PMID- 15673542 OWN - NLM STAT- MEDLINE DCOM- 20050616 LR - 20061115 IS - 0195-668X (Print) IS - 0195-668X (Linking) VI - 26 IP - 5 DP - 2005 Mar TI - Predictors of the rise in vWF after ST elevation myocardial infarction: implications for treatment strategies and clinical outcome: An ENTIRE-TIMI 23 substudy. PG - 440-6 AB - AIMS: 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). METHODS AND 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. CONCLUSION: 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. FAU - Ray, Kausik K AU - Ray KK AD - TIMI Study Group and Cardiovascular Division, Department of Medicine, Brigham & Women's Hospital/Harvard Medical School, Boston, MA, USA. kkray@partners.org FAU - Morrow, David A AU - Morrow DA FAU - Gibson, C Michael AU - Gibson CM FAU - Murphy, Sabina AU - Murphy S FAU - Antman, Elliott M AU - Antman EM FAU - Braunwald, Eugene AU - Braunwald E LA - eng PT - Clinical Trial PT - Journal Article PT - Multicenter Study PT - Research Support, Non-U.S. Gov't DEP - 20050126 PL - England TA - Eur Heart J JT - European heart journal JID - 8006263 RN - 0 (Enoxaparin) RN - 0 (Fibrinolytic Agents) RN - 0 (Platelet Glycoprotein GPIIb-IIIa Complex) RN - 0 (von Willebrand Factor) SB - IM CIN - Eur Heart J. 2005 Mar;26(5):421-2. PMID: 15695531 MH - Blood Flow Velocity/physiology MH - Coronary Circulation MH - Coronary Vessels/physiology MH - Enoxaparin/*therapeutic use MH - Female MH - Fibrinolytic Agents/*therapeutic use MH - Humans MH - Male MH - Myocardial Infarction/*blood/drug therapy/mortality/physiopathology MH - Platelet Glycoprotein GPIIb-IIIa Complex/antagonists & inhibitors MH - Thrombolytic Therapy/*methods MH - Treatment Outcome MH - von Willebrand Factor/*metabolism EDAT- 2005/01/28 09:00 MHDA- 2005/06/17 09:00 CRDT- 2005/01/28 09:00 PHST- 2005/01/28 09:00 [pubmed] PHST- 2005/06/17 09:00 [medline] PHST- 2005/01/28 09:00 [entrez] AID - ehi104 [pii] AID - 10.1093/eurheartj/ehi104 [doi] PST - ppublish SO - Eur Heart J. 2005 Mar;26(5):440-6. doi: 10.1093/eurheartj/ehi104. Epub 2005 Jan 26.