Myocarditis is a disease of the myocardium caused by various infectious (or non-infectious) factors. “Definite” diagnosis of myocarditis is made by a combination of histological, immunohistochemical and immunological criteria (myocardial biopsy is required). However, in the vast majority of cases the working diagnosis is the so-called a “possible” diagnosis based on patient’s clinical presentation (signs and symptoms), laboratory (myocardial necrosis markers), imaging and electrocardiographic findings. In clinical routine, the main diagnostic test is magnetic resonance imaging (MRI) of the heart (CMR) in which a characteristic pattern is identified.
Viral infections are the leading cause of myocarditis. It used to be due to adenoviruses or enteroviruses (eg Cocsakie). Viral myocarditis is now thought to be more commonly caused by herpetoviruses (eg HHV-6, CMV) and parvo B-19 virus (parvoB19). In addition, it should be noted that coronaviruses (eg SARS-CoV-2) can also cause myocarditis – although myocardial injury in COVID-19 may have multiple causes.
The exact mechanism of myocardial injury in cases of viral myocarditis has not been fully elucidated. There are some theoretical hypotheses, with the predominant one being the immune response to the infectious agent. If the reaction of the organism successfully leads to the complete removal of the virus from the myocardium, then the adverse consequences are gradually reversed. Still, if this is not possible, then a persistent inflammatory response may eventually lead to fibrosis, dilatation and remodeling of the left ventricle increasing the possibility of dilated cardiomyopathy. Given that myocardial involvement in the case of a viral infection does not occur in everyone, along with the observation that same-family members suffer more frequently, indicates that there is a genetic substrate in those who are eventually infected.
Treatment of myocarditis involves avoidance of any intense physical activity (non-compliance with this may result in an increased in viral load and increased in mortality). Exercise abstinence is recommended for all patients for 6 months from diagnosis. If cardiac function is normal after this time, the patient is monitored periodically at sparse intervals for up to 3 years after the episode to rule out late complications (dilated cardiomyopathy or heart failure with a normal left ventricular ejection fraction).
Pharmaceutical treatments depends on patient’s clinical presentation and local protocols. In the case thata decrease in left ventricular ejection fraction is observed, appropriate medication is administered (β-adrenergic blockers, angiotensin converting enzyme inhibitors, diuretics, saline inhibitors). For those patients in whom left ventricular ejection fraction remains normal, there is no consensus on the benefit of using the abovementioned treatment, with the possible exception of β-blockers.