Myocarditis

Template:Adult patient

Background

File:Triggers of myocarditis.png
Triggers of myocarditis. Myocarditis can be induced by both infectious and non-infectious pathogens, with viral infection being the most common cause (red background).
  • Inflammatory cardiomyopathy caused by damage and necrosis of myocytes
  • Viral-induced is the most common etiology[1]
  • Clinical presentation ranges from smoldering heart failure to fulminant cardiogenic shock or sudden death
  • Maintain high index of suspicion in younger patients without traditional CAD risk factors
  • Incidence: estimated 1.5 million cases worldwide annually
  • Giant cell myocarditis is a rapidly fatal variant requiring early recognition

Causes

  • Viral (most common):
    • Enterovirus (Coxsackie B) and adenovirus (historically most common)
    • Parvovirus B19 and HHV-6 (currently most detected on biopsy)
    • Influenza A and B, HIV, hepatitis B/C, COVID-19
  • Bacterial: Lyme disease, beta-hemolytic strep, Mycoplasma, diphtheria
  • Parasitic: Chagas disease (most common cause worldwide), toxoplasma, trichinosis
  • Autoimmune: sarcoidosis, SLE, giant cell myocarditis
  • Drugs/toxins: cocaine, doxorubicin, immune checkpoint inhibitors, amphetamines

Phases

  • Acute: direct cytotoxicity and focal necrosis from viral, autoimmune, or toxins
  • Subacute: host immune response (viral molecular mimicry, anti-myocyte antibody production)
  • Chronic: diffuse myocardial fibrosis and cardiac dysfunction

Clinical Features

  • Typically young patients (20-50 years) with few risk factors for CAD
  • Preceding viral illness in 50-80% of cases (1-2 weeks prior)
  • Chest pain or chest pressure/tightness (mimics ACS)
  • Flu-like symptoms: fever, fatigue, myalgias, nausea/vomiting
  • Tachycardia out of proportion to fever
  • New-onset heart failure: fatigue, orthopnea, dyspnea on exertion
  • Consider this diagnosis in the septic-appearing patient who worsens after IV fluids
  • May present with sudden cardiac arrest (especially in young athletes)
  • Pediatric patients: see myocarditis (peds)

Differential Diagnosis

Template:Chest pain DDX

Evaluation

File:12 lead EKG ST elevation with myocarditis.jpg
Diffuse ST elevation in a patient with combined myocarditis and pericarditis.

ECG

  • Must be obtained to rule out STEMI
  • Sinus tachycardia (most common finding)
  • Diffuse ST changes, nonspecific ST-T wave abnormalities
  • Low voltages
  • Prolonged QTc
  • AV block (especially with Lyme disease or sarcoidosis)
  • Wide QRS / new LBBB
  • Normal ECG does NOT rule out myocarditis

Labs

  • Troponin: elevated in ~50% of cases; sensitivity limited
  • BNP/NT-proBNP: reflects degree of heart failure
  • CBC, BMP, LFTs
  • ESR, CRP (usually elevated but nonspecific)
  • Consider viral serologies, Lyme titer, ANA (if autoimmune suspected)
  • Blood cultures (if infectious etiology suspected)

Imaging

  • CXR: cardiomegaly, pulmonary edema, or pleural effusion
  • Echocardiography (essential in ED):
    • Decreased LVEF, global hypokinesis or regional wall motion abnormalities
    • Can detect pericardial effusion (myopericarditis)
    • Fulminant myocarditis may show normal LV dimensions with increased wall thickness
  • Cardiac MRI (noninvasive gold standard): myocardial edema and late gadolinium enhancement
  • Endomyocardial biopsy: invasive gold standard, reserved for unexplained cardiomyopathy or suspected giant cell myocarditis

Management

ED Management

  • IV access, continuous monitoring, 12-lead ECG
  • Rule out ACS: may require coronary angiography if ST elevation or high clinical suspicion
  • Avoid NSAIDs and aspirin in acute phase (animal studies suggest increased inflammation)
  • Volume status: use caution with IV fluids — may worsen heart failure
  • Dysrhythmia management:
    • Avoid class IC antiarrhythmics
    • Amiodarone for sustained VT
    • Temporary pacing for complete heart block
  • Anticoagulation consideration if severely reduced LVEF with LV thrombus risk

Definitive Treatment

  • Supportive care is mainstay; most viral myocarditis self-resolves
  • GDMT for heart failure: ACE-I/ARB, beta-blockers, diuretics (as tolerated by hemodynamics)
  • Mechanical circulatory support (ECMO, VAD) for refractory cardiogenic shock
  • Giant cell myocarditis: requires immunosuppression (cyclosporine + corticosteroids)
  • Cardiac transplant for end-stage disease
  • Activity restriction: no competitive sports for 3-6 months per AHA guidelines[2]

Disposition

  • Admit all patients with suspected myocarditis to a monitored bed
  • ICU admission for hemodynamic instability, arrhythmias, or reduced LVEF
  • Early cardiology consultation
  • Consider transfer to center with mechanical circulatory support capability

Prognosis

  • Fulminant myocarditis paradoxically has the best long-term prognosis if patient survives the acute phase
  • Overall mortality: ~20% at 1 year, ~50% at 5 years for non-fulminant forms
  • Children: ~70% survival rate at 5 years
  • Most patients with mild disease recover completely

Complications

See Also

External Links

References

  1. ↑ Cooper LT Jr. Myocarditis. N Engl J Med. 2009;360(15):1526-38. PMID 19357408
  2. ↑ Caforio ALP, et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the ESC. Eur Heart J. 2013;34(33):2636-2648. PMID 23824828
  • Ammirati E, et al. Clinical presentation and outcome in a contemporary cohort of patients with acute myocarditis. Circulation. 2018;138(11):1088-1099. PMID 29764898
  • Tschöpe C, et al. Myocarditis and inflammatory cardiomyopathy: current evidence and future directions. Nat Rev Cardiol. 2021;18(3):169-193. PMID 33046850
  • Writing Committee; Drazner MH, et al. 2024 ACC Expert Consensus Decision Pathway on Myocarditis. J Am Coll Cardiol. 2025;85(4):391-431. PMID 39665703
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