Viral Myocarditis and Dilated Cardiomyopathy: Mechanisms of Cardiac Injury, Inflammation, and Fibrosis

Myocarditis is an inflammation of the myocardium, which often follows infection with one of many different pathogens including viruses, bacteria, protozoa, helminths, or fungi. Enteroviruses of the family of Picornaviruses (small, positive-sense, single-stranded RNA viruses) are a major etiological agent causing the clinical disease. Myocyte injury results from the direct infection and replication of the pathogen, from the innate and adaptive host immune responses to the infection, and from induction of autoimmunity to heart antigens. Chronic inflammation is likely due to autoimmunity, persistent viral infection in the heart, and an attempt to heal scar tissue laid down as a consequence of acute inflammation-induced remodeling. Profibrotic cytokines and mediators released during acute myocarditis in susceptible individuals activate fibroblasts and recruit new fibroblast differentiation via endothelial mesenchymal transition leading to cardiac remodeling and dilated cardiomyopathy.