title: Residual platelet activity is increased in clopidogrel- and ASA-treated patients with coronary stenting for acute coronary syndromes compared with stable coronary artery disease.
abstract: OBJECTIVE
  To evaluate residual platelet activity in a consecutive cohort of patients treated with dual antiplatelet therapy after coronary stent implantation
  
  
  METHODS
  Prospective single-centre cohort study.
  
  
  METHODS
  University hospital in Germany.
  
  
  METHODS
  480 patients with symptomatic coronary artery disease (n = 221 (46%) or acute coronary syndrome (ACS; n = 259 (54%) stable angina) were studied. Platelet activity was measured by collagen- (5 microg/ml) and adenosine diphosphate- (ADP; 20 micromol/l) induced platelet aggregation to assess post-treatment activity in patients treated with acetylsalicylic acid (500 mg bolus intravenously followed by 100 mg once a day) and clopidogrel (600 mg loading dose followed by 75 mg once a day)
  
  
  METHODS
  Increased residual platelet activity (IRPA) was defined if platelet aggregation was in the upper tertile of values in the patient collective. Association of epidemiological factors with IRPA was evaluated in a multivariate logistic regression analysis.
  
  
  RESULTS
  IRPA-ADP was found in 53 patients (11.0%) and IRPA-collagen in 42 patients (8.8%). ACS was associated with IRPA independently from other factors (for IRPA-collagen: odds ratio (OR) = 2.3, 95% confidence interval (CI) 1.2 to 4.5, p<0.05; for IRPA-ADP: OR = 2.4; 95% CI 1.3 to 4.4, p<0.01; for IRPA-ADP/collagen: OR = 4.5, 95% CI 1.2 to 16.9, p<0.05).
  
  
  CONCLUSIONS
  The data suggest that ACS is independently associated with IRPA despite conventional antiplatelet therapy. Further studies are warranted to demonstrate the effects of intensified antiplatelet therapy for patients with acute coronary events.
authors.affiliation: Medizinische Klinik III, Universitätsklinikum Tübingen, Eberhard Karls-Universität Tübingen, Germany.
authors.forename: T
authors.initials: T
authors.lastname: Geisler
authors.forename: M
authors.initials: M
authors.lastname: Kapp
authors.forename: K
authors.initials: K
authors.lastname: Göhring-Frischholz
authors.forename: K
authors.initials: K
authors.lastname: Daub
authors.forename: C
authors.initials: C
authors.lastname: Dösch
authors.forename: B
authors.initials: B
authors.lastname: Bigalke
authors.forename: H
authors.initials: H
authors.lastname: Langer
authors.forename: C
authors.initials: C
authors.lastname: Herdeg
authors.forename: M
authors.initials: M
authors.lastname: Gawaz
mesh_terms: D054058:Acute Coronary Syndrome / Q000188:drug therapy* / Q000503:physiopathology; D000368:Aged; D001241:Aspirin / Q000008:administration & dosage; D000077144:Clopidogrel; D015331:Cohort Studies; D003324:Coronary Artery Disease / Q000188:drug therapy* / Q000503:physiopathology; D003328:Coronary Thrombosis / Q000150:complications*; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D008297:Male; D015539:Platelet Activation / Q000187:drug effects* / Q000502:physiology; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000097:blood / Q000627:therapeutic use*; D011446:Prospective Studies; D012307:Risk Factors; D015607:Stents; D013988:Ticlopidine / Q000008:administration & dosage / Q000031:analogs & derivatives; D016896:Treatment Outcome
chemical_list: D010975:Platelet Aggregation Inhibitors; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin