Poststroke venous thromboembolism and neutrophil activation: an illustrated review.

Poststroke venous thromboembolism and neutrophil activation: an illustrated review.
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脑卒中后静脉血栓栓塞和中性粒细胞活化:一个图解的回顾。

DOI:
10.1016/j.rpth.2023.100170
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发表时间:
2023-05
影响因子:
4.6
通讯作者:
Stokes, Karen Y.
Stokes, Karen Y.
中科院分区:
医学2区
文献类型:
--
作者:
Dhanesha, Nirav;Ansari, Junaid;Pandey, Nilesh;Kaur, Harpreet;Virk, Chiranjiv;Stokes, Karen Y.

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急性缺血性卒中患者发生静脉血栓栓塞(VTE)的风险很高,如深静脉血栓形成(DVT),据估计,美国每年约有80,000名卒中患者受到影响。急性卒中后症状性深静脉血栓的发生率约为10%。静脉血栓栓塞与院内死亡和致残率升高、院内并发症发生率升高以及卒中患者1年死亡率升高有关。目前的指南建议在急性缺血性卒中患者中使用药理学预防静脉血栓栓塞。然而,血栓预防只能预防一半的预期静脉血栓栓塞事件,并且与出血的高风险相关,这表明需要有针对性的替代治疗来降低这些患者的静脉血栓栓塞风险。中性粒细胞是缺血性中风后血液中最先反应的细胞之一。重要的是,中性粒细胞、血小板和内皮细胞之间的协调相互作用有助于DVT的发展。在中风和其他相关免疫疾病,如抗磷脂综合征的情况下,中性粒细胞通过形成中性粒细胞-血小板聚集体、分泌炎症介质、激活补体、释放组织因子、产生中性粒细胞胞外陷阱等途径促进血栓的传播。在这篇有插图的综述文章中,我们介绍了卒中后静脉血栓栓塞的流行病学和治疗,卒中中性粒细胞过度激活的临床前和临床证据,以及卒中背景下中性粒细胞介导的静脉血栓栓塞的机制。鉴于卒中患者中循环中性粒细胞的过度激活,我们建议更好地了解导致中性粒细胞激活的分子机制,可能会导致开发新的治疗方法,以降低卒中患者中静脉血栓栓塞的风险。急性缺血性脑卒中患者发生静脉血栓栓塞(VTE)的风险很高。静脉血栓栓塞与卒中患者死亡和残疾风险增加有关。中性粒细胞与其他细胞和因素之间的相互作用增加了静脉血栓栓塞的风险。目前的文献支持中性粒细胞依赖机制在促进静脉血栓栓塞中的关键作用。
Patients with acute ischemic stroke are at a high risk of venous thromboembolism (VTE), such as deep vein thrombosis (DVT), estimated to affect approximately 80,000 patients with stroke each year in the United States. The prevalence of symptomatic DVT after acute stroke is approximately 10%. VTE is associated with increased rates of in-hospital death and disability, with higher prevalence of in-hospital complications and increased 1-year mortality in patients with stroke. Current guidelines recommend the use of pharmacologic VTE prophylaxis in patients with acute ischemic stroke. However, thromboprophylaxis prevents only half of expected VTE events and is associated with high risk of bleeding, suggesting the need for targeted alternative treatments to reduce VTE risk in these patients. Neutrophils are among the first cells in blood to respond after ischemic stroke. Importantly, coordinated interactions among neutrophils, platelets, and endothelial cells contribute to the development of DVT. In case of stroke and other related immune disorders, such as antiphospholipid syndrome, neutrophils potentiate thrombus propagation through the formation of neutrophil-platelet aggregates, secreting inflammatory mediators, complement activation, releasing tissue factor, and producing neutrophil extracellular traps. In this illustrated review article, we present epidemiology and management of poststroke VTE, preclinical and clinical evidence of neutrophil hyperactivation in stroke, and mechanisms for neutrophil-mediated VTE in the context of stroke. Given the hyperactivation of circulating neutrophils in patients with stroke, we propose that a better understanding of molecular mechanisms leading to neutrophil activation may result in the development of novel therapeutics to reduce the risk of VTE in this patient population. Patients with acute ischemic stroke are at a high risk of venous thromboembolism (VTE). VTE is associated with increased risk of death and disability in patients with stroke. Interactions between neutrophils and other cells and factors contribute to risk of VTE. Current literature supports a key role of neutrophil-dependent mechanisms in promoting VTE.
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期刊: BLOOD
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