Viral myocarditis (VM) is a type of inflammatory myocarditis, a broad heading under which bacterial, protozoal, fungal infections, toxic substances, medications, and systemic immune-system mediated diseases are also classified as causative agents.

VM is a dynamic, multi-phasic (acute and chronic) condition characterized by a wide range of clinical presentations including acute coronary syndrome-type chest pain, acute heart failure, chronic dilated cardiomyopathy (DCM), and sudden cardiac death. Its acute phase is infection driven, while its chronic phase is dominated by autoimmunity, likely triggered through molecular mimicry by persistent viral presence. Chronic viral inflammation ultimately leads to tissue remodeling and the development of DCM and heart failure (HF).

VM is known to affect all age groups, ethnicities and genders. It is mainly found in young and middle-aged adults, with the median age at diagnosis being roughly 42 years old.

Though its exact pathophysiology remains unknown to date, COVID-19 myocarditis is caused by the SARS-CoV2 virus. Direct cardiotoxic effects and cytokine storm are two prevailing hypotheses for its occurrence, although echocardiographic and endomyocardial biopsy (EMB) findings to distinguish it from other viral causes remain non-specific. It is differentiated from other viral causes by evidence of SARS-CoV2 polymerase chain reaction (PCR) testing, and clinical clues in the history, such as the development of acute respiratory distress syndrome, or history of exposure. Dyspnea is the main presenting symptom, and hypertension is the most common comorbidity.

Disease complications of VM include but are not exclusively limited to:

1. Acute heart failure, found in the acute phase of VM.
2. DCM, the end result of chronic VM.
3. Life-threatening arrhythmias, including monomorphic ventricular tachycardia, and atrial fibrillation.
4. Cardiogenic shock.
5. Conduction abnormalities, and variable degrees of heart block requiring treatment.
6. Sudden cardiac death.