Silicon-carbide coated coronary stents have low platelet and leukocyte adhesion during platelet activation.
BACKGROUND: Stent thrombosis and restenosis are of great clinical significance. We constructed a closed loop in vitro heparinized whole human blood circulation model for testing hemocompatibility of coronary stents. This model allows evaluation of human blood activation by blood-stent interaction in a well-controlled setting. Until now these interactions were studied in the highly coagulable pig coronary artery model. METHODS: We evaluated activation of the coagulation system and blood components by uncoated, heparin-coated, and silicon-carbide coated tantalum stents. The effects, measured by biochemical assays, were compared with stainless-steel stents. Also the inhibitory effect on platelet activation by indomethacin equal to the oral effect of 325 mg acetylsalicylic acid daily, was measured and visualized by scanning electron microscopy. RESULTS: Both activation of the coagulation system and platelets were counteracted by indomethacin, suggesting an important role for platelets in activation of the coagulation system in this model. Despite platelet activation by all stents, the SiC-coated tantalum stent demonstrates a significantly lower GpIIIa receptor-mediated platelet adhesion at the stent surface (21.7 x 10(3) counts per second/mg stent weight) compared to all other stents (stainless-steel 54.0, heparin-coated 95.7 and uncoated 76.2 x 10(3) cps/mg). Also activated leukocytes demonstrated a significantly lower CD11b receptor-mediated adhesion at the SiC-coated stent (37.0 x 10(3) cps/mg) than at the stainless-steel stent (114.5 x 10(3) cps/mg). CONCLUSIONS: Data from this in vitro circulation study show a significantly lower platelet and leukocyte adhesion at the surface of the SiC-coated tantalum stent than at the surface of stainless-steel stents or uncoated and heparin-coated tantalum stents.[1]References
- Silicon-carbide coated coronary stents have low platelet and leukocyte adhesion during platelet activation. Monnink, S.H., van Boven, A.J., Peels, H.O., Tigchelaar, I., de Kam, P.J., Crijns, H.J., van Oeveren, W. J. Investig. Med. (1999) [Pubmed]
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