Last updated on:December 21st, 2022
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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's clinical course is variable. Infection can result in one of three outcomes. These include full viral clearance with no residual inflammation; viral persistence with or without inflammation; or autoimmune-mediated inflammation despite viral clearance. Genetic factors have been hypothesized to influence the clinical outcome, although the precise mechanism is yet to be elucidated.
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.
Parvovirus B19 (parvoB19V) appears to be the most common agent. Other notable agents include adenovirus, enterovirus (coxsackie virus), herpesvirus (human herpesvirus 6, Epstein Barr virus), hepatitis C virus (HCV), human immunodeficiency virus (HIV) and influenza A.
Though the pathogenesis of VM can vary according to each virus's mode of invasion, the main stages of infection are largely the same. Direct viral entry of cardiomyocytes occurs via receptor-mediated endocytosis of cardiotropic viruses and may be followed by an inflammatory phase, dominated by adaptive immune and autoimmune processes triggered by persistent viral presences. Multiple immune system cells are involved, including natural killer cells and macrophages, which in turn may lead to cytokine-mediated inflammation. In endomyocardial biopsy-proven myocarditis, inflammatory infiltrate is most commonly lymphocytic, borderline, granulomatous, giant cell and eosinophilic, in that order.
Coronavirus disease of 2019 (COVID-19) myocarditis
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.
Most cases of acute myocarditis in children are viral in nature. As with adult cases, the clinical course and most clinical features are similar. The most recent development involves the ventricular dysfunction seen in children, notably part of the multisystem inflammatory syndrome in children that involves inflammation of the heart and vessels during or after the active infectious phase. Signs of myocardial inflammation and viral nucleic acid were often found on autopsy in these cases.
Disease complications of VM include but are not exclusively limited to: