title: Impact of clopidogrel response on the clinical evolution in patients with acute coronary syndromes.
abstract: OBJECTIVE
  the purpose of the present study was to determine the relationship between the Clopidogrel genetic response (based on laboratory specific tests) and the worse evolution of the patients with acute coronary syndromes.
  
  
  METHODS
  The study included 80 patients (11 females and 69 males), aged between 45 - 85 years, admitted in the 1st Department of Cardiology, between January June 2012, diagnosed with acute coronary syndromes (especially unstable angina). All the patients received Clopidogrel as antiplatelet agent, in some cases associated with aspirin. The diagnosis of acute coronary syndrome was based on clinical, ECG, echocardiographic and enzymatic signs. All the patients accepted to be included in the present study and signed a consent formulary. The Clopidogrel resistance was determined by specific genetic laboratory tests.
  
  
  CONCLUSIONS
  Of 80 cases, 4 patients were identified as normal responders (5%), 3 patients were low responders (3.75%), 58 patients were high responders (72.5%) and 15 patients were unpredictable (18.75%). In the high responders' group a lot of hemorrhagic disorders in different territories were identified. Normal responders had a good evolution. In patients with low response and unpredictable status the recurrence of angina and left ventricular failure as complications were frequent.
  
  
  CONCLUSIONS
  The present study allowed a positive correlation between the haemorrhagic events and the high responder status to Clopidogrel. Low responder patients or those with an unpredictable phenotype had a worse evolution caused by the recurrence of angina or left ventricular failure.
authors.affiliation: University of Medicine and Pharmacy Grigore T Popa Iasi, Faculty of Medicine.
authors.forename: Irina Iuliana
authors.initials: II
authors.lastname: Costache
authors.forename: Cristina
authors.initials: C
authors.lastname: Rusu
authors.forename: I
authors.initials: I
authors.lastname: Ivanov
authors.forename: Roxana
authors.initials: R
authors.lastname: Popescu
authors.forename: A
authors.initials: A
authors.lastname: Petriş
mesh_terms: D054058:Acute Coronary Syndrome / Q000175:diagnosis / Q000188:drug therapy* / Q000235:genetics; D000368:Aged; D000369:Aged, 80 and over; D000483:Alleles; D001189:Aryl Hydrocarbon Hydroxylases / Q000235:genetics*; D001241:Aspirin / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D000077144:Clopidogrel; D065731:Cytochrome P-450 CYP2C19; D004359:Drug Therapy, Combination; D005260:Female; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D011110:Polymorphism, Genetic; D012008:Recurrence; D012307:Risk Factors; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D017211:Treatment Failure; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D010975:Platelet Aggregation Inhibitors; D000077144:Clopidogrel; D001189:Aryl Hydrocarbon Hydroxylases; C045793:CYP2C19 protein, human; D065731:Cytochrome P-450 CYP2C19; D013988:Ticlopidine; D001241:Aspirin