Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is presenting as a systemic disease associated with vascular inflammation and endothelial injury. Severe forms of SARS-CoV-2 infection induce acute respiratory distress syndrome (ARDS) and there is still an ongoing debate on whether COVID-19 ARDS and its perfusion defect differs from ARDS induced by other causes. Beside pro-inflammatory cytokines (such as interleukin-1 β [IL-1β] or IL-6), several main pathological phenomena have been seen because of endothelial cell (EC) dysfunction: hypercoagulation reflected by fibrin degradation products called D-dimers, micro- and macrothrombosis and pathological angiogenesis. Direct endothelial infection by SARS-CoV-2 is not likely to occur and ACE-2 expression by EC is a matter of debate. Indeed, endothelial damage reported in severely ill patients with COVID-19 could be more likely secondary to infection of neighboring cells and/or a consequence of inflammation. Endotheliopathy could give rise to hypercoagulation by alteration in the levels of different factors such as von Willebrand factor. Other than thrombotic events, pathological angiogenesis is among the recent findings. Overexpression of different proangiogenic factors such as vascular endothelial growth factor (VEGF), basic fibroblast growth factor (FGF-2) or placental growth factors (PlGF) have been found in plasma or lung biopsies of COVID-19 patients. Finally, SARS-CoV-2 infection induces an emergency myelopoiesis associated to deregulated immunity and mobilization of endothelial progenitor cells, leading to features of acquired hematological malignancies or cardiovascular disease, which are discussed in this review. Altogether, this review will try to elucidate the pathophysiology of thrombotic complications, pathological angiogenesis and EC dysfunction, allowing better insight in new targets and antithrombotic protocols to better address vascular system dysfunction. Since treating SARS-CoV-2 infection and its potential long-term effects involves targeting the vascular compartment and/or mobilization of immature immune cells, we propose to define COVID-19 and its complications as a systemic vascular acquired hemopathy.

由严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 引起的 2019 年冠状病毒病 (COVID-19) 是一种与血管炎症和内皮损伤相关的全身性疾病。严重形式的 SARS-CoV-2 感染会诱发急性呼吸窘迫综合征 (ARDS)，关于 COVID-19 ARDS 及其灌注缺陷是否与其他原因诱发的 ARDS 不同，仍有争议。除了促炎细胞因子（如白细胞介素 1 β [IL-1β] 或 IL-6）外，由于内皮细胞 (EC) 功能障碍，已观察到几种主要病理现象：由称为 D-二聚体的纤维蛋白降解产物反映的高凝状态，微血栓和大血栓以及病理性血管生成。SARS-CoV-2 引起的直接内皮感染不太可能发生，EC 表达 ACE-2 是一个有争议的问题。确实，在 COVID-19 重症患者中报告的内皮损伤可能更可能继发于邻近细胞的感染和/或炎症的结果。内皮病可能通过改变不同因子（如血管性血友病因子）的水平而导致高凝状态。除了血栓形成事件之外，病理性血管生成也是最近的发现之一。在 COVID-19 患者的血浆或肺活检中发现了不同的促血管生成因子，如血管内皮生长因子 (VEGF)、碱性成纤维细胞生长因子 (FGF-2) 或胎盘生长因子 (PlGF) 的过度表达。最后，SARS-CoV-2 感染诱导了与免疫失调和内皮祖细胞动员相关的紧急骨髓生成，导致获得性血液系统恶性肿瘤或心血管疾病的特征，本文将对此进行讨论。总之，本综述将试图阐明血栓并发症、病理性血管生成和 EC 功能障碍的病理生理学，从而更好地了解新靶点和抗血栓方案，以更好地解决血管系统功能障碍。由于治疗 SARS-CoV-2 感染及其潜在的长期影响涉及靶向血管室和/或未成熟免疫细胞的动员，我们建议将 COVID-19 及其并发症定义为全身性血管获得性血液病。可以更好地了解新靶点和抗血栓形成方案，以更好地解决血管系统功能障碍。由于治疗 SARS-CoV-2 感染及其潜在的长期影响涉及靶向血管室和/或未成熟免疫细胞的动员，我们建议将 COVID-19 及其并发症定义为全身性血管获得性血液病。可以更好地了解新靶点和抗血栓形成方案，以更好地解决血管系统功能障碍。由于治疗 SARS-CoV-2 感染及其潜在的长期影响涉及靶向血管室和/或未成熟免疫细胞的动员，我们建议将 COVID-19 及其并发症定义为全身性血管获得性血液病。