To the Editor,
We read with interest the article by Nishioka et al. 1 on a 15‐year‐old male diagnosed with acute myocarditis 2 days after clinical onset of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection. The patient was admitted because of heart failure and atrioventricular (AV) block III and was treated with mechanical ventilation, extra‐corporal membrane oxygenation (ECMO), steroids, remdesivir, and dobutamine. 1 He was extubated 8 days after admission and was transferred for further rehabilitation. 1 The study is promising but raises concerns that should be discussed.
We disagree with the diagnosis of myocarditis. 1 Myocarditis is either diagnosed by endomyocardial biopsy or by contrast‐enhanced cardiac magnetic resonance imaging (MRI). Neither investigation was carried out. Therefore, the diagnosis of myocarditis is based at best on speculation rather than evidence. The frequent occurrence of arrhythmias is not an argument for myocarditis, since arrhythmias can also arise from other heart diseases. In myocarditis, cardiac MRI may show subendocardial, subepicardial, mid‐myocardial, or trans‐myocardial gadolinium enhancement of the myocardium. 2 Magnetic resonance elastography (MRE) can show increased stiffening of the myocardium due to fibrosis and inflammation, and oxygen extraction fraction MRI can show decreased oxygen utilization. 3 Biopsy may show infiltration of inflammatory cells of the myocardium. The reader should know whether biopsy or cardiac MRI was performed.
Differential diagnoses of elevated creatine‐kinase (CK), heart failure, and AV‐block were not adequately ruled out. An important unconsidered differential diagnosis was Takotsubo syndrome (TTS). 4 This is a known complication of SARS‐CoV‐2 infections and, as in the index patient, can be complicated by arrhythmias and heart failure. 5 Takotsubo syndrome is diagnosed according to the Mayo Clinic criteria, which include ruling out coronary heart disease. Takotsubo syndrome mimics myocardial infarction, clinically, electrocardiographically, blood chemically, and echocardiographically.
A shortcoming of the study is that it was not stated whether the index patient's condition had been diagnosed as viral myocarditis or immune myocarditis. Viral myocarditis is rare and SARS‐CoV‐2‐related myocarditis is more common as a result of immune mechanisms. Another shortcoming is that reference limits were not specified for any of the laboratory parameters presented.
The long‐term outcome of the patient is missing. We should know if the heart failure and AV block completely disappeared and after what time. Of particular interest is whether or not the patient requires permanent pacemaker implantation. There is no information as to whether the patient was vaccinated against SARS‐CoV‐2, with which brand, how often, and with what latency until the current cardiac impairment.
We should be aware of the criteria used to distinguish ventilatory‐associated pneumonia from SARS‐CoV‐2 pneumonia. COVID‐19 pneumonia can vary in intensity and extent over time. Was a pathogen isolated from the tracheal secretions?
Overall, the interesting study has limitations that call the results and their interpretation into question. Clarifying these weaknesses would strengthen the conclusions and could improve the study. Myocarditis should not be diagnosed by clinical criteria alone but substantiated by biopsy or cardiac MRI.
AUTHOR CONTRIBUTIONS
Josef Finsterer conducted the design, literature search, discussion, first draft, critical comments, and final approval of this study. Sounira Mehri conducted the literature search, discussion, critical comments, and final approval.
CONFLICT OF INTEREST
The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
ETHICS STATEMENT
This article is based on previously conducted studies and does not contain any new studies with human participants or animals performed by any of the authors.
REFERENCES
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