title: Severe left ventricular systolic dysfunction is independently associated with high on-clopidogrel platelet reactivity.
abstract: OBJECTIVE
  The purpose of the present study was to investigate the association between left ventricular systolic function and the response to clopidogrel.
  
  
  METHODS
  The efficacy of clopidogrel was measured by the vasodilator-stimulated phosphoprotein phosphorylation 20 ± 4 h after 600 mg of clopidogrel. High on-clopidogrel platelet reactivity (HCPR) was defined as a platelet reactivity index (PRI) ≥50%. The 30-day combined incidence of death, non-fatal acute coronary syndrome, re-percutaneous coronary intervention (PCI), stent thrombosis, and stroke was also investigated.
  
  
  RESULTS
  The study group consisted of 519 patients undergoing PCI. The values (mean and 95% confidence interval) of the PRI were as follows: 40.4% (37.8-43.0) in patients with left ventricular ejection fraction (LVEF) >50%, 42.4% (39.3-45.6) in patients with LVEF 35-50%, and 46.7% (40.6-52.9) in patients with LVEF <35% (p = 0.013). The proportions of patients with HCPR were 35.9% in patients with LVEF ≥35 and 51.9% in patients with LVEF <35% (p = 0.022). After adjustment for variables that significantly influenced clopidogrel efficacy, LVEF <35% was found to be independently associated with HCPR (p = 0.039). The 30-day combined clinical endpoint occurred in 18% of patients with LVEF <35% and in 7.3% of patients with LVEF ≥35% (p = 0.026). The 30-day incidence of all-cause mortality was 14% in patients with LVEF <35 and 1.0% in patients with LVEF ≥35% (p < 0.001).
  
  
  CONCLUSIONS
  An LVEF <35% was found to be independently associated with HCPR.
authors.affiliation: Third Medical Faculty of Charles Univ. and Univ. Hospital Kralovske Vinohrady, Srobarova 50, 100 34, Prague, Czech Republic, motovska.zuzana@gmail.com.
authors.forename: Zuzana
authors.initials: Z
authors.lastname: Motovska
authors.forename: Martina
authors.initials: M
authors.lastname: Ondrakova
authors.forename: Magdalena
authors.initials: M
authors.lastname: Doktorova
authors.forename: Petr
authors.initials: P
authors.lastname: Widimsky
mesh_terms: D054058:Acute Coronary Syndrome / Q000453:epidemiology; D000368:Aged; D001792:Blood Platelets / Q000378:metabolism*; D015815:Cell Adhesion Molecules / Q000378:metabolism; D000077144:Clopidogrel; D005260:Female; D006801:Humans; D008297:Male; D008840:Microfilament Proteins / Q000378:metabolism; D008875:Middle Aged; D062645:Percutaneous Coronary Intervention; D010750:Phosphoproteins / Q000378:metabolism; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D012189:Retrospective Studies; D015607:Stents; D020521:Stroke / Q000453:epidemiology; D013318:Stroke Volume; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy* / Q000453:epidemiology / Q000503:physiopathology; D000098662:Vasodilator-Stimulated Phosphoprotein
chemical_list: D015815:Cell Adhesion Molecules; D008840:Microfilament Proteins; D010750:Phosphoproteins; D010975:Platelet Aggregation Inhibitors; D000098662:Vasodilator-Stimulated Phosphoprotein; D000077144:Clopidogrel; D013988:Ticlopidine