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药物洗脱支架植入术后的新型动脉粥样硬化:作用与机制

Neoatherosclerosis after Drug-Eluting Stent Implantation: Roles and Mechanisms.

作者信息

Cui Yuanyuan, Liu Yue, Zhao Fuhai, Shi Dazhuo, Chen Keji

机构信息

Cardiovascular Diseases Center, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China; China Heart Institute of Chinese Medicine, China Academy of Chinese Medical Sciences, Beijing 100091, China.

出版信息

Oxid Med Cell Longev. 2016;2016:5924234. doi: 10.1155/2016/5924234. Epub 2016 Jun 30.

DOI:10.1155/2016/5924234
PMID:27446509
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4944075/
Abstract

In-stent neoatherosclerosis (NA), characterized by a relatively thin fibrous cap and large volume of yellow-lipid accumulation after drug-eluting stents (DES) implantation, has attracted much attention owing to its close relationship with late complications, such as revascularization and late stent thrombosis (ST). Accumulating evidence has demonstrated that more than one-third of patients with first-generation DES present with NA. Even in the advent of second-generation DES, NA still occurs. It is indicated that endothelial dysfunction induced by DES plays a critical role in neoatherosclerotic development. Upregulation of reactive oxygen species (ROS) induced by DES implantation significantly affects endothelial cells healing and functioning, therefore rendering NA formation. In light of the role of ROS in suppression of endothelial healing, combining antioxidant therapies with stenting technology may facilitate reestablishing a functioning endothelium to improve clinical outcome for patients with stenting.

摘要

支架内新生动脉粥样硬化(NA)的特征是在药物洗脱支架(DES)植入后有相对较薄的纤维帽和大量黄色脂质堆积,由于其与晚期并发症如血管重建和晚期支架血栓形成(ST)密切相关,已引起广泛关注。越来越多的证据表明,超过三分之一的第一代DES患者会出现NA。即使在第二代DES出现后,NA仍然会发生。有迹象表明,DES诱导的内皮功能障碍在新生动脉粥样硬化发展中起关键作用。DES植入诱导的活性氧(ROS)上调显著影响内皮细胞的愈合和功能,从而导致NA形成。鉴于ROS在抑制内皮愈合中的作用,将抗氧化治疗与支架技术相结合可能有助于重建有功能的内皮,从而改善支架植入患者的临床结局。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e1/4944075/95716987ec41/OMCL2016-5924234.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e1/4944075/748779ee499d/OMCL2016-5924234.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e1/4944075/95716987ec41/OMCL2016-5924234.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e1/4944075/748779ee499d/OMCL2016-5924234.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e1/4944075/95716987ec41/OMCL2016-5924234.002.jpg

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