The coronavirus disease 2019 (COVID-19) pandemic, although no longer a global public health emergency since 2023, is formally still ongoing, and as of May 2024, over 775 million confirmed cases and more than seven million deaths have been reported worldwide. An association between COVID-19 infection and thrombosis was observed very early in the beginning of the pandemic [1]. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was found to have a high affinity for the endothelium; infection predisposes to excessive inflammation, platelet activation, and endothelial cell activation and injury, resulting, among others, in a hypercoagulability state [2, 3]. This pathophysiological association has been clinically translated into thromboembolic events. In particular, patients hospitalised with COVID-19 exhibited an increased incidence of pulmonary embolism (PE), likely contributing to an increased case fatality of the infection in the acute phase [4, 5].

2019 年冠状病毒病 (COVID-19) 大流行虽然自 2023 年以来不再是全球公共卫生紧急事件，但形式上仍在持续，截至 2024 年 5 月，全球报告了超过 7.75 亿确诊病例和超过 700 万人死亡。在大流行开始之初就观察到了 COVID-19 感染与血栓形成之间的关联[1]。严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）被发现与内皮细胞具有高亲和力；感染容易引起过度炎症、血小板活化以及内皮细胞活化和损伤，从而导致高凝状态等[2, 3]。这种病理生理学关联已在临床上转化为血栓栓塞事件。特别是，因 COVID-19 住院的患者肺栓塞 (PE) 的发生率增加，可能导致急性期感染病死率增加 [4, 5]。