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裸钽镍钛自膨支架植入后猪股浅动脉的异质性血管反应。

Heterogeneous vascular response after implantation of bare nitinol self-expanding stents in the swine femoropopliteal artery.

机构信息

Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shimmachi, Suita city, Osaka, 564-8565, Japan.

Kawarada Cardio Foot Vascular Clinic, Osaka, Japan.

出版信息

Cardiovasc Interv Ther. 2023 Apr;38(2):210-222. doi: 10.1007/s12928-022-00889-5. Epub 2022 Oct 18.

DOI:10.1007/s12928-022-00889-5
PMID:36255689
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10020252/
Abstract

BACKGROUND

Mechanism of femoropopliteal in-stent restenosis has been underappreciated.

AIM

The aim of this animal study was to elucidate vascular response after femoropopliteal bare nitinol self-expanding stents (SESs) implantation.

METHODS

Misago, Smart Flex, or Innova stent was randomly implanted in 36 swine femoropopliteal arteries. At week 4, quantitative vessel analysis (QVA) was performed on 36 legs, of which 18 underwent histological evaluation after angiography. The remaining 18 legs underwent QVA and histological evaluation at week 13.

RESULTS

Fibrin deposition was excessive at week 4. Internal elastic lamina (IEL) progressively enlarged over time, and vessel injury developed from mild level at week 4 to moderate level at week 13. Vessel inflammatory reaction was mild to moderate at week 4, and was moderate to severe at week 13. Increased fibrin deposition was an early-acting, IEL enlargement and increased vessel inflammation were long-acting, and increased vessel injury and giant cells infiltration were late-acting contributors to neointimal hyperplasia (NIH). Stent type altered time-dependent process of vessel injury, vessel inflammation, eosinophils and giant cells infiltration. Misago had less fibrin deposition and vessel enlargement, and less progressive vessel injury, vessel inflammation, and eosinophils and giant cells infiltration. Net lumen as assessed by percent diameter stenosis or minimum lumen diameter was preserved with Misago, but was not preserved with the other stents.

CONCLUSIONS

In the context of bare nitinol SES platform with less progressive mechanical stress and inflammatory reaction, the advantage of less NIH outweighed the disadvantage of less vessel enlargement, leading to net lumen preservation.

摘要

背景

股浅动脉内支架再狭窄的机制尚未得到充分认识。

目的

本动物研究旨在阐明股浅动脉裸钽镍钛自膨支架(SES)植入后的血管反应。

方法

将 Misago、Smart Flex 或 Innova 支架随机植入 36 只猪的股浅动脉。第 4 周时对 36 条腿进行定量血管分析(QVA),其中 18 条在血管造影后进行组织学评估。其余 18 条腿在第 13 周时进行 QVA 和组织学评估。

结果

第 4 周时纤维蛋白沉积过多。内弹性膜(IEL)随时间逐渐增大,血管损伤从第 4 周的轻度发展到第 13 周的中度。第 4 周时血管炎症反应为轻至中度,第 13 周时为中至重度。纤维蛋白沉积增加是早期作用,IEL 增大和血管炎症是长期作用,而血管损伤和巨细胞浸润是向心性内膜增生(NIH)的晚期作用。支架类型改变了血管损伤、血管炎症、嗜酸性粒细胞和巨细胞浸润的时间依赖性过程。Misago 支架的纤维蛋白沉积和血管扩张较少,血管损伤、血管炎症、嗜酸性粒细胞和巨细胞浸润的进展较少。通过百分比直径狭窄或最小管腔直径评估的净管腔保留用 Misago,但其他支架则没有保留。

结论

在裸钽镍钛 SES 平台的背景下,机械应力和炎症反应的进展较小,较少的 NIH 优势超过了较少的血管扩张的劣势,从而导致净管腔保留。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/356f/10020252/23a74fefcc57/12928_2022_889_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/356f/10020252/2353cec9f483/12928_2022_889_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/356f/10020252/b324e8863a59/12928_2022_889_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/356f/10020252/373aa75ddc89/12928_2022_889_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/356f/10020252/23e2731844c2/12928_2022_889_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/356f/10020252/a0df2ac28885/12928_2022_889_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/356f/10020252/f8445b2f785f/12928_2022_889_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/356f/10020252/23a74fefcc57/12928_2022_889_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/356f/10020252/2353cec9f483/12928_2022_889_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/356f/10020252/b324e8863a59/12928_2022_889_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/356f/10020252/373aa75ddc89/12928_2022_889_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/356f/10020252/23e2731844c2/12928_2022_889_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/356f/10020252/a0df2ac28885/12928_2022_889_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/356f/10020252/f8445b2f785f/12928_2022_889_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/356f/10020252/23a74fefcc57/12928_2022_889_Fig7_HTML.jpg

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