title: Detection of clopidogrel resistance using ADP induced aggregometry with specific inhibitor PGE1.
abstract: BACKGROUND
  Antiaggregation therapy is still the most frequently used approach to prevent thrombotic events in cardiovascular diseases. It has a good clinical effect but increasing evidence shows high residual platelet aggregation activity in a number of patients. Laboratory methods only allow us to detect clopidogrel "non-responders" or "low responders". Recent methods are based on monitoring residual platelet aggregation activity (aggregation methods) or detecting the number of free epitopes for binding a specific monoclonal antibody such as vasodilator-stimulated phosphoprotein phosphorylation (VASP).
  
  
  METHODS
  The aims of our study were comparison light transmission aggregometry (LTA) and multiple electrode platelet aggregometry (MEA) with induction by ADP in concentrations of 20 micromol/L with or without prostaglandin E1 (PGE1) for monitoring clopidogrel resistance.
  
  
  RESULTS
  In the group of 84 patients with cardiovascular disease (CAD) studied, an impaired individual response to clopidogrel therapy was found 11.9% and 10.7% of the patients using MEA and LTA, respectively, induced by ADP with PGE1. The LTA and MEA methods with induction by ADP with PGE1 and without PGE1 were statistically compared using Spearman's nonparametric correlation analysis. Both methods with using PGE, showed a positive significant correlation (p = 0.003) in contrast with the results without PGE1 with a no significant correlation (p = 0.732).
  
  
  CONCLUSIONS
  The sensitivity for detecting clopidogrel resistance correlates well with other data in the literature suggesting that there are 5%-30% clopidogrel low-responders depending on the type of platelet function assay used and the criteria for defining a low-responder [16-18]. These results favor implementation of the ADP test with PGE1 by MEA specifically for identification of low-responders to clopidogrel.
authors.forename: L
authors.initials: L
authors.lastname: Slavik
authors.forename: J
authors.initials: J
authors.lastname: Ulehlova
authors.forename: V
authors.initials: V
authors.lastname: Krcova
authors.forename: A
authors.initials: A
authors.lastname: Hlusi
authors.forename: J
authors.initials: J
authors.lastname: Indrakova
authors.forename: M
authors.initials: M
authors.lastname: Hutyra
authors.forename: J
authors.initials: J
authors.lastname: Galuszka
authors.forename: K
authors.initials: K
authors.lastname: Indrak
mesh_terms: D000244:Adenosine Diphosphate; D000328:Adult; D000368:Aged; D000527:Alprostadil; D002318:Cardiovascular Diseases / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy*; D000077144:Clopidogrel; D004351:Drug Resistance; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D010979:Platelet Function Tests; D011237:Predictive Value of Tests; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D010975:Platelet Aggregation Inhibitors; D000244:Adenosine Diphosphate; D000077144:Clopidogrel; D000527:Alprostadil; D013988:Ticlopidine