Effects of unfractionated and low molecular weight heparins on plasma levels of hemostatic factors in patients with acute coronary syndromes

Background and Objectives. Unfractionated heparin (UFH) and enoxaparin (low molecular weight heparin) constitute fundamental therapies in the treatmen t of patients with acute coronary syndrome (ACS). Since enoxaparin appears to offer clinical advantages over UFH in managing ACS, markers of thrombin generation, endothelial function and acute phase response could manifest di fferent responses to UFH or enoxaparin. The purpose of the present study wa s to investigate the effect that treatment with either UFH or enoxaparin ha s on plasma hemostatic markers in 24 patients with ACS. Design and Methods. The patients were randomized to receive 5,000 IU intrav enous bolus acid continuous infusion of 18 IU/Kg/h UFH (n=11) or 1 mg/kg/12 h subcutaneous enoxaparin (n-13). The plasma levels of fibrinogen (Fg), pro thrombin fragment 1+2 (F1+2), thrombin antithrombin complex (TAT), von Will ebrand factor (VWF), tissue factor (TF) and tissue factor pathway inhibitor (TFPI) were assayed at admission and 6, 12, 24 and 48 hours after heparin treatment. Results. Upon admission, UFH and enoxaparin patients showed a significant i ncrease in ail the hemostatic parameters measured with respect to the level s in the control subjects. In comparison with the baseline levels of the UF H- and enoxaparin-treated patients, Fg showed a significant increase at 48 h and TFPI at 6, 12 and 24 hours. However, at 48 hours TFPI levels were not significantly higher than the basal values. There were no significant chan ges in F1+2, TAT, VWF or TF. Interpretation and Conclusions. Markers of thrombin generation, endothelial function and acute-phase reactants manifest a similar response to UFH and enoxaparin. An increase in thrombin generation may be a result of persisten tly activated inflammatory and endothelial processes, despite UFH and enoxa parin treatment. (C) 2001; Ferrata Storti Foundation.