.2% of patients, respectively. Obesity (body mass index >30 kg/m(2)) and multivessel disease were the only independent factors associated with high on-treatment platelet reactivity (p = 0.006 and p = 0.045, respectively). At 30 days, there was no major bleeding complication (BARC grade 3 or 5), and 1.6% of patients had recurrent ischemic events. Nuisance bleeding (BARC grade 1) and minor bleeding (BARC grade 2) occurred in 14.2% (n = 63) and 2.5% (n = 11) of patients, respectively, but were not predicted by VASP index. In conclusion, patients with acute coronary syndromes receiving maintenance doses of prasugrel have low rates of HPR and ischemic events within the first month. Minor or minimal bleeding is frequent, but not major bleeding. VASP was poorly correlated with the risk for minor or minimal bleeding.
authors.affiliation: Institut de Cardiologie, INSERM UMRS937, Pitié-Salpêtrière Hospital, Université Paris 6, Paris, France.
authors.forename: Guillaume
authors.initials: G
authors.lastname: Cayla
authors.forename: Thomas
authors.initials: T
authors.lastname: Cuisset
authors.forename: Johanne
authors.initials: J
authors.lastname: Silvain
authors.forename: Stephen A
authors.initials: SA
authors.lastname: O'Connor
authors.forename: Mathieu
authors.initials: M
authors.lastname: Kerneis
authors.forename: Christel
authors.initials: C
authors.lastname: Castelli
authors.forename: Jacques
authors.initials: J
authors.lastname: Quilici
authors.forename: Jean-Louis
authors.initials: JL
authors.lastname: Bonnet
authors.forename: Marie-Christine
authors.initials: MC
authors.lastname: Alessi
authors.forename: Pierre-Emmanuel
authors.initials: PE
authors.lastname: Morange
authors.forename: Jean-Philippe
authors.initials: JP
authors.lastname: Collet
authors.forename: Gilles
authors.initials: G
authors.lastname: Montalescot
mesh_terms: D054058:Acute Coronary Syndrome / Q000628:therapy*; D005260:Female; D005602:France / Q000453:epidemiology; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic / Q000379:methods*; D062645:Percutaneous Coronary Intervention; D010879:Piperazines / Q000008:administration & dosage* / Q000009:adverse effects; D010974:Platelet Aggregation / Q000187:drug effects*; D019106:Postoperative Hemorrhage / Q000097:blood* / Q000139:chemically induced / Q000453:epidemiology; D000068799:Prasugrel Hydrochloride; D011379:Prognosis; D058921:Purinergic P2Y Receptor Antagonists / Q000008:administration & dosage / Q000009:adverse effects; D013876:Thiophenes / Q000008:administration & dosage* / Q000009:adverse effects
chemical_list: D010879:Piperazines; D058921:Purinergic P2Y Receptor Antagonists; D013876:Thiophenes; D000068799:Prasugrel Hydrochloride