What are the typical presentation, diagnostic work‑up, and management recommendations for acute myocarditis caused by COVID‑19 infection?

COVID-19 Myocarditis: Presentation, Diagnosis, and Management

Clinical Presentation

Chest pain is the predominant symptom in COVID-19 myocarditis, typically accompanied by dyspnea, palpitations, or syncope, with symptom onset occurring during acute infection or delayed up to 1 month post-infection. 1

• Fever occurs in approximately 57% of patients with COVID-19 myocarditis 2
• Cardiac symptoms may be subtle or absent in critically ill, intubated patients 1
• Delayed-onset myocarditis can present as multisystem inflammatory syndrome in adults (MIS-A), characterized by hemodynamic compromise, acute heart failure, or cardiogenic shock without sepsis 1
• Young males (median age 43.4 years) are disproportionately affected, with 71.4% of cases occurring in men 2

Common pitfall: Do not dismiss cardiac involvement in patients with minimal respiratory symptoms—myocarditis can occur even with mild COVID-19 infection. 3

Diagnostic Work-Up

Initial Testing (All Suspected Cases)

Obtain ECG, high-sensitivity cardiac troponin, and transthoracic echocardiography immediately when cardiac involvement is suspected. 1

• ECG findings: ST-segment elevation without reciprocal depression (most common), diffuse T-wave inversion, or QRS prolongation 1
• Troponin elevation: Present in ~90% of cases; marked elevation (>5× upper limit of normal) strongly suggests myocarditis, Takotsubo syndrome, or type 1 MI 1, 2
• Mild troponin elevation (<2-3× upper limit of normal) in older patients with pre-existing cardiac disease does not require invasive work-up unless anginal chest pain or ECG changes are present 1
• BNP/NT-proBNP: Elevated in 87% of cases, reflecting both pre-existing disease and acute hemodynamic stress 1, 2

Echocardiography

• Assess for left ventricular wall motion abnormalities in non-coronary distribution 1
• Left ventricular ejection fraction <50% occurs in a minority but indicates higher risk 1
• Normal LV function does not exclude myocarditis—proceed to cardiac MRI 4

Cardiology Consultation

Obtain immediate cardiology consultation for rising troponin, concerning ECG abnormalities, or echocardiographic wall motion abnormalities. 1

Cardiac MRI (Essential Before Discharge)

Cardiac MRI must be performed before hospital discharge in all hemodynamically stable patients with suspected myocarditis, ideally >10 days from symptom onset. 1, 5, 4

• Diagnostic criteria (Updated Lake Louise Criteria): Requires ≥1 T2-based criterion (myocardial edema) AND ≥1 T1-based criterion (late gadolinium enhancement indicating injury/fibrosis) 4
• Prognostic value: Late gadolinium enhancement (LGE) is the strongest independent predictor of sudden cardiac death, cardiac mortality, and all-cause mortality 4
• Pattern recognition: Non-ischemic epicardial or mid-wall LGE pattern distinguishes myocarditis from ischemic injury 4
• Risk stratification: Extensive LGE involving multiple segments or mid-septal involvement identifies patients requiring ICD consideration 4

Critical pitfall: Never assume normal echocardiographic LVEF means low risk—echocardiography cannot detect myocardial edema or subepicardial/mid-myocardial LGE typical of myocarditis. 4

Endomyocardial Biopsy (Rarely Indicated)

• Reserve for suspected giant cell myocarditis or when diagnosis remains uncertain despite CMR 1
• Histopathology in COVID-19 myocarditis typically shows CD68+ macrophage/monocytic infiltration, endothelialitis, and individual cell necrosis—not the diffuse lymphocytic infiltrates seen in classic viral myocarditis 1, 2, 6
• SARS-CoV-2 viral RNA is rarely detected in myocardium 1, 6

Coronary Angiography

• Indicated only when type 1 MI is suspected (anginal chest pain, ischemic ECG pattern) 1
• Exclude flow-limiting coronary disease in men >50 years and women >55 years before confirming myocarditis diagnosis 1

Management

Hospitalization and Monitoring

Hospitalize all patients with definite COVID-19 myocarditis at an advanced heart failure center; transfer fulminant cases to centers with mechanical circulatory support and transplant capabilities. 5, 7

• Patients with chest pain, elevated troponin, abnormal ECG/echo/CMR, concerning arrhythmias, or hemodynamic instability require inpatient monitoring 1
• Close surveillance for clinical deterioration is essential, as troponin elevation correlates with worse outcomes 1

Guideline-Directed Medical Therapy

Initiate guideline-directed heart failure therapy before discharge and titrate in the outpatient setting. 1, 5, 7

• ACE inhibitors or ARBs: First-line for neurohormonal blockade 5, 7
• Beta-blockers: Use cautiously and only in hemodynamically stable patients; can precipitate cardiogenic shock in those with compromised cardiac function 1, 5
• Aldosterone antagonists: Consider for mildly reduced LV function with stable hemodynamics 7

Immunosuppressive Therapy

Intravenous corticosteroids should be considered in three specific scenarios: 1, 5

1. COVID-19 myocarditis with concurrent pneumonia requiring supplemental oxygen
2. Hemodynamic compromise or MIS-A (hyperinflammatory state with acute heart failure/cardiogenic shock without sepsis)
3. Fulminant myocarditis with biopsy-proven severe myocardial inflammatory infiltrates

• MIS-A is associated with delayed-onset myocarditis, high inflammatory biomarkers, and elevated ferritin 1
• Balance immunosuppression against infection risk 1
• For rapidly improving symptoms with normal/improving troponin and normal LVEF, anti-inflammatory medications may not be needed 1

Anti-Inflammatory Medications (Non-Fulminant Cases)

• NSAIDs, colchicine, or corticosteroids: Consider for ongoing symptoms or pericardial involvement 1, 5
• Avoid NSAIDs in isolated myocarditis without pericardial involvement due to increased inflammation and mortality risk 5

Mechanical Circulatory Support

• Initiate urgently if cardiogenic shock does not reverse rapidly with pharmacologic therapy 7
• Options include percutaneous cardiopulmonary support, ECMO, or intra-aortic balloon pump 7

Activity Restriction (Critical for All Patients)

Mandate complete exercise abstinence for 3-6 months after diagnosis, as sustained aerobic exercise during acute viral myocarditis increases mortality and sudden death risk. 1, 5, 7

Return-to-Play Criteria (After 3-6 Months)

Clearance requires all of the following: 5

• Absence of cardiopulmonary symptoms
• Resolution of laboratory evidence of myocardial injury (normal troponin)
• Normalization of LV systolic function on echocardiography
• Absence of spontaneous or inducible arrhythmias on ECG monitoring and exercise stress testing

Follow-Up Surveillance

Perform comprehensive cardiac testing at 3-6 months to assess recovery, guide heart failure management, and assess prognosis. 1, 5, 7

• Required tests: ECG, echocardiogram, ambulatory rhythm monitor, and cardiac MRI 1, 5
• Repeat CMR confirms resolution of inflammation and quantifies residual fibrosis 4
• Dilated cardiomyopathy develops in 21% of patients during long-term follow-up 7

If follow-up CMR shows extensive LGE (multiple segments) or mid-septal involvement, arrange urgent cardiology follow-up within 1-2 weeks for ICD discussion and close arrhythmia monitoring. 4

Prognosis

• Most patients with non-fulminant COVID-19 myocarditis have symptom resolution and improved cardiac function with or without treatment 1, 3
• Fulminant myocarditis carries 28% mortality at 60 days despite aggressive treatment 7
• Recovery rate is approximately 67%, with mortality around 19% in published case series 2
• Patients requiring vasopressor support (38% of cases) have higher mortality 2