title: Association between admission mean platelet volume and coronary patency after thrombolytic therapy for acute myocardial infarction.
abstract: OBJECTIVE
  High levels of mean platelet volume (MPV) have been shown to be a predictor of poor clinical outcome among survivors of myocardial infarction. We evaluated the association between admission MPV and infarct-related artery (IRA) patency in patients treated with thrombolytic therapy for acute myocardial infarction (AMI).
  
  
  METHODS
  We retrospectively evaluated 133 consecutive patients with ST-elevation AMI, who received thrombolytic therapy within 12 hours of chest pain. Sixty-five patients received streptokinase and 68 patients received recombinant tissue-type plasminogen activator, based on the discretion of the physician. Blood samples were taken before thrombolytic therapy and MPV was measured. Coronary angiography was performed within a mean of two days after thrombolytic therapy and the flow in the IRA was assessed with the TIMI flow grade and corrected TIMI frame count (CTFC).
  
  
  RESULTS
  After thrombolytic therapy, TIMI 3 flow was achieved in 62 patients (46.6%), whereas 71 patients (53.4%) had insufficient TIMI flow. Patients with insufficient TIMI flow had a significantly higher mean admission MPV (9.8+/-1.5 fl vs. 8.6+/-1.4 fl; p<0.001) and were more likely to have been given streptokinase (p=0.02). The two groups were similar with respect to the type of IRA and the number of diseased vessels (p>0.05). There was a weak correlation between MPV and CTFC (p=0.01). Multivariate analysis showed MPV (OR 1.871, 95% CI 1.402-2.498; p<0.001) and the type of thrombolytic agent (OR 2.915; 95% CI 1.333-6.374; p=0.007) as independent predictors of insufficient TIMI flow. The receiver operating characteristic analysis yielded a cutoff value of 8.885 fl for MPV to predict insufficient TIMI flow, with sensitivity and specificity being 70.4% and 66.1%, respectively.
  
  
  CONCLUSIONS
  Our findings show that a higher admission MPV is associated with an increased risk for insufficient TIMI flow in the IRA after thrombolytic therapy for AMI.
authors.affiliation: Department of Cardiology, Atatürk Education and Research Hospital, Ankara, Turkey. drasaatciyasar@yahoo.com
authors.forename: Ayşe Saatci
authors.initials: AS
authors.lastname: Yaşar
authors.forename: Emine
authors.initials: E
authors.lastname: Bilen
authors.forename: Isa Oner
authors.initials: IO
authors.lastname: Yüksel
authors.forename: Uğur
authors.initials: U
authors.lastname: Arslantaş
authors.forename: Fatih
authors.initials: F
authors.lastname: Karakaş
authors.forename: Ozgür
authors.initials: O
authors.lastname: Kirbaş
authors.forename: Mehmet
authors.initials: M
authors.lastname: Bilge
mesh_terms: D017023:Coronary Angiography; D003331:Coronary Vessels / Q000503:physiopathology*; D006801:Humans; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy*; D010343:Patient Admission; D010976:Platelet Count; D013300:Streptokinase / Q000627:therapeutic use*; D015912:Thrombolytic Therapy / Q000379:methods*; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use*; D014654:Vascular Patency / Q000502:physiology*
chemical_list: D013300:Streptokinase; D010959:Tissue Plasminogen Activator