We thank Dr. Jiang F for the positive feedback, and we appreciate the interest in our article describing electrocardiographic markers of increased risk of sudden cardiac death in patients with COVID-19 pneumonia and for taking the time to express his comments (Alareedh et al., 2021).

In his letter to the editor, Dr. Jiang F discussed the association of myocardial or cardiac injury related to COVID-19 infection with ECG changes and adverse clinical outcome. We also thought that the presence of cardiac injury related to COVID-19 infection is associated with significant alterations in cardiac conduction and/or repolarization properties, which can predispose to malignant ventricular arrhythmias and sudden cardiac death (Wang et al., 2020).

Different mechanisms have been suggested for cardiac injury related to COVID-19 infection, including myocardial expression of ACE2 on their surface leading to direct myocardial injury, hypoxia, alterations in ion channels, and cytokines storm. All these potential mechanisms potentiate myocardial injury associated with COVID-19 infection that might be detected as various changes in surface ECG (Mehraeen et al., 2020; Wang et al., 2020).

However, the diagnosis of myocarditis is difficult to confirm consistently as diagnosis of possible myocarditis associated with COVID-19 is based on clinical presentation and results of noninvasive imaging without myocardial biopsy or autopsy examinations (Bonow et al., 2020).

In our study, we did not assess the possibility of cardiac involvement by echocardiography or serum markers of cardiac damage, such as troponin or D-dimer, to exclude myocardial injury as we mentioned in the limitation section of our article.

In his letter, Dr. Jiang F mentioned the importance of prethrombotic state and thrombotic state associated with COVID-19 infection, which may lead to pulmonary embolism or coronary thrombosis even in the absence of cardiac risk factors. We agree with the Dr. that prethrombotic state and thrombotic state could potentially play a role in ECG changes or adverse clinical outcome associated with COVID-19 infection. The possible underlying causes of ECG changes, such as pulmonary embolism or coronary disease, were beyond the scope of our study aims because of logistic limitations posed by isolation wards and shortage of health resources, which limits the assessment of all possible confounding factors that might influence ECG changes as we mentioned in the limitation section of our article.

Finally, as the clinical course of COVID-19 evolves rapidly, ECG provides a quick, simple, and effective assessment of the patient's prognosis, and ECG changes detected on admission may be used as a sixth vital sign with possible prognostic value (Elias et al., 2020).

The limitations of our study should be kept in mind while interpreting its results and it would be of particular interest to assess the underlying causes of ECG changes and to determine the prognostic value of these ECG changes in patients with COVID-19 infection in follow-up studies.

我们感谢 Jiang F 博士的积极反馈，感谢您对我们描述 COVID-19 肺炎患者心源性猝死风险增加的心电图标志物的文章感兴趣，并感谢您花时间发表评论（Alareedh 等，2017）。 ， 2021 ）。

Jiang F博士在给编辑的信中讨论了与COVID-19感染相关的心肌或心脏损伤与心电图变化和不良临床结果的关联。我们还认为，与 COVID-19 感染相关的心脏损伤的存在与心脏传导和/或复极特性的显着改变有关，这可能导致恶性室性心律失常和心源性猝死（Wang et al., 2020 ）。

人们提出了与 COVID-19 感染相关的心脏损伤的不同机制，包括心肌表面 ACE2 的表达导致直接心肌损伤、缺氧、离子通道改变和细胞因子风暴。所有这些潜在机制都会加剧与 COVID-19 感染相关的心肌损伤，这可能会通过表面心电图的各种变化来检测（Mehraeen 等人， 2020 ；Wang 等人， 2020 ）。

然而，心肌炎的诊断很难一致地确认，因为对可能与 COVID-19 相关的心肌炎的诊断是基于临床表现和无创成像结果，无需心肌活检或尸检（Bonow 等， 2020 ）。

在我们的研究中，我们没有通过超声心动图或心脏损伤的血清标志物（例如肌钙蛋白或 D-二聚体）评估心脏受累的可能性，以排除心肌损伤，正如我们在文章的限制部分中提到的。

江芳博士在信中提到了与COVID-19感染相关的血栓前状态和血栓状态的重要性，即使在没有心脏危险因素的情况下，也可能导致肺栓塞或冠状动脉血栓形成。我们同意博士的观点，即血栓前状态和血栓状态可能在心电图变化或与 COVID-19 感染相关的不良临床结果中发挥作用。心电图变化的可能根本原因，例如肺栓塞或冠状动脉疾病，超出了我们的研究目标范围，因为隔离病房造成的后勤限制和卫生资源的短缺，限制了对可能影响的所有可能的混杂因素的评估正如我们在文章的限制部分中提到的，心电图会发生变化。

最后，随着COVID-19临床病程的迅速发展，心电图可以快速、简单、有效地评估患者的预后，入院时检测到的心电图变化可作为第六生命体征，具有可能的预后价值（Elias等） ., 2020 ).

在解释其结果时应牢记我们研究的局限性，评估心电图变化的根本原因并确定这些心电图变化对 COVID-19 感染患者随访的预后价值将特别有意义研究。