Key result
Acenocoumarol and polymer coating prevented the 38% early thrombotic occlusion rate seen with uncoated stents and no medication, but did not affect neointimal hyperplasia.
Why the study?
Does polymer coating of self-expanding stents prevent early thrombotic occlusion and reduce neointimal hyperplasia compared to uncoated stents with or without antithrombotic medication in normal porcine coronary arteries?
Does polymer coating of self-expanding stents prevent early thrombotic occlusion and reduce neointimal hyperplasia compared to uncoated stents with or without antithrombotic medication in normal porcine coronary arteries?
Polymer coating of self-expanding stents prevents early thrombotic occlusion without affecting neointimal hyperplasia in a porcine model.
Polymer coating may avert early porcine stent thrombosis without curbing hyperplasia; leaves open human translation.
Background: Preliminary clinical reports suggest that metallic stents are thrombogenic during the first days to weeks after implantation but that restenosis rates after this period may be reduced. Methods: We investigated the angiographic patency and histologically measured neointimal hyperplasia of 48 uncoated self-expanding, stainless steel mesh stents (Wallstent, Schneider [Europe] AG, Bulach, Switzerland) placed in normal coronary arteries of three groups of eight pigs that received postprocedure aspirin (ASA, group B), acenocoumarol (group C), or no medication (group A). The results were compared with those obtained in a fourth group of eight pigs (group D) receiving 15 polymer-coated (BioGold, PlasmaCarb Inc., Bedford, NH, USA) Wallstent stents, which are designed to reduce thrombogenicity without additional medication. After 1, 4, and 12 weeks, angiography was repeated. After the last angiogram the coronary arteries were pressure-fixated followed by light microscopy, immunocytochemistry, and electron microscopic examination. Results: Group A showed a 38% thrombotic occlusion rate within 1 week, which was prevented by acenocoumarol or polymer coating, but not by ASA. Histologic analysis showed no difference in the thickness of neointimal hyperplasia between the groups (median values: 134, 101, 143 and 113 μm for groups A, B, C, and D, respectively). Polymer coating did not induce an inflammatory reaction. Conclusions: Acenocoumarol and the polymer coating protected against early thrombotic occlusion of stainless steel self-expanding stents, but neointimal hyperplasia was not affected by preventive measures against stent thrombosis.
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Giessen et al. (1992) studied Normal coronary arteries (animal model) (n=32). Polymer-coated stents or uncoated stents with acenocoumarol/aspirin vs. Uncoated stents with no medication was evaluated on Thrombotic occlusion rate within 1 week. Acenocoumarol and polymer coating prevented the 38% early thrombotic occlusion rate seen with uncoated stents and no medication, but did not affect neointimal hyperplasia.
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