Abstract
BACKGROUND: Titanium-alloys (Ti) are widely used as blood biocompatible material for blood pumps and coronary stents. Thrombus formation on the Ti surface often results from high shear stress induced-platelet activation, and it is contributory to pump failure and coronary reocclusion, respectively. Although heparin and aspirin are routinely used to prevent thrombus formation in clinical settings, the efficacy is not satisfactory. The aim of this study was to elucidate the mechanisms of thrombus formation on Ti surface induced by high shear stress and to evaluate the efficacy of antithrombotic agents. METHODS: A cone-and-plate viscometer and a parallel flow chamber were used for shear-induced platelet aggregation and adhesion studies, respectively. Platelet microaggregation of citrate anticoagulated platelet rich plasma samples were measured by flow cytometry. Anti-GPIIIa antibody was used to identify the number of platelets adhering to the Ti surface after infusion of heparinized whole blood. RESULTS: Heparin (10 unit/ml) enhanced shear (108 dynes/cm2) induced human platelet aggregation by 22%. Absorptions of vWF and fibrinogen onto Ti surface were increased within 60 min after incubation with plasma and both plasma proteins enhanced platelet adhesion induced by high shear stress (111 dynes/cm2). Indomethacin (30 mM) had no effect on shear-induced platelet adhesion. Maximal concentration of TAK-029, a GPIIb/IIIa antagonist, prevented the platelet adhesions to non-, vWF- and fibrinogen-coated Ti surface by 89%, 75% and 98%, respectively. CONCLUSION: Treatment with a GPIIb/IIIa antagonist is an appropriate option to prevent shear-induced thrombus formation on Ti surface.
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