Do unapposed stent struts endothelialise? In vivo demonstration with optical coherence tomography.

Do unapposed stent struts endothelialise? In vivo demonstration with optical coherence tomography.
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DOI:
10.1136/hrt.2006.091876
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发表时间:
2007-03-01
期刊:
Heart (British Cardiac Society)
影响因子:
--
通讯作者:
Di Mario, C
Di Mario, C
中科院分区:
其他
文献类型:
--
作者:
Tanigawa, J;Barlis, P;Di Mario, C

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尽管药物洗脱支架显著降低了经皮冠状动脉介入治疗后的再狭窄率,但关于支架血栓形成的潜在风险仍然值得关注。对于分叉病变,报告的支架内血栓形成率高达3.6%,支架贴壁不完全被认为是一种可能的机制。我们报告的情况下,52岁的男子与糖尿病和三血管疾病。最初,将三个重叠的西罗莫司洗脱支架(Cypher,Cordis)展开到左前降支动脉。由于对角支的TIMI-3级血流,未进行进一步的对吻后扩张。4个月随访时的血管造影显示支架广泛通畅,两个对角线的TIMI-3血流(图A)。在左前降支动脉分叉处至第一对角线(箭头)的最佳相干断层扫描(LightLab Imaging Inc,Westford,马萨诸塞州,USA)显示支架贴壁良好,几乎所有支柱上的内膜层(图B,箭头)极小(< 0.07 mm)。一个支柱在对角分支的起点处突出到管腔中,周围覆盖有厚组织层(0.25 mm,图C),延伸至其与近端和远端血管壁的连接处。根据组织密度和游离支柱上的均匀生长以及其他贴壁支柱上的最小生长,该病例强烈表明该组织由血栓组成,可能完全组织化和内皮化。这些发现引出了两个关于药物洗脱支架贴壁不良时支架内血栓形成的想法。首先,未贴壁的支柱可嵌套血栓触发支架闭塞,其次,该过程可能是自限性的,最终允许组织在支架支柱上生长,并可能促进其完全内皮化。
Although drug-eluting stents have dramatically reduced restenosis rates after percutaneous coronary intervention, concerns remain with regard to the potential risk of stent thrombosis. For bifurcation lesions, a stent thrombosis rate up to 3.6% has been reported, and incomplete stent apposition has been proposed as a possible mechanism. We report the case of a 52-year-old man with diabetes and three-vessel disease. Initially, three overlapping sirolimus-eluting stents (Cypher, Cordis) were deployed to the left anterior descending artery. No further kissing post-dilatation was performed because of TIMI-3 flow in the diagonal branches. Angiography at 4 months of follow-up showed widely patent stents with TIMI-3 flow to both diagonals (panel A). Optimal coherence tomography (LightLab Imaging Inc, Westford, Massachusetts, USA) at the bifurcation of the left anterior descending artery to the first diagonal (arrow) showed good stent apposition, with minimal (< 0.07 mm) intimal layer (panel B, arrow) on almost all struts. One strut was protruding into the lumen at the origin of the diagonal branch circumferentially covered by a thick tissue layer (0.25 mm, panel C) extending to its connection with the vessel wall proximally and distally. On the basis of tissue density and uniform growth on the free strut with minimal growth on other apposed struts, the case strongly suggests that this tissue consists of thrombus, likely fully organised and endothelialised. These findings lead to two thoughts on stent thrombosis in the presence of malapposed drug-eluting stents. Firstly, unapposed struts can nestle thrombus triggering stent occlusion and secondly, the process can be self-limiting, eventually allowing growth of tissue on the stent strut and possibly promoting its complete endothelialisation.