Predictors of the rise in vWF after ST elevation myocardial infarction: implications for treatment strategies and clinical outcome

Abstract

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 (ΔvWF), 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. TFGP=0.0042) or CTFC≥40 at 60 min (P=0.0035) were associated with a higher ΔvWF. ΔvWF ≥75th percentile was associated with a higher incidence of death or myocardial infarction (MI) at 30 days, compared with P=0.027). Enoxaparin independently reduced the ΔvWF (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 ΔvWF. Enoxaparin is independently associated with a reduction in ΔvWF 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.