title: High post-treatment platelet reactivity is associated with a high incidence of myonecrosis after stenting for non-ST elevation acute coronary syndromes.
abstract: High post-treatment platelet reactivity (HPPR=adenosine diphosphate [ADP] 10 microM-induced platelet aggregation >70%) identifies low responders to dual antiplatelet therapy with increased risk of recurrent cardiovascular (CV) events after stenting for non-ST elevation acute coronary syndromes (NSTE-ACS). This study was designed to compare the incidence of periprocedural myocardial infarction (MI) after stenting for NSTE-ACS patients between non-responders to dual antiplatelet therapy defined by HPPR and normo-responders. One hundred ninety NSTE-ACS consecutive patients undergoing coronary stenting were included in this prospective study. They received 250 mg aspirin and a 600 mg loading dose of clopidogrel at least 12 hours (h) before percutaneous coronary intervention (PCI). A single post-treatment blood sample was obtained before PCI to analyze maximal intensity of ADP-induced platelet aggregation, and troponin levels were analyzed before PCI, and 12 and 24 h after PCI. Troponin I was considered elevated if >0.4 ng/ml. HPPR was present in 22% of patients (n=42). Periprocedural MI occurred significantly more frequently in patients with HPPR than in the normo-responders (43% vs. 24%, p=0.014). After being correlated with recurrent ischemic events after stenting for NSTE-ACS, the HPPR seems to be also a marker of increased risk of periprocedural MI for NSTE-ACS patients.
authors.affiliation: Department of Cardiology, CHU Timone, Boulevard Saint Pierre, Marseille, Bouches du rhone, 13005 France. thomascuisset@voila.fr
authors.forename: Thomas
authors.initials: T
authors.lastname: Cuisset
authors.forename: Corinne
authors.initials: C
authors.lastname: Frere
authors.forename: Jacques
authors.initials: J
authors.lastname: Quilici
authors.forename: Pierre-Emmanuel
authors.initials: PE
authors.lastname: Morange
authors.forename: Lyassine
authors.initials: L
authors.lastname: Nait-Saidi
authors.forename: Christopher
authors.initials: C
authors.lastname: Mielot
authors.forename: Laurent
authors.initials: L
authors.lastname: Bali
authors.forename: Marc
authors.initials: M
authors.lastname: Lambert
authors.forename: Marie-Christine
authors.initials: MC
authors.lastname: Alessi
authors.forename: Jean-Louis
authors.initials: JL
authors.lastname: Bonnet
mesh_terms: D000208:Acute Disease; D000244:Adenosine Diphosphate; D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D001241:Aspirin / Q000494:pharmacology; D000077144:Clopidogrel; D005260:Female; D005602:France; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D017202:Myocardial Ischemia / Q000097:blood* / Q000188:drug therapy / Q000628:therapy; D016017:Odds Ratio; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D010979:Platelet Function Tests; D011237:Predictive Value of Tests; D011379:Prognosis; D011446:Prospective Studies; D012107:Research Design; D012307:Risk Factors; D015607:Stents; D013577:Syndrome; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000494:pharmacology; D013997:Time Factors; D019210:Troponin I / Q000097:blood
chemical_list: D010975:Platelet Aggregation Inhibitors; D019210:Troponin I; D000244:Adenosine Diphosphate; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin