Histopathological Evaluation of Pulmonary Arterial Remodeling in COVID-19.

Sergiy G Gychka, Sofiia I Nikolaienko, Nataliia V Shults, Volodymyr M Vasylyk, Bohdan O Pasichnyk, Iryna V Kagan, Yulia V Dibrova, Muin Tuffaha, Yuichiro J Suzuki
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Abstract

A positive-sense single-stranded RNA virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), caused the coronavirus disease 2019 (COVID-19) pandemic that devastated the world. While this is a respiratory virus, one feature of the SARS-CoV-2 infection was recognized to cause pathogenesis of other organs. Because the membrane fusion protein of SARS-CoV-2, the spike protein, binds to its major host cell receptor angiotensin-converting enzyme 2 (ACE2) that regulates a critical mediator of cardiovascular diseases, angiotensin II, COVID-19 is largely associated with vascular pathologies. In fact, we have previous reported that postmortem lung tissues collected from patients who died of COVID-19 exhibited thickened pulmonary vascular walls and reduced vascular lumen. The present study extended these findings by further characterizing the pulmonary vasculature of COVID-19 patients using larger sample sizes and providing mechanistic information through histological observations. The examination of 56 autopsy lung samples showed thickened vascular walls of small pulmonary arteries after 14 days of disease compared to H1N1 influenza patients who died before COVID- 19 pandemic started. Pulmonary vascular remodeling in COVID-19 patients was associated with hypertrophy of the smooth muscle layer, perivascular fibrosis, edema and lymphostasis, inflammatory infiltration, perivascular hemosiderosis and neoangiogenesis. We found a correlation between the duration of hospital stay and the thickness of the muscular layer of pulmonary arterial walls. These results further confirm that COVID-19 affects the pulmonary vasculature and warrants an evaluation of patients that survived COVID-19 for possible future development of pulmonary arterial hypertension.

新冠肺炎患者肺动脉重构的组织病理学评价。
一种正义单链RNA病毒——严重急性呼吸综合征冠状病毒2 (SARS-CoV-2),引发了席卷全球的2019冠状病毒病(COVID-19)大流行。虽然这是一种呼吸道病毒,但SARS-CoV-2感染的一个特征被认为会导致其他器官的发病机制。由于SARS-CoV-2的膜融合蛋白(刺突蛋白)与其主要宿主细胞受体血管紧张素转换酶2 (ACE2)结合,而ACE2调节心血管疾病的关键介质血管紧张素II,因此COVID-19在很大程度上与血管病变相关。事实上,我们之前曾报道过,从COVID-19死亡患者身上收集的死后肺组织显示出肺血管壁增厚和血管管腔减少。本研究通过使用更大的样本量进一步表征COVID-19患者的肺血管,并通过组织学观察提供机制信息,从而扩展了这些发现。对56个尸检肺样本的检查显示,与COVID- 19大流行开始前死亡的H1N1流感患者相比,患病14天后小肺动脉血管壁增厚。COVID-19患者肺血管重构与平滑肌层肥大、血管周围纤维化、水肿和淋巴淤积、炎症浸润、血管周围含铁血黄素沉着和新生血管生成有关。我们发现住院时间与肺动脉壁肌层厚度之间存在相关性。这些结果进一步证实了COVID-19影响肺血管系统,值得对COVID-19存活患者进行评估,以了解未来可能发展为肺动脉高压。
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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