血栓形成在腹主动脉瘤发病机制中的作用

Q3 Medicine JVS-vascular science Pub Date : 2023-01-01 DOI:10.1016/j.jvssci.2023.100106
Jack Bontekoe MD , Jon Matsumura MD , Bo Liu PhD
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摘要

背景腹主动脉瘤(AAAs)是老年人较为常见的血管性病变,具有较高的发病率。不可逆的主动脉壁退化如果不及时治疗会导致致命的破裂。几乎所有的AAA都不同程度地含有腔内血栓(ILT),但血栓形成在AAA中受到干扰的机制相对未知。本文综述了与AAA相关的血栓性并发症、血栓形成对AAA手术结果的影响、AAA发病机制以及抗血栓治疗在该疾病治疗中的应用。方法采用血栓形成、AAAs相关关键词检索PubMed数据库的文献。结果血栓性并发症在AAA患者中相对少见,但有显著的发病率风险。ILT可以通过限制解剖适应性和影响血管内泄漏的风险来影响血管内动脉瘤的修复。AAA发展的许多病理机制,包括血流动力学、炎症、氧化应激和主动脉壁重塑,都包含与血栓形成相互作用的途径。相反,ILT也可能是生化应激的来源,并加剧这些动脉瘤的过程。在动物AAA模型中,抗血栓治疗在预防和稳定AAA方面显示出良好的效果。抗血小板药物可能有助于降低AAA患者主要不良心血管事件的风险;结论血栓形成和ILT可能对动脉瘤生长、破裂风险和患者预后有不利影响,但在分子水平上对动脉瘤疾病的病理性血栓形成机制的了解有限。使用血小板和凝血抑制剂预防ILT可能是动脉瘤进展和稳定的合理理论目标;然而,目前抗血栓治疗在AAA中的实际益处尚不清楚。需要进一步的研究来证明血栓形成对AAA发病机制的影响程度,并为这种疾病的医学管理开发新的药理学策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Thrombosis in the pathogenesis of abdominal aortic aneurysm

Background

Abdominal aortic aneurysms (AAAs) are a relatively common vascular pathology of the elderly with high morbidity potential. Irreversible degeneration of the aortic wall leads to lethal rupture if left untreated. Nearly all AAAs contain intraluminal thrombus (ILT) to a varying degree, yet the mechanisms explaining how thrombosis is disturbed in AAA are relatively unknown. This review examined the thrombotic complications associated with AAA, the impact of thrombosis on AAA surgical outcomes and AAA pathogenesis, and the use of antithrombotic therapy in the management of this disease.

Methods

A literature search of the PubMed database was conducted using relevant keywords related to thrombosis and AAAs.

Results

Thrombotic complications are relatively infrequent in AAA yet carry significant morbidity risks. The ILT can impact endovascular aneurysm repair by limiting anatomic suitability and influence the risk of endoleaks. Many of the pathologic mechanisms involved in AAA development, including hemodynamics, inflammation, oxidative stress, and aortic wall remodeling, contain pathways that interact with thrombosis. Conversely, the ILT can also be a source of biochemical stress and exacerbate these aneurysmal processes. In animal AAA models, antithrombotic therapies have shown favorable results in preventing and stabilizing AAA. Antiplatelet agents may be beneficial for reducing risks of major adverse cardiovascular events in AAA patients; however, neither antiplatelet nor anticoagulation is currently used solely for the management of AAA.

Conclusions

Thrombosis and ILT may have detrimental effects on AAA growth, rupture risk, and patient outcomes, yet there is limited understanding of the pathologic thrombotic mechanisms in aneurysmal disease at the molecular level. Preventing ILT using platelet and coagulation inhibitors may be a reasonable theoretical target for aneurysm progression and stability; however, the practical benefits of current antithrombotic therapies in AAA are unclear. Further research is needed to demonstrate the extent to which thrombosis impacts AAA pathogenesis and to develop novel pharmacologic strategies for the medical management of this disease.

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