The association between coronavirus disease 2019 (COVID19) and cardiovascular diseases is of great concern. Zeng and colleagues reported for the first time a patient with COVID19 complicated with fulminant myocarditis [1, 2]. Several concerns should improve the implication of their finding. The electrocardiogram on admission indicates right ventricular loading, given elevated R waves and strain pattern with inverted T wave in V1-2 leads, as well as deep S waves in V5-6 leads, in addition to left atrial loading, given biphasic P wave in V1 lead. Invasive right heart catheterization would have been useful to more accurately assess right ventricular function, using central venous pressure, right ventricular stroke work index, and pulmonary artery pulsatility index [3]. Hemodynamic monitoring using right heart catheterization might also have clarified the mechanism of hemodynamic deterioration on day 29. Furthermore, a concomitant endo-myocardial biopsy from the right ventricular septum would have contributed to pathological diagnosis concluding definite causality of COVID-19: direct myocardial injury or indirect immune-associated myocardial depression. Complete recovery of myocardial function in their case might support the latter causality. Recently, percutaneous minimal axial-flow left ventricular assist device is considered concomitantly with extracorporeal membrane oxygenation for biventricular unloading (i.e., ECPELLA) [4]. If the patient already had a severe biventricular failure on admission, such a more intensified mechanical circulatory support might have been recommended, instead of extracorporeal membrane oxygenation alone. On the contrary, we should understand that such intensified mechanical therapy increases the risk of devicerelated comorbidities including bleeding, thrombosis, and infection. The appropriate device selection and estimated support length for those with COVID-19-related fulminant myocarditis remain unknown. Nevertheless, we should consider also the challenging situation in the management of COVID-19 patients using personal protective equipment and restrictive medical resources, and such optimal strategies might not always be realistic. I again congratulate the authors’ devoted management.

中文翻译：

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COVID-19 引起的暴发性心肌炎的详细血流​​动力学

2019 年冠状病毒病 (COVID19) 与心血管疾病之间的关联备受关注。Zeng 及其同事首次报道了 COVID19 患者并发暴发性心肌炎 [1, 2]。一些问题应该会改善他们发现的含义。入院时的心电图显示右心室负荷，考虑到升高的 R 波和应变模式，V1-2 导联中的倒置 T 波，以及 V5-6 导联中的深 S 波，除了左心房负荷，给定双相​​ P 波V1 领先。使用中心静脉压、右心室卒中工作指数和肺动脉搏动指数，侵入性右心导管插入术有助于更准确地评估右心室功能 [3]。使用右心导管术进行血流动力学监测也可能阐明了第 29 天血流动力学恶化的机制。此外，同时进行的右室间隔心内膜活检有助于病理诊断得出 COVID-19 的明确因果关系：直接心肌损伤或间接免疫相关的心肌抑制。在他们的情况下，心肌功能的完全恢复可能支持后一种因果关系。最近，经皮最小轴流左心室辅助装置被认为与体外膜肺氧合用于双心室卸荷（即 ECPELLA）[4]。如果患者在入院时已经有严重的双心室衰竭，可能会推荐这种更强化的机械循环支持，而不是单独的体外膜肺氧合。相反，我们应该理解，这种强化机械治疗会增加设备相关并发症的风险，包括出血、血栓形成和感染。对于 COVID-19 相关的暴发性心肌炎患者，合适的设备选择和估计的支持长度仍然未知。尽管如此，我们还应该考虑使用个人防护设备和限制性医疗资源管理 COVID-19 患者的挑战性情况，而且这种最佳策略可能并不总是现实的。我再次祝贺作者的敬业管理。对于 COVID-19 相关的暴发性心肌炎患者，合适的设备选择和估计的支持长度仍然未知。尽管如此，我们还应该考虑使用个人防护设备和限制性医疗资源管理 COVID-19 患者的挑战性情况，而且这种最佳策略可能并不总是现实的。我再次祝贺作者的敬业管理。对于 COVID-19 相关的暴发性心肌炎患者，合适的设备选择和估计的支持长度仍然未知。尽管如此，我们还应该考虑使用个人防护设备和限制性医疗资源管理 COVID-19 患者的挑战性情况，而且这种最佳策略可能并不总是现实的。我再次祝贺作者的敬业管理。