Both the infectious agent and development of inflammatory response to infection can lead to irreversible myocardial injury, which affects the outcome of short- and long-term prognosis. In the case of the rapid elimination of the infectious agent and rapid withholding of inflammatory process, changes in myocardium are small. If the immune response does not lead to complete elimination of infectious agent or inflammation progresses after removing the virus, chronic myocardial damage may develop. Persistence of the virus in myocardium, postinfectious immune reaction, autoimmunity, and primary cardiac damage may result in the development of progressive ventricular dysfunction, development of cardiac arrhythmias, and exacerbation of symptom. Because of the long-term consequences, it is important to diagnose infective cardiomyopathy (IC) quickly and start appropriate treatment. However, IC is still a diagnostic challenge. Infective cardiomyopathy is often underdiagnosed because of a wide spectrum of factors causing IC—infectious, toxic, immunologic, and various clinical manifestation. The processes responsible for the development of IC take place at the cellular level, which is why it is important to make the diagnosis not only based on clinical symptoms and imaging but also to confirm it with the use of histological, immunohistochemical, and molecular studies. Progress in the diagnosis and understanding of the pathomechanisms responsible for the development of IC contributed to the use of new therapeutic options. Immunosuppresive and immunomodulative treatment is still of limited use. However, in some cases of viral IC, targeted antiviral treatment can be added to the standard heart failure therapy resulting in improvement of the prognosis.
Part of the book: Cardiomyopathies