viral myocarditis

Viral myocarditis results from direct viral cytotoxicity and subsequent T-cell mediated immune injury to cardiac myocytes. Coxsackievirus B is the classic cause, but other viruses include adenovirus, parvovirus B19, HHV-6, echovirus, and in immunocompromised patients, CMV. Pathogenesis involves three phases: (1) viral entry and replication causing direct myocyte damage, (2) immune-mediated injury from cytotoxic T cells and cytokines (this autoimmune phase may persist after virus clearance), and (3) chronic remodeling that can lead to dilated cardiomyopathy in a subset of patients. Clinical presentation ranges from asymptomatic to fulminant heart failure; classic scenario is a young adult with recent viral prodrome (fever, myalgias) followed by chest pain (mimicking MI but with normal coronaries), palpitations, syncope, or signs of heart failure. Can cause sudden cardiac death in young athletes due to arrhythmias. ECG may show diffuse ST changes, arrhythmias, or heart block. Cardiac biomarkers (troponin) are often elevated. Echocardiography may show global hypokinesis or wall motion abnormalities. Cardiac MRI with late gadolinium enhancement is useful for diagnosis. Endomyocardial biopsy is the gold standard (Dallas criteria: lymphocytic infiltrate with myocyte necrosis) but has low sensitivity due to patchy involvement. Management is largely supportive (heart failure therapy, arrhythmia management); immunosuppression is controversial and generally reserved for specific subtypes like giant cell myocarditis. Complications include dilated cardiomyopathy, arrhythmias, and sudden death. It's a key cause of sudden death in young, otherwise healthy individuals and should be considered in the differential for myocarditis-associated pericarditis (myopericarditis) as well.