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This is a clinician-written, evidence-based summary aligned to the USMLE Step 2 CK Content Outline. It is intended for medical students preparing for USMLE Step 2 CK. Management reflects current ACC/AHA, USPSTF, and APA guidelines. Always cross-reference with UpToDate, institutional protocols, and clinical judgment.
Key points
- Classic presentation: young patient with recent viral illness + chest pain + troponin elevation + ECG changes (mimics ACS but coronaries are normal)
- Most common cause: viral (Coxsackie B, parvovirus B19, adenovirus, HHV-6). Also: autoimmune, drug hypersensitivity (eosinophilic), giant cell myocarditis (fulminant)
- Cardiac MRI is the non-invasive diagnostic gold standard: myocardial edema (T2), epicardial/mid-wall LGE (NOT subendocardial like ischemia)
- Management is supportive: standard HF therapy if LV dysfunction; avoid NSAIDs in acute phase (controversial); restrict exercise until resolved
- Giant cell myocarditis: fulminant course, high mortality, suspect if rapid deterioration + VT. Biopsy to confirm. Immunosuppression + consider transplant
Overview
Myocarditis is inflammation of the myocardium that can result from infectious, autoimmune, or toxic etiologies. Viral infection is the most common cause in developed countries. The clinical spectrum ranges from subclinical (mild troponin elevation) to fulminant (cardiogenic shock requiring mechanical support). Myocarditis is an important cause of new-onset heart failure and sudden cardiac death in young adults. Diagnosis relies on clinical presentation, biomarkers, and cardiac MRI; endomyocardial biopsy is reserved for specific clinical scenarios.
Clinical Features
Symptoms
Chest pain (often pleuritic, may mimic ACS), preceded by viral URI or GI illness days to weeks before
Dyspnea, fatigue (new-onset HF)
Palpitations, syncope (arrhythmias — VT, AF, heart block)
Fulminant: cardiogenic shock with rapid deterioration (giant cell, eosinophilic)
Signs
Tachycardia disproportionate to fever
S3 gallop, signs of HF if significant LV dysfunction
Pericardial friction rub if concurrent pericarditis (myopericarditis)
Hypotension, cool extremities in fulminant disease
Investigations
First-line
TroponinElevated (often mildly to moderately). Rise and fall pattern similar to ACS
ECGDiffuse ST elevation (like pericarditis), ST changes mimicking ACS, low voltage, arrhythmias (VT, AF, AV block), or may be normal
EchocardiogramRegional or global wall motion abnormalities, reduced LVEF (may be severe in fulminant), pericardial effusion
LabsCBC, BMP, CRP/ESR (elevated), BNP (if HF)
Second-line
Cardiac MRINon-invasive gold standard. Updated Lake Louise criteria: T2 mapping (myocardial edema), T1 mapping (fibrosis/inflammation), LGE in epicardial or mid-wall pattern (distinguishes from ischemic injury which is subendocardial). Sensitivity ~75-80%
Coronary assessmentAngiography or CTA to rule out ACS (especially if presentation mimics STEMI/NSTEMI). Young patient with chest pain + troponin + normal coronaries = myocarditis is top differential
Specialist
Endomyocardial biopsyGold standard but limited sensitivity. Indicated for: suspected giant cell myocarditis (fulminant + VT), cardiac sarcoidosis, unexplained new-onset HF with rapid deterioration, failure to improve on standard therapy. Dallas criteria: inflammatory infiltrate + myocyte necrosis
1
Supportive care (viral myocarditis)
- Standard HFrEF GDMT if LV dysfunction: ACEi/ARB, beta-blocker (when stable), diuretics as needed
- Avoid strenuous exercise for 3-6 months (risk of arrhythmia and sudden death). Return to activity only after symptoms resolve, troponin normalizes, LV function recovers, and no significant arrhythmias on monitoring
- Avoid NSAIDs in acute myocarditis (may impair healing — animal studies, though human evidence is limited)
- No role for routine antiviral therapy or immunosuppression in viral myocarditis
2
Fulminant myocarditis
- Aggressive hemodynamic support: inotropes, vasopressors, mechanical circulatory support (ECMO, Impella)
- High recovery rate if patient survives the acute phase (~70% with aggressive support)
- Giant cell myocarditis: immunosuppression (cyclosporine + corticosteroids) + consideration for urgent transplant listing (median survival without transplant is ~5 months)
3
Specific etiologies
- Eosinophilic myocarditis: stop offending drug, corticosteroids
- Cardiac sarcoidosis: corticosteroids + steroid-sparing agents (methotrexate)
- Chagas disease (endemic in Latin America): benznidazole or nifurtimox in acute phase
USMLE Step 2 CK Exam Tips
- 1Young patient + viral prodrome + chest pain + troponin elevation + normal coronaries = myocarditis
- 2Cardiac MRI LGE pattern: epicardial/mid-wall = myocarditis. Subendocardial = ischemic MI. This distinction is heavily tested
- 3Restrict exercise for 3-6 months — exertion during active myocarditis increases risk of SCD
- 4Giant cell myocarditis: suspect if fulminant HF + VT in a young person. Biopsy confirms. Treat with immunosuppression, consider transplant
- 5Do NOT give immunosuppression for viral myocarditis — only for specific pathologies (giant cell, sarcoid, eosinophilic)
- 6Myocarditis is a common cause of sudden death in young athletes (second to HCM)
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