What findings, including lab results and physical exam findings, are indicative of fulminant myocarditis?

Diagnostic Findings for Fulminant Myocarditis

Fulminant myocarditis is characterized by sudden and severe diffuse cardiac inflammation leading to cardiogenic shock, ventricular arrhythmias, or multiorgan failure requiring inotropic or mechanical circulatory support for survival. 1

Clinical Presentation

• Acute onset of cardiac symptoms with rapid progression to hemodynamic instability
• Key physical exam findings:
  • Hypotension (systolic BP <90 mmHg)
  • Signs of cardiogenic shock
  • Tachycardia
  • Elevated jugular venous pressure
  • S3 gallop
  • Pulmonary rales
  • Cool extremities with decreased peripheral pulses
  • Altered mental status due to hypoperfusion

Laboratory Findings

• Cardiac biomarkers:
  • Significantly elevated troponin T/I (often markedly higher than typical myocarditis)
  • Elevated creatine kinase
• Inflammatory markers:
  • Elevated C-reactive protein
  • Elevated erythrocyte sedimentation rate
• Other laboratory abnormalities:
  • Elevated lactate (>2 mmol/L) - indicates tissue hypoperfusion
  • Metabolic acidosis (low pH <7.35)
  • Elevated liver enzymes and creatinine (indicating end-organ damage)
  • BNP/NT-proBNP elevation

Electrocardiographic Findings

• Diffuse ST-segment elevation without reciprocal depression
• T-wave inversions
• Prolonged QRS complex duration
• Ventricular arrhythmias
• Advanced atrioventricular blocks
• Low voltage QRS complexes 2

Imaging Findings

• Echocardiography:

  • Severe global systolic dysfunction (reduced ejection fraction)
  • Ventricular dilatation
  • Increased wall thickness due to edema
  • Regional or global wall motion abnormalities
  • Possible pericardial effusion
  • Intracavitary thrombi 2, 3

• Cardiac MRI (if patient is stable enough):

  • Myocardial edema on T2-weighted imaging
  • Early gadolinium enhancement indicating hyperemia/capillary leak
  • Late gadolinium enhancement in non-ischemic pattern
  • According to Lake Louise Criteria: at least one T2-based criterion and one T1-based criterion 3

Hemodynamic Parameters

• Elevated filling pressures (PCWP >18 mmHg)
• Reduced cardiac output (<4 L/min)
• Elevated systemic vascular resistance
• Mixed venous oxygen saturation <65%

Distinguishing Fulminant from Non-Fulminant Myocarditis

Fulminant myocarditis is distinguished from non-fulminant forms by:

1. Hemodynamic instability requiring inotropic support and/or mechanical circulatory support 2, 4
2. Rapid progression from symptom onset to severe heart failure (typically days)
3. Higher mortality rate (35% short-term mortality even with VA-ECMO support) 5
4. Histologic subtype impacts prognosis (giant cell myocarditis having worse outcomes than eosinophilic or lymphocytic forms) 4

Management Considerations

Patients with fulminant myocarditis should be managed at centers with expertise in:

• Advanced heart failure
• Mechanical circulatory support (including VA-ECMO)
• Cardiac transplantation capabilities 2, 1

Prognostic Indicators

Poor prognostic factors in fulminant myocarditis include:

• Low pH
• High lactate levels
• Absence of functional cardiac recovery on mechanical support
• Increased burden of malignant arrhythmias
• High peak cardiac biomarkers 5

Early recognition and aggressive intervention are critical for improving outcomes in fulminant myocarditis, as timely implementation of mechanical circulatory support before multi-organ failure develops can be life-saving.