Background Current COVID-19 pandemic reveals thrombotic, vascular and endothelial disfunctions at peak disease, or even after vaccination. However, the duration, degree of damage, and appropriate long-term therapeutic strategies are unclear. Most post-COVID data are yielded from random clinical observations or autopsy of postmortem samples, while precise cellular data in survivors are insufficient. Methods We analyzed blood erythrocytes (RBC), endotheliocytes, and echinocytes by electron microscopy and flow cytometry in patients with confirmed COVID-19 (n=31) and matched controls (n=32) on admission and at hospital discharge. Results All patients experienced mild disease, none required pulmonary support, and all survived. Admission number of circulating endotheliocytes was significantly (40-100 times) higher in COVID-19 patients. Cells were massively damaged by multiple fenestrae in membranes with diameter comparable to the size of supercapsid in SARS CoV-2 virus. COVID-19 also provoked formation of stacked aggregated RBC capable to clog microvascular bed and to diminish oxygen supply. In some patients, such abnormalities persisted at hospital discharge revealing remaining penetration of COVID-19 intracellular where it may be replicated and returned to circulation. Conclusion Cell-endothelial injury cause blood vessels denuded; their increased permeability resulted in tissue edema, inflammation, platelet activation, and augmented thrombosis. Such sequelae can provoke long-term delayed vascular complications following COVID-19. Controlled outcome-driven trials are urgently needed for exploring optimal antithrombotic and vascular protection strategies following even mild COVID-19.

中文翻译：

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轻度 COVID-19 和受损的细胞内皮串扰：考虑长期抗血栓形成和血管保护？

背景 当前的 COVID-19 大流行揭示了在疾病高峰期，甚至在接种疫苗后出现血栓、血管和内皮功能障碍。然而，持续时间、损伤程度和适当的长期治疗策略尚不清楚。大多数 COVID 后数据来自随机临床观察或尸检样本的尸检，而幸存者的精确细胞数据不足。方法 我们通过电子显微镜和流式细胞术分析了入院和出院时确诊的 COVID-19 患者（n=31）和匹配对照（n=32）的血红细胞 (RBC)、内皮细胞和棘细胞。结果所有患者病情轻微，无一例需要肺支持，均存活。COVID-19 患者的循环内皮细胞入院数显着增加（40-100 倍）。细胞被膜中的多个窗孔严重破坏，其直径与 SARS CoV-2 病毒中的超级衣壳大小相当。COVID-19 还引发了堆积聚集的红细胞的形成，这些红细胞能够堵塞微血管床并减少氧气供应。在一些患者中，这种异常在出院时仍然存在，这表明 COVID-19 仍然渗透到细胞内，在那里它可能被复制并返回循环。结论细胞-内皮损伤导致血管剥脱；它们增加的通透性导致组织水肿、炎症、血小板活化和血栓形成增加。这种后遗症会引发 COVID-19 后长期延迟的血管并发症。