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动脉粥样硬化性血管疾病中的纤维蛋白凝块特性:从病理生理学到临床结果

Fibrin Clot Properties in Atherosclerotic Vascular Disease: From Pathophysiology to Clinical Outcomes.

作者信息

Ząbczyk Michał, Natorska Joanna, Undas Anetta

机构信息

John Paul II Hospital, 31-202 Kraków, Poland.

Institute of Cardiology, Jagiellonian University Medical College, 31-202 Kraków, Poland.

出版信息

J Clin Med. 2021 Jul 5;10(13):2999. doi: 10.3390/jcm10132999.

DOI:10.3390/jcm10132999
PMID:34279484
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8268932/
Abstract

Fibrin is a major component of thrombi formed on the surface of atherosclerotic plaques. Fibrin accumulation as a consequence of local blood coagulation activation takes place inside atherosclerotic lesions and contributes to their growth. The imbalance between thrombin-mediated fibrin formation and fibrin degradation might enhance atherosclerosis in relation to inflammatory states reflected by increased fibrinogen concentrations, the key determinant of fibrin characteristics. There are large interindividual differences in fibrin clot structure and function measured in plasma-based assays and in purified fibrinogen-based systems. Several observational studies have demonstrated that subjects who tend to generate denser fibrin networks displaying impaired clot lysis are at an increased risk of developing advanced atherosclerosis and arterial thromboembolic events. Moreover, the majority of cardiovascular risk factors are also associated with unfavorably altered fibrin clot properties, with their improvement following effective therapy, in particular with aspirin, statins, and anticoagulant agents. The prothrombotic fibrin clot phenotype has been reported to have a predictive value in terms of myocardial infarction, ischemic stroke, and acute limb ischemia. This review article summarizes available data on the association of fibrin clot characteristics with atherosclerotic vascular disease and its potential practical implications.

摘要

纤维蛋白是在动脉粥样硬化斑块表面形成的血栓的主要成分。局部血液凝固激活导致的纤维蛋白积累发生在动脉粥样硬化病变内部,并促进其生长。凝血酶介导的纤维蛋白形成与纤维蛋白降解之间的失衡,可能会因纤维蛋白原浓度升高所反映的炎症状态而加剧动脉粥样硬化,纤维蛋白原浓度是纤维蛋白特性的关键决定因素。在基于血浆的检测和基于纯化纤维蛋白原的系统中,纤维蛋白凝块的结构和功能存在很大的个体差异。多项观察性研究表明,倾向于生成密度更高、凝块溶解受损的纤维蛋白网络的受试者,发生晚期动脉粥样硬化和动脉血栓栓塞事件的风险增加。此外,大多数心血管危险因素也与纤维蛋白凝块特性的不利改变有关,有效治疗后,尤其是使用阿司匹林、他汀类药物和抗凝剂后,这些特性会得到改善。据报道,促血栓形成的纤维蛋白凝块表型对心肌梗死、缺血性中风和急性肢体缺血具有预测价值。这篇综述文章总结了关于纤维蛋白凝块特征与动脉粥样硬化性血管疾病的关联及其潜在实际意义的现有数据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ef9/8268932/cdc09ce747f3/jcm-10-02999-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ef9/8268932/019956033d64/jcm-10-02999-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ef9/8268932/cdc09ce747f3/jcm-10-02999-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ef9/8268932/019956033d64/jcm-10-02999-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ef9/8268932/cdc09ce747f3/jcm-10-02999-g002.jpg

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