Viral infections often affect the heart. In the majority of cases, the course of the disease is benign and patients recover spontaneously. However,
viral infection may persist and lead to acute
cardiac failure or progress to
dilated cardiomyopathy.
Viral infections are considered to be the most common causes of
myocarditis. There is evidence that intramyocardial viral persistence is associated with progressive
ventricular dysfunction, even when the infiltrate is sparse or missing. The diagnosis of viral
myocarditis necessitates the detection of viral genome by molecular biology techniques and the evaluation of myocardial
inflammation by the immunohistochemistry on endomyocardial biopsy samples. Autoreactive
myocarditis can also only be diagnosed by endomyocardial biopsy. Infiltration of leukocytes and a negative polymerase chain reaction on microbial agents are their hallmarks. Apart from symptomatic or supportive
therapy, etiologic treatment strategies have to address the underlying causative virus or the autoimmune process. In symptomatic or deteriorating patients, targeted
antiviral therapy is a reasonable algorithm to eradicate the virus, which will contribute to resolving
inflammation or apoptosis, thus confining myocardial damage. The Marburg registry favors
intravenous immunoglobulin treatment in biopsy-proven adenovirus and parvovirus B19
myocarditis combined with optimal conventional
therapy to achieve virus clearance. In fulminant
myocarditis, biopsy is mandatory to identify giant cell
myocarditis and cardiac
sarcoidosis to be treated by immunosuppression. In
cardiogenic shock, the use of mechanical circulatory support by means of a
ventricular assist device as a bridge to recovery may be a lifesaving approach. In perimyocarditis with dominant pericardial affection,
colchicine over a period of 1 to 6 months can dissolve the
pericardial effusion effectively in more than 80% of cases.