title: Predictors of the rise in vWF after ST elevation myocardial infarction: implications for treatment strategies and clinical outcome: An ENTIRE-TIMI 23 substudy.
abstract: OBJECTIVE
  Prior studies suggest that acute coronary syndromes (ACSs) are associated with endothelial activation and that this is of prognostic significance. We hypothesized that endothelial activation, as measured by a rise in von Willebrand Factor (DeltavWF), was influenced by the thrombolysis in myocardial infarction flow grade (TFG), the corrected TIMI frame count (CTFC) and the choice of anticoagulant therapy after fibrinolysis in ST elevation myocardial infarction (STEMI).
  
  
  RESULTS
  Data were drawn from the enoxaparin and tenecteplase tissue plasminogen activator (TNK-tpa) with or without GPIIb/IIIa inhibitor as the reperfusion strategy in the STEMI trial (ENTIRE-TIMI 23). Three hundred and fourteen patients had serial measurements of vWF (baseline and 48-72 h) and angiographic data available. TFG<3 (P=0.0042) or CTFC>/=40 at 60 min (P=0.0035) were associated with a higher DeltavWF. DeltavWF >/=75th percentile was associated with a higher incidence of death or myocardial infarction (MI) at 30 days, compared with <75th percentile (11.2 vs. 4.1%, P=0.027). Enoxaparin independently reduced the DeltavWF (P=0.019) and also the composite of death or MI (OR 0.33, 95% CI 0.12-0.91, P=0.03) compared with unfractionated heparin.
  
  
  CONCLUSIONS
  In STEMI treated by fibrinolysis, coronary flow at 60 min and choice of adjunctive anticoagulant appear to be independent determinants of DeltavWF. Enoxaparin is independently associated with a reduction in DeltavWF and a reduction in death or MI. The clinical benefits of enoxaparin as an adjunctive treatment in STEMI may be mediated in part by a reduction in vWF release.
authors.affiliation: TIMI Study Group and Cardiovascular Division, Department of Medicine, Brigham & Women's Hospital/Harvard Medical School, Boston, MA, USA. kkray@partners.org
authors.forename: Kausik K
authors.initials: KK
authors.lastname: Ray
authors.forename: David A
authors.initials: DA
authors.lastname: Morrow
authors.forename: C Michael
authors.initials: CM
authors.lastname: Gibson
authors.forename: Sabina
authors.initials: S
authors.lastname: Murphy
authors.forename: Elliott M
authors.initials: EM
authors.lastname: Antman
authors.forename: Eugene
authors.initials: E
authors.lastname: Braunwald
mesh_terms: D001783:Blood Flow Velocity / Q000502:physiology; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000502:physiology; D017984:Enoxaparin / Q000627:therapeutic use*; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy / Q000401:mortality / Q000503:physiopathology; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D015912:Thrombolytic Therapy / Q000379:methods*; D016896:Treatment Outcome; D014841:von Willebrand Factor / Q000378:metabolism*
chemical_list: D017984:Enoxaparin; D005343:Fibrinolytic Agents; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D014841:von Willebrand Factor