Long COVID Myocarditis: Incidence, Mechanisms, Clinical Implications, and Management

Long coronavirus disease (COVID) (post-acute sequelae of severe acute respiratory syndrome coronavirus 2 infection) is characterized by persistent or new health issues weeks or months after acute COVID-19. Cardiac involvement, including myocarditis, is a notable complication that can occur even after an initially mild infection. To review current literature (2022-2025) on myocarditis in Long COVID, focusing on incidence, pathophysiological mechanisms, clinical presentation, diagnosis, management, prognosis, and future directions. Post-COVID myocarditis remains relatively uncommon but is significantly more frequent than pre-pandemic rates. Myocardial injury in Long COVID is hypothesized to result from multiple mechanisms: persistent viral antigen or RNA in cardiac tissue causing chronic immune activation, immune-mediated damage (including autoimmunity such as anti-heart antibodies), microvascular endothelial dysfunction with impaired perfusion, and maladaptive inflammatory responses. Patients may present with typical myocarditis symptoms (exertional chest pain, dyspnea, palpitations) or atypical features like exercise intolerance, orthostatic tachycardia, or unexplained fatigue. Management is supportive and guided by myocarditis severity: exercise restriction for 3-6 months in confirmed cases, guideline-directed heart failure therapy if ventricular dysfunction is present, anti-inflammatory or immunosuppressive therapy in specific scenarios (eg, corticosteroids in fulminant cases or overlapping multisystem inflammatory syndrome), and therapies targeting pericardial involvement (nonsteroidal anti-inflammatory drugs, colchicine) if present.