Viral myocarditis

Abstract

Purpose of the review This article traces the pathways leading from viral infection of the heart by coxsackievirus B3 to autoimmune myocarditis in its various manifestations. Recent findings Myocarditis can be induced by a number of different infectious agents and represents a significant cause of death especially in young individuals. Following infection patients may develop lymphocytic, eosinophilic, or giant cell/granulomatous myocardial inflammation. It can lead to infectious dilated cardiomyopathy, a disease frequently requiring cardiac transplantation. Although acute viral myocarditis is frequently sub-clinical and recovery may be spontaneous, treatment of chronic myocarditis is presently unsatisfactory. Ongoing disease may be due to persistent virus in the heart or to immunopathic attack. Depending on the etiology, treatment may be antiviral or immunosuppressive. Endomyocardial biopsy is proving of value in determining etiology and deciding future therapy. A great deal of information about the pathogenesis of myocarditis has been gained from experimental models in rodents using heart disease induced by infection using coxsackievirus B3 or by immunization with cardiac myosin. Summary Treatment of myocarditis is still problematic and may depend on etiologic diagnosis to distinguish infectious from immune mediated disease. Both pathogenic mechanisms may co-occur in individual patients. In the future, treatment may depend upon endomyocardial biopsy, immunohistologic testing, improved imaging, and molecular genetic analysis for providing more precise diagnoses.

Cardiac Autoimmunity: Myocarditis

“…All these viruses cause myocarditis with similar inflammatory features, and all could lead to DCM. The real prevalence of progression to DCM for each specific virus is not known [6, 64, 72]. …”

“…T cells play an important role in the clearance of viruses. Specific T cell clones have the capacity to destroy and lysate infected cardiomyocytes, according to in vitro data [72, 76]. Overall, this antiviral response has a dual effect: (a) it controls viral infection and limits its cytotoxic effects, and (b) the tissue damage associated with the T cell response leads to exposure of cryptic antigens like myosin-derived peptides, which could eventually generate an autoimmune cardiac-specific response [79].…”

“…That exposure, in the context of a proper pro-inflammatory microenvironment, triggers the adaptive immune response leading to myocarditis in genetically susceptible individuals [6, 72, 76]. Thus, different triggers could lead to myocarditis and eventually chronic autoimmune myocarditis.…”

“…Fortunately, there is a growing body of therapeutic knowledge which, despite frequently based on case reports and uncontrolled trials, suggests that immune modulation/suppression is a useful approach in myocarditis, even in viral-triggered cases if it is used together with proper antiviral treatment [72, 153]. …”

“…The main antiviral drugs studied in myocarditis have been acyclovir, peramivir, ganciclovir, ribavirin, and artesunate, in well-defined viral myocarditis patients (etiology was specifically determined: parvovirus B19, influenza, cytomegalovirus, parainfluenza, herpesvirus, respectively) [6, 72, 153]. All of them have been either small studies or case reports, but overall the benefit of antiviral treatment seems to be consistent in terms of ejection fraction, survival, and decreased viral load.…”