症状性颈动脉狭窄支架置入术后并发症：临床危险因素与蛋白质组学机制的研究进展

Research Progress on Clinical Risk Factors and Proteomic Mechanisms of Postoperative Complications after Symptomatic Carotid Artery Stenosis Stent Implantation

摘要: 症状性颈动脉狭窄是导致缺血性脑卒中的重要病因，颈动脉支架置入术(carotid artery stenting, CAS)是其血运重建的关键手段。然而，术后30天内卒中、心肌梗死及远期支架内再狭窄等并发症仍严重影响患者预后。识别高危人群并阐明再狭窄的发生机制，是优化临床决策和改善远期结局的关键。本文系统综述了CAS术后并发症的临床危险因素及代谢综合征背景下血管再狭窄的蛋白质组学分子机制，并探讨二者之间的内在关联。临床研究显示，除年龄、高血压等传统危险因素外，主动脉弓形态与变异、颈内动脉扭曲指数、颈总动脉开口病变等解剖学特征在手术风险中发挥独立作用，复杂解剖结构可增加操作难度、诱发血管损伤和血流动力学紊乱。蛋白质组学研究揭示，代谢综合征环境下血管壁发生显著的分子重构，主要涉及细胞外基质重塑、炎症免疫应答、氧化应激及细胞骨架调控等通路，这些事件共同驱动血管平滑肌细胞增殖迁移和内膜增生。进一步分析表明，临床危险因素可通过改变局部力学微环境或放大损伤反应，启动或加剧上述分子事件，从而构成“解剖–分子”级联的病理基础。本文旨在整合临床表型与分子机制的研究进展，为深入理解再狭窄的发生发展提供理论依据，并为优化风险评估和干预策略提供新视角。

Abstract: Symptomatic carotid artery stenosis is an important cause of ischemic stroke, and carotid artery stenting (CAS) is a key means of revascularization. However, complications such as stroke, myocardial infarction and long-term in-stent restenosis within 30 days after surgery still seriously affect the prognosis of patients. Identifying high-risk groups and elucidating the mechanism of restenosis are the keys to optimizing clinical decision-making and improving long-term outcomes. This article systematically reviews the clinical risk factors of complications after CAS and the molecular mechanism of proteomics of vascular restenosis in the context of metabolic syndrome, and explores the intrinsic relationship between the two. Clinical studies have shown that in addition to traditional risk factors such as age and hypertension, anatomical features such as aortic arch morphology and variation, internal carotid artery tortuosity index, and common carotid artery opening lesions play an independent role in surgical risks. Complex anatomical structures can increase the difficulty of operation and induce vascular injury and hemodynamic disorders. Proteomics studies have revealed that significant molecular remodeling of vascular wall occurs in the environment of metabolic syndrome, mainly involving extracellular matrix remodeling, inflammatory immune response, oxidative stress and cytoskeleton regulation. These events jointly drive the proliferation and migration of vascular smooth muscle cells and intimal hyperplasia. Further analysis shows that clinical risk factors can initiate or aggravate the above molecular events by changing the local mechanical microenvironment or amplifying the damage response, thus forming the pathological basis of the ‘anatomical-molecular’ cascade. This article aims to integrate the research progress of clinical phenotypes and molecular mechanisms, provide a theoretical basis for in-depth understanding of the occurrence and development of restenosis, and provide a new perspective for optimizing risk assessment and intervention strategies.