Partner und Internationale Organisationen
(Englisch)
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TINOX GmbH München, University Hospital Utrecht (NL), University of Bristol (UK), Freeman Hospital, Newcastle (UK)
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Abstract
(Englisch)
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STENT COATING FOR PREVENTION OF INSTENT-RESTENOSIS
S Windecker, I Mayer, G de Pasquale, O Dirsch, P de Groot,
B Leskosek, B Meier, OM Hess.
Cardiology, Swiss Cardiovascular Center, Bern, Switzerland.
Background: Coronary stents reduce restenosis by preventing constrictive arterial remodeling, but stimulate neointimal hyperplasia. The purpose of this study was to investigate the effect of a novel stent coating, titanium-nitride-oxide (TiNOX), on coronary artery remodeling in animals.
Methods: Twelve pigs were each instrumented with 3 stainless steel stents (15 mm length, 2.5-3.0 mm diameter): one control and two TiNOX coated stents (TiNOX 1 = ceramic; TiNOX 2 = metallic). Animals were allowed to survive for 6 weeks. Histologic specimens of stented segments were analyzed by digital morphometry. In vitro adhesion studies with fluorescent platelets were performed in a perfusion chamber using stainless steel and TiNOX-coated samples.
Results: Neointimal hyperplasia was larger in uncoated (2.61±1.12 mm2) than coated stents (TiNOX 1: 1.47±0.84 mm2, p<0.02; TiNOX 2: 1.39±0.93 mm2, p<0.02). Lumen diameter was increased in all stented segments regardless of coating. Linear regression analysis revealed a significant inverse relationship between neointimal hyperplasia and lumen (controls: r=0.82, p<0.005, y=4.3-0.5x; coated stents: r=0.51, p<0.02, y=2.4-0.3x), as well as between restenosis rate and lumen (controls: r=0.96, p<0.001, y=90-12x; coated stents: r=0.71, p<0.001, y=55-7x). Restenosis rate was reduced by 40% in coated stents. Strong platelet adhesion was found in stainless steel, but attenuated adhesion in TiNOX-coated samples.
Conclusions: TiNOX coating of coronary stents reduces neointimal hyperplasia (44% reduction for TiNOX 1 and 47% for TiNOX 2, respectively) in the pig. Reduced platelet adhesion to TiNOX coated stents may be the underlying mechanism for the attenuated neointimal hyperplasia.
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