ABSTRACT
Inflammatory processes induced by viral or bacterial infections are believed to be one of the major pathogenetic mechanisms in myocarditis and inflammatory cardiomyopathy (dilated cardiomyopathy, inflammatory; DCMI). Although virtually any microbial agent can cause myocardial inflammation and dysfunction, bacterial infections are rare in these conditions in western countries and viral forms are considered the most common cause of acquired cardiomyopathies nowadays. While Coxsackievirus involvement is well established in pediatric myocarditis due to direct isolation of infectious virus, its involvement in adult heart disease rests primarily upon serological evidence and direct detection of enterovirus RNA in heart muscle by nucleic acid hybridization and RT-PCR. Subsequent molecular biological studies have identified distinct genotypes of different viruses and virus subtypes in myocardial tissues of patients with acute, chronic, and end-stage heart diseases. Spontaneous improvement of ventricular function following virus clearance, complete or partial reversibility of ventricular dysfunction after antiviral treatment, progression of myocardial dysfunction in patients with persisting viral infections, and adverse prognosis in virus-positive patients on the other hand have led to the assumption that dilated cardiomyopathy (DCM) may be a late sequela of viral myocarditis.
