Acute Myocarditis in the Hospital Setting: Triage, Targeted Therapy, and the Genetics of Sudden Death

In this episode of Hospital Medicine Unplugged, we tackle myocarditis in hospitalized patients—recognize fast, stratify risk, escalate support, and target therapy when needed.

We start with the do-firsts: triage to the right care setting, exclude obstructive coronary artery disease, and launch diagnostic testing with ECG, hs-troponin, natriuretic peptides, CRP, and echocardiography. If the picture remains uncertain, CMR confirms inflammation and endomyocardial biopsy (EMB) is reserved for high-risk or atypical cases where histology can guide therapy.

Risk stratification drives location of care: • Stable patients (preserved EF, no arrhythmias or instability) → general ward with monitoring. • High-risk patients (reduced EF, sustained arrhythmias, advanced AV block, cardiogenic shock, fulminant onset, or biopsy-proven giant cell/eosinophilic myocarditis) → ICU, where rapid deterioration and need for mechanical circulatory support is common.

Supportive care anchors management. Remove inciting agents, maintain continuous monitoring, and manage chest pain cautiously (NSAIDs/colchicine if EF preserved, but avoid NSAIDs in heart failure/shock).

For heart failure, follow guideline-directed therapy: diuretics, ACEi/ARB/ARNI, beta-blockers, MRA, SGLT2i as tolerated. Escalate to inotropes and temporary support (VA-ECMO, Impella, IABP) if cardiogenic shock persists. LVAD or transplant enter the discussion if recovery stalls.

Arrhythmia management is essential: • Continuous telemetry for all. • Antiarrhythmics, pacing, or defibrillation for unstable rhythms. • ICD placement considered before discharge in select high-risk cases.

Immunosuppression is targeted, not routine. Corticosteroids ± calcineurin inhibitors are reserved for biopsy-proven noninfectious immune-mediated myocarditis (giant cell, eosinophilic, sarcoid, immune checkpoint inhibitor–related). Viral PCR must guide therapy—avoid immunosuppression if active viral infection is present. Antivirals may be used in rare cases with proven viral triggers.

Prognosis splits two ways: • Most uncomplicated cases (chest pain, preserved EF, no arrhythmias) recover fully, with excellent short- and long-term outcomes. • Severe presentations (shock, fulminant myocarditis, sustained arrhythmias, giant cell disease) carry in-hospital mortality or transplant rates of 8–28%, with long-term risk of progression to dilated cardiomyopathy, arrhythmias, or death in up to 25%.

Follow-up is mandatory: early post-discharge visits, repeat echo at 2–4 weeks, CMR at 3–6 months in higher-risk patients, and strict exercise restriction for 3–6 months. Return-to-play requires normalized biomarkers, normal LV function, and arrhythmia-free surveillance.

Key takeaways: recognize fast, risk-stratify, monitor aggressively, use CMR for diagnosis, biopsy selectively, treat heart failure per guidelines, immunosuppress only when indicated, and never miss fulminant disease. Most patients recover, but severe myocarditis demands escalation to advanced therapies and multidisciplinary care.