We have read with great interest the article “Electrocardiographic markers of increased risk of sudden cardiac death in patients with COVID-19 pneumonia” by Alareedh et al., (2021).

The difference between respiratory system virus, circulatory system virus, pulmonary hemorrhagic fever virus, and enterovirus is not very important. Is there still less virus in E. coli culture? ACE2 mediates the destruction of endothelial cells, and thrombosis may be the mechanism. Where is prethrombotic state and hypercoagulable state? It is just an academic discussion of assumptions. The ECG of pulmonary embolism is the camouflager of the heart world. It has various manifestations. Autopsy seems to have proved everything and myocardial infarction.

Acute cardiac injury incidence in COVID-19 is about 13 times higher in the intensive care unit /severely ill than in less critical patients. The cytokine release with complement and iNO dysregulation are established mechanisms potentially leading to sepsis-related cardiomyopathy, making sepsis per se one of the potential mechanism leading to acute cardiac injury in COVID-19 patients. Moreover, the hyper-inflammation with endothelial dysfunction is likely be responsible of both pulmonary in situ platelet aggregation and deep thrombosis potentially leading to severe pulmonary embolism and right ventricular failure(Tavazzi et al., 2020). Coronavirus disease 2019 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) primarily affects the lungs but can involve any organ. Patients who have recovered from COVID-19 have presented with complications such as thrombotic episodes in various organs both during and after being infected with SARS-CoV-2. A COVID-19-associated prothrombotic state has been mentioned in multiple recent research articles (Iqbal et al., 2021). The COVID-19, due to SARS-CoV-2, has uncovered many real-world issues when it comes to healthcare management and has led to widespread mortality. These include myopericarditis, acute coronary syndromes, thrombosis, arrhythmias, hypertension, and heart failure (Veldtman et al., 2020). Novel coronavirus disease (COVID-19) has led to a major public health crisis globally. Currently, myocardial damage is speculated to be associated with COVID-19, which can be seen as one of the main causes of death of patients with COVID-19 (Liaqat et al., 2021). These cases suggest a possible connection between acute elevated right ventricular afterload and acute respiratory distress in patients affected by SARS-CoV-2 (Martínez-Mateo et al., 2020). Acute coronary syndrome-ST-elevation myocardial infarction is a relevant complication of COVID-19. Due to high levels of pro-inflammatory mediators, diffuse coronary thrombosis could occur even in patients without cardiac history or comorbidities (Tedeschi et al., 2020).

我们饶有兴趣地阅读了 Alareedh 等人（2021 年）的文章“COVID-19 肺炎患者心源性猝死风险增加的心电图标志物” 。

呼吸系统病毒、循环系统病毒、肺出血热病毒和肠道病毒之间的区别不是很重要。大肠杆菌培养物中的病毒是否仍然较少？ACE2介导内皮细胞的破坏，血栓形成可能是其机制。血栓前状态和高凝状态在哪里？这只是对假设的学术讨论。肺栓塞的心电图是心脏世界的伪装。它有多种表现形式。尸检似乎已经证明了一切和心肌梗塞。

COVID-19 中重症监护病房/重症患者的急性心脏损伤发生率大约是不太危重的患者的 13 倍。细胞因子释放与补体和 iNO 失调是可能导致败血症相关心肌病的既定机制，使败血症本身成为导致 COVID-19 患者急性心脏损伤的潜在机制之一。此外，内皮功能障碍的过度炎症可能是肺原位血小板聚集和深部血栓形成的原因，可能导致严重的肺栓塞和右心室衰竭（Tavazzi 等，  2020）。由严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 引起的 2019 年冠状病毒病主要影响肺部，但可累及任何器官。从 COVID-19 中康复的患者在感染 SARS-CoV-2 期间和之后都出现了并发症，例如各种器官的血栓形成。最近的多篇研究文章中都提到了与 COVID-19 相关的血栓前状态（Iqbal 等人，  2021 年）。由于 SARS-CoV-2，COVID-19 在医疗保健管理方面揭示了许多现实问题，并导致了广泛的死亡。这些包括心肌心包炎、急性冠状动脉综合征、血栓形成、心律失常、高血压和心力衰竭（Veldtman 等，  2020）。新型冠状病毒病 (COVID-19) 已在全球引发重大公共卫生危机。目前，推测心肌损伤与 COVID-19 相关，这可以看作是 COVID-19 患者死亡的主要原因之一（Liaqat 等，  2021）。这些病例表明，在受 SARS-CoV-2 影响的患者中，急性右心室后负荷升高与急性呼吸窘迫之间可能存在联系（Martínez-Mateo 等人，  2020 年）。急性冠状动脉综合征-ST 段抬高心肌梗死是 COVID-19 的相关并发症。由于高水平的促炎介质，即使在没有心脏病史或合并症的患者中也可能发生弥漫性冠状动脉血栓形成（Tedeschi 等，  2020）。