Is fulminant myocarditis caused by circulating human coronaviruses?

This Commentary refers to: ‘Coronavirus fulminant myocarditis saved with glucocorticoid and human immunoglobulin’, by H. Hu et al., doi: 10.1093/eurheartj/ehaa190.

I read with interest the recent Cardiovascular Flashlight publication by Hu et al.¹ In December 2019, a cluster of pneumonia cases of unknown aetiology were identified in Wuhan, Hebei, China caused by a novel coronavirus, later named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).² According to the Johns Hopkins coronavirus resource centre, there have been 2,090,110 reported cases with 139,469 deaths worldwide as of 16 April 2020. Patients with SARS-CoV-2 infection can have acute respiratory distress syndrome (ARDS) followed by multiorgan failure including fulminant myocarditis.³ Appropriate treatment for severe SARS-CoV-2 infections is unknown. Treatment with corticosteroids is discouraged by the World Health Organization,⁴ and immunoglobulin use is controversial.

Hu and colleagues report a fascinating case of a young patient presenting acutely with chest pain and dyspnoea found to be in cardiogenic shock with an ST elevation myocardial infarction and dilated cardiomyopathy. A sputum sample revealed the presence of coronavirus RNA and the patient was treated with methylprednisolone and immunoglobulin, with clinical improvement.

While it is possible coronavirus was responsible for his fulminant myocarditis, it is unlikely. First, it should be clarified that this patient was not infected with SARS-CoV-2 and was rather infected with a one of the four commonly circulating coronaviruses (OC43, HKU1, NL63, and 229E). SARS-CoV-2 is not detected on routine respiratory pathogen panels and additional SARS-CoV-2 testing was not pursued in this patient. This is an important clarification as SARS-CoV-2 is known to cause ARDS and ultimately fulminant myocarditis, while circulating human coronaviruses typically do not. Secondly, identification of coronavirus RNA from sputum could simply be a colonizer rather than a true pathogen. There is no mention of fever or acute respiratory illness and, while the chest imaging is abnormal with evidence of fluid overload, it does not appear to be consistent with viral pneumonia. A case–control study in Asia reported that human coronaviruses did not cause pneumonia and, interestingly, coronavirus RNA could be identified in 2% of healthy asymptomatic patients.⁵ A myocardial biopsy would be needed to prove coronavirus myocarditis, while a coronavirus PCR from a respiratory sample is not specific.

While immune modulation with corticosteroids and immunoglobulin is a mainstay for fulminant myocarditis, it is controversial in SARS-CoV-2 fulminant infection. One should be cautious in extrapolating the successful treatment of this patient to guide treatment of fulminant SARS-CoV-2 infection.