How is myocarditis diagnosed in a patient of any age presenting with recent chest pain, dyspnea, palpitations, or unexplained heart failure after a viral prodrome or systemic illness?

Diagnosis of Myocarditis

Myocarditis is diagnosed through a systematic approach combining clinical presentation, cardiac biomarkers, ECG abnormalities, echocardiography, and cardiac MRI—with CMR serving as the gold-standard non-invasive test in stable patients, while endomyocardial biopsy is reserved for fulminant cases or when specific etiologies require confirmation. 1

Initial Clinical Assessment

Presenting Symptoms

Suspect myocarditis in patients presenting with:

• Chest pain (pericarditic or pseudo-ischemic character), present in 82–95% of adult cases 2
• Dyspnea (19–49% of cases), either acute onset or progressive over days to weeks 3, 2
• Palpitations, syncope, or aborted sudden cardiac death 3
• Signs of acute heart failure with or without cardiogenic shock 3, 4
• Recent viral prodrome or systemic illness preceding cardiac symptoms 3, 1

Critical First Step

Immediately exclude acute coronary syndrome and stress-induced cardiomyopathy before confirming myocarditis, particularly in patients with chest pain, heart failure, or new arrhythmia. 3

Mandatory Initial Diagnostic Tests

12-Lead Electrocardiogram

Obtain immediately in all suspected cases. 1 Look for:

• Diffuse ST-segment elevation without reciprocal depression 3, 1
• Diffuse T-wave inversion 3, 1
• QRS prolongation (>120 ms), which predicts life-threatening arrhythmias 4
• New AV block (first- to third-degree) or bundle-branch block 4
• Ventricular or atrial arrhythmias 4

Important caveat: ECG findings are neither sufficiently sensitive nor specific to establish or exclude myocarditis as a stand-alone test. 3, 4

Cardiac Biomarkers

• Serial high-sensitivity cardiac troponin measurements are required for diagnosis; troponin may be only mildly elevated despite severe ventricular dysfunction. 1
• Elevated troponin indicates myocyte necrosis and is present in the vast majority of cases. 3, 4
• Persistently elevated or fluctuating troponin levels signal ongoing myocardial injury and clinical deterioration. 4
• Creatine kinase may be elevated but is not diagnostic. 3

Transthoracic Echocardiography

Perform immediately to assess: 1

• Non-coronary distribution wall-motion abnormalities 3, 1
• Reduced ejection fraction and ventricular dilation 1
• Increased wall thickness from myocardial edema 1
• Pericardial effusion 1
• Progressive wall-motion abnormalities and worsening LV function indicate clinical deterioration 4

Echocardiography helps exclude valvular disease, congenital heart disease, and other cardiomyopathies, but findings are nonspecific for myocarditis. 3, 4

Baseline Laboratory Panel

Obtain CBC, electrolytes, BUN, creatinine, glucose, calcium, magnesium, phosphorus, and chest radiograph. 3, 1

Serum inflammatory markers (CRP, ESR) have low sensitivity and should not be relied upon for diagnosis. 3, 4

Advanced Imaging: Cardiac Magnetic Resonance

Cardiac MRI should be performed in all hemodynamically stable patients with suspected myocarditis to confirm the diagnosis; it is the gold-standard non-invasive test and should be completed before discharge. 1

CMR Diagnostic Criteria

• Non-ischemic late gadolinium enhancement pattern 3, 1
• Prolonged native T1 and T2 relaxation times indicating myocardial edema and inflammation 3
• Myocardial edema on T2-weighted imaging 3, 4

CMR provides incremental diagnostic information beyond endomyocardial biopsy and correlates well with histologic findings. 3, 1 Optimal sensitivity for CMR is within a few weeks of symptom onset. 3

Endomyocardial Biopsy

Biopsy has a low diagnostic yield (5–10% with strict histologic criteria) and is reserved for specific high-risk scenarios. 3, 1

Indications for Endomyocardial Biopsy

Perform biopsy when: 3, 1

• Fulminant myocarditis with cardiogenic shock requiring inotropic or mechanical circulatory support
• High-grade AV block (Mobitz type 2 or complete heart block)
• Sustained or symptomatic ventricular tachycardia
• Failure to respond to guideline-directed therapy
• Suspected specific etiologies: giant-cell myocarditis, cardiac sarcoidosis, eosinophilic myocarditis, or immune-checkpoint-inhibitor-related myocarditis

Histologic diagnosis requires inflammatory cells with myocyte necrosis. 4

Tests NOT Recommended

Routine viral serology testing is not recommended because of limited clinical utility and low specificity. 3, 1 Increasing serum antibody titers provide only circumstantial evidence and are of little clinical help. 3

Diagnostic Certainty Classification

The 2022 ACC Expert Consensus defines three levels: 3

Possible Myocarditis

• Cardiac symptoms + elevated troponin + abnormal ECG/echo findings
• Without CMR or biopsy confirmation, or when neither was performed

Probable Myocarditis

• All features of possible myocarditis
• Plus follow-up CMR or biopsy within 6 months showing abnormalities consistent with previous myocarditis

Definite Myocarditis

• All features of possible myocarditis
• Plus CMR or biopsy at time of acute illness demonstrating active myocarditis

Risk Stratification for Urgent Cardiology Consultation

All patients meeting criteria for definite myocarditis require admission to an advanced heart-failure center. 1

Fulminant Myocarditis Criteria (Immediate Transfer to Tertiary Center)

• Cardiogenic shock 1
• Need for inotropic support 1
• Sustained ventricular arrhythmias 1
• High-grade AV block 1

Fulminant myocarditis carries approximately 28% 60-day mortality but survivors have more favorable long-term prognosis than non-fulminant cases. 1

Common Diagnostic Pitfalls

• Do not rely on ECG alone—insufficient sensitivity and specificity 3, 4
• Do not perform routine viral serology—adds little clinical value 3, 1
• Do not delay CMR in stable patients—it is the definitive non-invasive test 1
• Do not perform routine endomyocardial biopsy—reserve for the specific high-risk scenarios listed above 3, 1
• Do not miss the diagnostic window—CMR sensitivity is optimal within weeks of presentation 3