Published: July 9, 2025
Myocarditis represents a significant cause of morbidity and mortality in pediatric patients, yet its clinical presentation can be deceptively subtle. As inflammation of the heart muscle and conduction system, myocarditis affects the heart’s ability to contract effectively and maintain normal rhythm, potentially leading to sudden cardiac death even in previously healthy children.
Cardiomyopathy affects approximately 1 to 1.5 per 100,000 children annually in the United States, with myocarditis accounting for roughly 16% of identifiable causes of dilated cardiomyopathy. Several demographic patterns emerge:
While any virus can trigger myocarditis, the most common causes include:
Historical viral patterns:
Noninfectious causes include autoimmune diseases (particularly lupus), hypersensitivity reactions, medications and toxins, though viral etiologies predominate.
The pathophysiology involves direct viral invasion and subsequent immune-mediated damage to myocardial tissue. This can occur during acute viral illness or in a postviral phase weeks after initial infection.
Perhaps the most critical clinical pearl is recognizing that gastrointestinal (GI) symptoms are the most common presenting complaint in pediatric heart failure, including myocarditis-induced cardiomyopathy. Studies consistently show that nausea, vomiting, abdominal pain and feeding intolerance are more common than classic dyspnea or chest pain.
Key clinical insight: More than half of pediatric heart failure cases are initially misdiagnosed, often as viral gastroenteritis. Consider cardiac etiology in children with:
Myocarditis presentations range from:
Modern diagnosis relies on clinical criteria rather than invasive biopsy:
Definite myocarditis: Positive endomyocardial biopsy
Probable myocarditis (acute or subclinical): Requires one or more of:
Laboratory testing:
Electrocardiography:
Imaging:
Biopsy considerations:
Acute phase
Hospitalization is standard for suspected myocarditis due to unpredictable clinical course and potential for rapid deterioration.
Immunomodulatory therapy:
Supportive care:
Monitoring and prognosis
Hospital course: Monitor until troponin trending down, ventricular function stable and arrhythmia burden controlled.
Key prognostic insight: Troponin levels don’t reliably predict severity. Patients with minimally elevated troponin can deteriorate rapidly, while those with very high levels may have preserved function.
Ventricular function patterns:
Goal-directed medical therapy (ACE inhibitors, aldosterone antagonists, beta-blockers) should continue for one year after normalization of cardiac function. The timeline begins when echocardiogram normalizes, not from initial diagnosis.
Long-term outcomes
Three-year follow-up studies reveal:
Pediatric myocarditis remains a diagnostic and management challenge requiring high clinical suspicion, particularly in children presenting with GI symptoms. Early recognition, appropriate supportive care and adherence to activity restrictions can significantly improve outcomes. The key to successful management lies in maintaining clinical vigilance, understanding the disease’s unpredictable nature and providing comprehensive, long-term follow-up care.
Health care providers must remember that myocarditis can present as a great mimicker, and maintaining a low threshold for cardiac evaluation in children with unexplained symptoms may be lifesaving. The combination of clinical acumen, appropriate diagnostic testing and evidence-based management strategies offers the best outcomes for these vulnerable patients.