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J Vasc Interv Radiol. 2019 Apr;30(4):616-617. doi: 10.1016/j.jvir.2018.09.032.
2
A polymer-coated, paclitaxel-eluting stent (Eluvia) versus a polymer-free, paclitaxel-coated stent (Zilver PTX) for endovascular femoropopliteal intervention (IMPERIAL): a randomised, non-inferiority trial.聚合物涂层紫杉醇洗脱支架(Eluvia)与无聚合物紫杉醇涂层支架(Zilver PTX)治疗下肢股腘动脉腔内介入治疗(IMPERIAL):一项随机非劣效试验。
Lancet. 2018 Oct 27;392(10157):1541-1551. doi: 10.1016/S0140-6736(18)32262-1. Epub 2018 Sep 24.
3
Pathologic intimal thickening in human atherosclerosis is formed by extracellular accumulation of plasma-derived lipids and dispersion of intimal smooth muscle cells.人动脉粥样硬化中的病理性内膜增厚是由血浆衍生脂质的细胞外积聚和内膜平滑肌细胞的分散形成的。
Atherosclerosis. 2018 Jul;274:235-242. doi: 10.1016/j.atherosclerosis.2018.03.039. Epub 2018 Mar 26.
4
Long-Term Results from the MAJESTIC Trial of the Eluvia Paclitaxel-Eluting Stent for Femoropopliteal Treatment: 3-Year Follow-up.Eluvia紫杉醇洗脱支架治疗股腘动脉疾病的MAJESTIC试验的长期结果:3年随访
Cardiovasc Intervent Radiol. 2017 Dec;40(12):1832-1838. doi: 10.1007/s00270-017-1771-5. Epub 2017 Sep 25.
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Cilostazol reduces angiographic restenosis after endovascular therapy for femoropopliteal lesions in the Sufficient Treatment of Peripheral Intervention by Cilostazol study.西洛他唑减少西洛他唑治疗股腘动脉病变的血管内治疗后的血管造影再狭窄。
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8
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股浅动脉裸金属支架植入18年后的病理评估

Pathological evaluation 18 years after bare-metal stent implantation in the superficial femoral artery.

作者信息

Ishihara Takayuki, Inoue Katsumi, Iida Osamu, Hata Yosuke, Mano Toshiaki

机构信息

Kansai Rosai Hospital Cardiovascular Center, Amagasaki, Japan.

Division of Laboratory Medicine, Kokura Memorial Hospital, Kitakyushu, Japan.

出版信息

J Cardiol Cases. 2020 Oct 28;23(2):94-97. doi: 10.1016/j.jccase.2020.10.006. eCollection 2021 Feb.

DOI:10.1016/j.jccase.2020.10.006
PMID:33520032
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7817911/
Abstract

Bare-metal stents (BMSs) have been generally applied for the treatment of peripheral artery disease in patients with femoropopliteal disease. However, very long-term pathological findings after BMS implantation have not been elucidated to date. We experienced an autopsy case in which we performed a pathological evaluation 18 years after BMS implantation in the right superficial femoral artery. The BMS was totally occluded and filled with remarkable neointima formation. Neointima was mainly composed of a lot of rather atrophic smooth muscles and intercellular spaces containing dense collagenous fibers. Furthermore, regional fatty infiltration was also observed, but inflammatory cell infiltration, such as macrophages and lymphocytes, was not recognized obviously even around the struts. Judging from the pathological findings, the main mechanism of the very long-term in-stent restenosis in the patients with femoropopliteal disease was continuous proliferation of smooth muscle cells that led to the totally occlusive disease. This observation leads us to speculate that continuous elution of an anti-proliferating drug over a longer duration, at least beyond 1 year, would be effective to prevent chronic-phase restenosis. Further development of devices that can be used in the femoropopliteal artery is needed in light of this speculation. Very long-term pathological findings after bare-metal stent (BMS) implantation in the femoropopliteal (FP) artery have not been elucidated to date. The BMS which was implanted in the FP artery 18 years before was totally occluded and filled with remarkable neointima formation due to smooth muscle cell (SMC) proliferation without any infiltration of inflammatory cells around the struts. The main mechanism of the very long-term in-stent restenosis of FP disease was continuous proliferation of SMC.>.

摘要

裸金属支架(BMS)已普遍应用于股腘动脉疾病患者的外周动脉疾病治疗。然而,迄今为止,BMS植入术后的极长期病理结果尚未阐明。我们遇到了一例尸检病例,在该病例中,我们对右股浅动脉植入BMS 18年后进行了病理评估。BMS完全闭塞,充满了显著的新生内膜形成。新生内膜主要由大量相当萎缩的平滑肌和含有密集胶原纤维的细胞间隙组成。此外,还观察到局部脂肪浸润,但即使在支架周围也未明显发现巨噬细胞和淋巴细胞等炎性细胞浸润。从病理结果判断,股腘动脉疾病患者极长期支架内再狭窄的主要机制是平滑肌细胞的持续增殖,导致完全闭塞性疾病。这一观察结果使我们推测,更长时间(至少超过1年)持续洗脱抗增殖药物将有效预防慢性期再狭窄。鉴于这一推测,需要进一步开发可用于股腘动脉的装置。迄今为止,股腘(FP)动脉植入裸金属支架(BMS)后的极长期病理结果尚未阐明。18年前植入FP动脉的BMS完全闭塞,由于平滑肌细胞(SMC)增殖而充满显著的新生内膜形成,支架周围没有任何炎性细胞浸润。FP疾病极长期支架内再狭窄的主要机制是SMC的持续增殖。