Coronavirus Disease 2019 (COVID-19) Coronary Vascular Thrombosis: Correlation with Neutrophil but Not Endothelial Activation.
Coronavirus Disease 2019 (COVID-19) Coronary Vascular Thrombosis: Correlation with Neutrophil but Not Endothelial Activation.
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DOI：
10.1016/j.ajpath.2021.09.004
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发表时间：
2022-01
期刊：
影响因子：
--
通讯作者：
Pober JS
中科院分区：
文献类型：
--
作者：
Johnson JE;McGuone D;Xu ML;Jane-Wit D;Mitchell RN;Libby P;Pober JS
2019年严重冠状病毒病（COVID-19）增加了导致死亡的心肌损伤风险。这项研究使用多参数免疫荧光技术广泛检查了7例死于COVID-19的患者的心脏尸检组织，并与12例对照标本进行了比较，无论是否患有心血管疾病。与之前的报告一致，没有发现表明心肌炎的病毒感染或淋巴细胞浸润的证据。然而，在COVID-19队列的心脏中观察到大血管和小血管中频繁和广泛的血栓形成，这些发现在对照组中很少见。血栓形成血管的内皮衬里通常缺乏精氨酸介导的内皮活化的证据，评估为转录因子p65（RelA）、pSTAT 1或pSTAT 3的核表达，或通过细胞内粘附分子-1（ICAM-1）、血管细胞粘附分子-1（VCAM-1）、组织因子或血管性血友病因子（VWF）的表达评估的炎症活化证据。内膜EC衬里也普遍保存，几乎没有细胞死亡或脱落的证据。相比之下，在COVID-19患者的心肌血栓内存在频繁的中性粒细胞活化标志物，包括嗜中性粒细胞-血小板聚集体、大血栓内富含嗜中性粒细胞的聚集体以及中性粒细胞胞外陷阱（NET）形成的证据。这些发现表明，循环中性粒细胞而不是内皮细胞的改变是COVID-19患者心脏血栓素质增加的原因。
Severe coronavirus disease 2019 (COVID-19) increases the risk of myocardial injury that contributes to mortality. This study used multiparameter immunofluorescence to extensively examine heart autopsy tissue of 7 patients who died of COVID-19 compared to 12 control specimens, with or without cardiovascular disease. Consistent with prior reports, no evidence of viral infection or lymphocytic infiltration indicative of myocarditis was found. However, frequent and extensive thrombosis was observed in large and small vessels in the hearts of the COVID-19 cohort, findings that were infrequent in controls. The endothelial lining of thrombosed vessels typically lacked evidence of cytokine-mediated endothelial activation, assessed as nuclear expression of transcription factors p65 (RelA), pSTAT1, or pSTAT3, or evidence of inflammatory activation assessed by expression of intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), tissue factor, or von Willebrand factor (VWF). Intimal EC lining was also generally preserved with little evidence of cell death or desquamation. In contrast, there were frequent markers of neutrophil activation within myocardial thrombi in patients with COVID-19, including neutrophil-platelet aggregates, neutrophil-rich clusters within macrothrombi, and evidence of neutrophil extracellular trap (NET) formation. These findings point to alterations in circulating neutrophils rather than in the endothelium as contributors to the increased thrombotic diathesis in the hearts of COVID-19 patients.
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