Myocarditis

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
• 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

• Acute coronary syndrome (most important to rule out)
• Pericarditis / myopericarditis
• Takotsubo cardiomyopathy (stress cardiomyopathy)
• Pulmonary embolism
• Pneumonia
• Sepsis from other cause

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
  • If cardiogenic shock: consider vasopressors/inotropes (dobutamine, milrinone)
• 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

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

• Ventricular dysrhythmias / sudden cardiac arrest
• Dilated cardiomyopathy
• Chronic heart failure
• LV aneurysm / thrombus formation

See Also

• Cardiomyopathy
• Pericarditis
• Heart failure
• Cardiogenic shock
• Myocarditis (peds)

External Links

• 2024 ACC Expert Consensus on Myocarditis

References

• 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