You are here

Article Text

Article menu
Download PDFPDF
EBM opinion and debate
General medicine
SARS-CoV-2 myocarditis: what physicians need to know
  1. Arsalan Khalil,
  2. Tamara Naneishvili,
  3. Neeraj Prasad,
  4. James Glancy
  1. Cardiology, County Hospital Hereford, Hereford, Herefordshire, UK
  1. Correspondence to Dr Arsalan Khalil, Cardiology, County Hospital Hereford, Hereford HR1 2BN, UK; arsalan.khalil{at}nhs.net

https://doi.org/10.1136/bmjebm-2020-111527

Statistics from Altmetric.com

    Request Permissions

    If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

    Introduction

    Myocarditis is one of the complications seen with viral infections like parvovirus B19, human herpes virus, Epstein-Barr virus, cytomegalovirus, adenovirus and enteroviruses. Recent data suggest that SARS-CoV-2 could be a possible aetiological agent for myocarditis in the current pandemic.1 Although we have some understanding of its respiratory manifestations, limited data are available regarding the involvement of the heart with this virus.

    Myocarditis secondary to SARS-CoV-2 has been reported as one of the causes of increased mortality.1 The European Society of Cardiology (ESC) states ‘in the absence of vaccines or curative medical treatment, SARS-CoV-2 exerts an unprecedented global impact on public health and healthcare delivery’.2

    In this article, we outline the pathophysiology, clinical manifestations, investigations and some of the treatment modalities that have been used so far for the management of SARS-CoV-2-related myocarditis. We also suggest areas for further research.

    What do we know so far?

    Multiple case reports have described SARS-CoV-2-related myocarditis.3–5 However; there are no randomised controlled trials or meta-analysis on this subject.

    Proposed mechanisms for injury to the myocardium include binding of SARS-CoV-2 spike protein to ACE 2 which facilitates virus entry into the target cells,6 immune-related myocardial inflammation and direct injury to the myocardium caused by hypoxemia.7 Furthermore, it has also been suggested that IL-6 plays an integral role in activation of helper T cells, which in turn release inflammatory cytokines ultimately resulting in myocardial inflammation and damage.8

    Age distribution and clinical presentation of SARS-CoV-2-related myocarditis is variable. Clinical manifestations can be as mild as fatigue and shortness of breath to devastating …

    View Full Text