Department of Cardiac Surgery, Centre Cardiologique du Nord, 93200 Saint-Denis, France.
Department of Cardiothoracic Surgery, Royal Infirmary of Edinburgh, Edinburgh EH16 4SA, UK.
Viruses. 2023 Apr 2;15(4):916. doi: 10.3390/v15040916.
In this review, we investigated whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can directly cause myocarditis with severe myocardial damage induced by viral particles. A review of the major data published from 2020 to 2022 was performed by consulting the major databases alongside first-hand experiences that emerged from the cardiac biopsies and autopsy examinations of patients who died of SARS-CoV-2 infections. From this study, a significantly large amount of data suggests that the Dallas criteria were met in a residual percentage of patients, demonstrating that SARS-CoV-2 myocarditis was a rare clinical and pathological entity that occurred in a small percentage of subjects. All cases described here were highly selected and subjected to autopsies or endomyocardial biopsies (EMBs). The most important discovery, through the detection of the SARS-CoV-2 genome using the polymerase chain reaction, consisted in the presence of the viral genome in the lung tissue of most of the patients who died from COVID-19. However, the discovery of the SARS-CoV-2 viral genome was a rare event in cardiac tissue from autopsy findings of patients who died of myocarditis It is important to emphasize that myocardial inflammation alone, as promoted by macrophages and T cell infiltrations, can be observed in noninfectious deaths and COVID-19 cases, but the extent of each cause is varied, and in neither case have such findings been reported to support clinically relevant myocarditis. Therefore, in the different infected vs. non-infected samples examined, none of our findings provide a definitive histochemical assessment for the diagnosis of myocarditis in the majority of cases evaluated. We report evidence suggesting an extremely low frequency of viral myocarditis that has also been associated with unclear therapeutic implications. These two key factors strongly point towards the use of an endomyocardial biopsy to irrefutably reach a diagnosis of viral myocarditis in the context of COVID-19.
在这篇综述中，我们调查了严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）是否可以直接导致心肌炎，以及病毒颗粒是否会导致严重的心肌损伤。通过查阅主要数据库并结合对死于 SARS-CoV-2 感染的患者的心脏活检和尸检检查中出现的第一手经验，对 2020 年至 2022 年发表的主要数据进行了综述。从这项研究中，大量数据表明，达拉斯标准在残留的患者中得到了满足，表明 SARS-CoV-2 心肌炎是一种罕见的临床和病理实体，在一小部分患者中发生。这里描述的所有病例都是高度选择的，并进行了尸检或心内膜心肌活检（EMB）。通过聚合酶链反应检测 SARS-CoV-2 基因组的最重要发现是，大多数死于 COVID-19 的患者的肺组织中存在病毒基因组。然而，在死于心肌炎的患者的尸检心脏组织中发现 SARS-CoV-2 病毒基因组是一个罕见事件。需要强调的是，巨噬细胞和 T 细胞浸润引起的心肌炎症仅在非传染性死亡和 COVID-19 病例中观察到，但每种原因的程度不同，在任何一种情况下，都没有发现这些发现支持临床上相关的心肌炎。因此，在检查的不同感染与非感染样本中，我们的发现都没有为大多数评估病例提供心肌炎的明确组织化学评估。我们报告的证据表明，病毒性心肌炎的频率极低，也与治疗意义不明确有关。这两个关键因素强烈指向使用心内膜心肌活检来无可争议地诊断 COVID-19 背景下的病毒性心肌炎。
