Owing to its beneficial pharmacological profile, the low-molecular-weight heparin (LMWH) enoxaparin is increasingly being taken as an alternative to UFH in the treatment of ACS with an early invasive strategy and in elective percutaneous coronary interventions (PCI). Insufficient anticoagulation increases the risk of catheter thrombus formation during PCI. The aim of the present study was to test in vitro the hypotheses that (i) inhibiting thrombin or thrombin generation by administering LMWH is a critical intervention in preventing catheter thrombus formation and (ii) other LMWH such as certoparin or dalteparin are as effective as enoxaparin. Blood pre-treated with the anticoagulants of interest was continuously circulated through a guiding catheter by using a roller pump for a maximum experimental period of 60 min or until the catheter became occluded. Overall thrombus weight, anti-Xa activity and electron microscopic features such as deposits of platelets, erythrocytes and fibrin on the catheter surface were quantified as endpoints. All LMWH tested significantly reduced catheter thrombus generation comparable to UFH treatment whereas there was no difference between the specific LMWH with respect to catheter thrombus formation or deposition of platelets, erythrocytes and fibrin. Thrombus generation was found to negatively correlate with anti-Xa activity. The additional use of eptifibatide did not affect thrombus formation. These data suggest that modulating plasmatic coagulation by employing LMWH is critical for preventing catheter thrombus formation and at the same time offer a potential for administering LMWH other than enoxaparin, such as certoparin or dalteparin, in the setting of PCI.

The direct thrombin inhibitor argatroban offers some significant advantages over unfractionated heparin (UFH) and is recommended as an alternative anticoagulant during percutaneous coronary interventions (PCI). The impact of argatroban on cardiac catheter thrombosis--a severe potential complication of PCI--has not been systematically studied yet. The aim of the present study was to test in vitro the hypothesis that argatroban is equivalent to the more established anticoagulants UFH and enoxaparin in preventing catheter thrombus formation. Blood pretreated with the anticoagulants of interest was continuously circulated through a guiding catheter by using a roller pump for a maximum experimental period of 60 minutes. In an alternate model, coagulation was mechanically induced by a magnetic stirrer. Coagulation parameters, overall thrombus weight and electron microscopic features (deposits of platelets and fibrin on the catheter surface) were quantified as endpoints. Argatroban (administered as bolus or continuous infusion), UFH (bolus), and enoxaparin (bolus) significantly reduced catheter thrombus formation compared to untreated controls. Here, neither overall thrombus weight nor platelet/fibrin deposition was different among the specific anticoagulants. Declining ACT (activated clotting time) levels--which were found in the argatroban bolus group--could be prevented by continuous infusion. In magnetic stirrer-induced coagulation, thrombus weight was lower following bolus treatment with UFH and enoxaparin compared to argatroban. These data suggest that the potential for argatroban in preventing catheter thrombosis is comparable to that of UFH and enoxaparin. However, the anticoagulatory efficacy varied, depending on the model of coagulation activation, which demonstrates the necessity for specific testing.

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