In-stent stenosis: pathology and implications for the development of drug eluting stents
In-stent stenosis: pathology and implications for the development of drug eluting stents
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DOI：
10.1136/heart.89.2.218
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发表时间：
2003-02-01
期刊：
影响因子：
5.7
通讯作者：
Bennett, MR
中科院分区：
文献类型：
--
作者：
Bennett, MR
全世界每年进行超过 150 万例经皮冠状动脉血运重建手术，其中大多数是冠状动脉内支架置入术。尽管设备取得了巨大进步，但主要的限制是支架内狭窄（ISS）（由 Bennett 和 O’Sullivan 审查1）。尽管选定患者的 ISS 率为 10-20%，但我们现在对完全闭塞、大隐静脉旁路移植物、血管成形术和 ISS 部位、糖尿病患者和小血管进行支架植入。因此，实际 ISS 率要高得多，在某些高风险病变中高达 59%。直到最近，治疗 ISS 的唯一有效方法是近距离放射治疗。与对照血管相比，近距离放射治疗降低了靶血管血运重建率和二元再狭窄率，并增加了最小管腔直径 (MLD)，可持续维持三年。 1 近距离放射治疗虽然有效，但并未得到普遍接受，主要是由于晚期血栓形成和放射治疗的后勤保障。相比之下，含有免疫抑制剂雷帕霉素和抗有丝分裂剂紫杉醇的药物洗脱支架已显示出令人鼓舞的减少新发病变中的 ISS 2 3 以及可能的 ISS 病变。这篇综述研究了 ISS 的病理学以及与支架结合的药物如何中断对血管损伤的正常反应。 c 再狭窄的机制 病变血管过度扩张导致内皮破坏、内弹力板断裂和内侧夹层。管腔扩大是由斑块减少（压缩/栓塞）、轴向斑块向支架外近端和远端部分重新分布、斑块挤出和血管扩张共同引起的。许多过程都会导致再狭窄（图 1 和表 1）。
Over 1.5 million percutaneous coronary revascularisation procedures are performed annually world wide, most being intracoronary stenting. Despite enormous advances in devices, the major limitation is in-stent stenosis (ISS)(reviewed by Bennett and O’Sullivan1). Although ISS rates are 10–20% in selected patients, we now stent total occlusions, saphenous vein bypass grafts, both angioplasty and ISS sites, diabetic patients, and small vessels. Thus, real ISS rates are much higher, up to 59% in some high risk lesions. Until recently, the only effective treatment for ISS was brachytherapy. Brachytherapy reduces target vessel revascularisation rates and binary restenosis rates, and increases minimum luminal diameters (MLDs) compared with control vessels, maintained to three years. 1 Although effective, brachytherapy is not universally accepted, due predominantly to late thrombosis and the logistics of administering radioactivity. In contrast, drug eluting stents containing the immunosuppressive agent rapamycin and the antimitotic agent paclitaxel have shown encouraging reductions in ISS in de novo lesions, 2 3 and possibly in ISS lesions. This review examines the pathology of ISS and how drugs bound to stents interrupt the normal response to vessel injury. c MECHANISMS OF RESTENOSISOverdistension of the diseased vessel causes endothelial disruption, internal elastic lamina fracture, and medial dissection. Lumen enlargement is caused by a combination of plaque reduction (compression/embolisation), axial plaque redistribution towards the proximal and distal segments outside the stent, plaque extrusion, and vessel expansion. Many processes then contribute to restenosis (fig 1 and table 1).