title: Prognostic significance of platelet function in the early phase of ST-elevation myocardial infarction treated with primary angioplasty.
abstract: BACKGROUND
  There are limited data concerning global platelet function response to antiplatelet therapy in ST-segment elevation myocardial infarction (STEMI). The aim was to determine the frequency and clinical significance of inadequate inhibition of two major platelet activation pathways: the thromboxane A2 (TXA2)- and ADP-dependent, in the early phase of STEMI.
  
  
  METHODS
  Platelet function was measured with a Platelet Function Analyzer-100 in 125 consecutive survivors of STEMI on days 3 (48+/-2 h) and 30 after stenting. Inadequate inhibition of the TXA2-dependent activation pathway was defined as a collagen-epinephrine closure time <193 and of the ADP-dependent as a collagen-adenosine closure time <130 seconds.
  
  
  RESULTS
  The study population was divided into groups I (n=67/53%; both pathways inhibited, complete inhibition), II (n=21/17%; one pathway inhibited, partial inhibition), and III (n=37/30%; neither pathway inhibited, no inhibition). LV remodeling occurred more frequently in groups II and III than in group I (40% and 62% vs. 14%, P=0.038 and <0.0001, respectively). At six months the combined rate of death, nonfatal reinfarction, stroke, and rehospitalization for heart failure was 3% in group I, 23.8% in II, and 54.1% in III (log rank=39.2, P for trend <0.0001). By multivariate regression analysis, no or partial inhibition were independent predictors of LV remodeling and combined clinical outcome.
  
  
  CONCLUSIONS
  Inadequate platelet function inhibition in acute phase STEMI despite standard antiplatelet therapy is associated with increased risk of poor LV performance and combined clinical events. This may suggest the need for intensified antiplatelet therapy in the early phase of STEMI.
authors.affiliation: 1st Department of Cardiology, Medical University of Warsaw, Warsaw, Poland. zhuczek@wp.pl
authors.forename: Zenon
authors.initials: Z
authors.lastname: Huczek
authors.forename: Krzysztof J
authors.initials: KJ
authors.lastname: Filipiak
authors.forename: Janusz
authors.initials: J
authors.lastname: Kochman
authors.forename: Radoslaw
authors.initials: R
authors.lastname: Piatkowski
authors.forename: Marcin
authors.initials: M
authors.lastname: Grabowski
authors.forename: Marek
authors.initials: M
authors.lastname: Roik
authors.forename: Janusz
authors.initials: J
authors.lastname: Kochanowski
authors.forename: Grzegorz
authors.initials: G
authors.lastname: Opolski
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology / Q000502:physiology; D000322:Adrenergic Agonists / Q000494:pharmacology; D000368:Aged; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology*; D003094:Collagen / Q000494:pharmacology; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D015539:Platelet Activation; D015607:Stents; D013928:Thromboxane A2 / Q000037:antagonists & inhibitors / Q000502:physiology; D016277:Ventricular Function, Left
chemical_list: D000322:Adrenergic Agonists; D013928:Thromboxane A2; D000244:Adenosine Diphosphate; D003094:Collagen; D004837:Epinephrine