How can I determine if my myocarditis is active and what is the appropriate management?

Determining Active Myocarditis and Management

Cardiac MRI with the updated 2018 Lake Louise Criteria is the definitive test to determine if myocarditis is active, requiring both a T2-based marker (indicating edema) and a T1-based marker (indicating injury) to confirm active inflammation. 1

Diagnostic Approach to Assess Disease Activity

Initial Assessment for Active Disease

• Measure cardiac troponin levels – elevated troponin indicates ongoing myocardial injury and active disease 2, 3
• Obtain 12-lead ECG – look for new conduction abnormalities (QRS >120 ms), PR-segment depression with diffuse ST-elevation, or low voltage with thickened LV walls suggesting active edema 4, 2
• Check inflammatory markers – ESR >60 mm/hr and CRP >3.0 mg/dL (often >7.0 mg/dL) strongly support acute/active myocarditis; normal values of both essentially rule out active inflammation 2
• Perform transthoracic echocardiography – assess for new or worsening wall motion abnormalities, increased wall thickness (edema), and ventricular dysfunction 4, 2

Definitive Assessment with Cardiac MRI

The 2018 Updated Lake Louise Criteria require BOTH:

T2-Based Criteria (Myocardial Edema = Active Inflammation)

• Elevated myocardial T2 relaxation time on T2-mapping (sensitivity 89%) 1
• Increased signal intensity on T2-weighted imaging 1

T2-mapping is specifically designed to detect acute inflammation and can discriminate active from healed myocarditis 1. This is the most specific marker for disease activity.

T1-Based Criteria (Myocardial Injury)

• Elevated native T1 relaxation time 1
• Late gadolinium enhancement (LGE) in non-ischemic pattern (epicardial/mid-wall) 1
• Increased extracellular volume (ECV) 1

Critical distinction: Native T1-mapping has the highest overall diagnostic accuracy (90% sensitivity, 91% specificity) but cannot reliably distinguish active from chronic disease alone because T1 remains elevated in chronic fibrosis 1. This is why the combination with T2-based markers is essential.

Interpreting CMR Results for Activity

• Active myocarditis: Positive T2-based marker (edema) + positive T1-based marker (injury) 1
• Healed/chronic myocarditis: Negative T2-based marker (no edema) but positive T1-based marker or LGE only 1
• High negative predictive value: Normal T2-mapping (92% NPV) effectively rules out active inflammation 1

Important caveat: LGE alone cannot differentiate recent from remote myocarditis episodes, as LGE persists chronically even after inflammation resolves 1. The presence of myocardial edema (T2-based criteria) is what confirms active disease.

Management Based on Disease Activity

For Active Myocarditis (Positive T2 + T1 Criteria)

Immediate Risk Stratification

Require hospital admission if ANY of the following are present: 2, 3

• Ventricular arrhythmias or heart block
• Hemodynamic compromise or acute heart failure
• Progressive wall motion abnormalities with deteriorating LV function
• Persistent or rising troponin levels
• Widening QRS complex
• Frequent non-sustained ventricular tachycardia

Pharmacologic Management

• Initiate standard heart failure therapy immediately: ACE inhibitors or ARBs for neurohormonal blockade 3
• Use beta-blockers cautiously – ensure hemodynamic stability first, particularly if supraventricular arrhythmias present 3
• NSAIDs are absolutely contraindicated – increase inflammation and mortality risk 3
• Immunosuppression is NOT indicated for typical lymphocytic or viral myocarditis; reserve only for specific subtypes (giant cell, eosinophilic, cardiac sarcoidosis) 3, 5

Activity Restrictions

• Avoid competitive sports for 3-6 months after diagnosis, even if symptoms resolve 3
• Restrict physical activity during the acute inflammatory phase 3

Arrhythmia Management

• Manage arrhythmias supportively – they often resolve with resolution of inflammation 3
• Consider permanent pacemaker for persistent high-grade AV block 3
• For drug-refractory ventricular arrhythmias, endocardial/epicardial radiofrequency catheter ablation may be effective 3

For Chronic/Healed Myocarditis (Negative T2, Positive T1/LGE Only)

• Continue standard heart failure therapy if dilated cardiomyopathy has developed 3
• Monitor for arrhythmias – LGE predicts subsequent risk of ventricular arrhythmias and cardiovascular death in biopsy-proven viral myocarditis 4, 3
• Regular echocardiography to monitor ventricular function 3
• Consider ICD placement if significant LGE burden and reduced ejection fraction, as LGE is a strong predictor of arrhythmic events 4

Role of Endomyocardial Biopsy

Biopsy is indicated (Class I) ONLY in specific high-risk scenarios: 2, 6

• Acute fulminant myocarditis with hemodynamic compromise
• New-onset heart failure with dilated ventricle and new ventricular arrhythmias
• Refractory sustained ventricular tachyarrhythmias
• Suspected giant cell myocarditis or cardiac sarcoidosis

Pre-procedural CMR localization of inflammatory changes reduces sampling errors and improves diagnostic yield 2. However, biopsy has low sensitivity due to patchy inflammation and is not routinely required for clinical management in most cases 2, 6.

Long-Term Monitoring Strategy

• Repeat cardiac MRI to track resolution of inflammation (disappearance of T2 signal) 3
• Serial troponin and natriuretic peptides to assess ongoing injury and heart failure severity 3
• Regular ECG monitoring for conduction abnormalities 3
• Monitor for development of dilated cardiomyopathy – occurs in 21% of patients during long-term follow-up 3

Common Pitfalls to Avoid

• Do not rely on LGE alone to determine disease activity – LGE persists chronically and cannot distinguish active from healed myocarditis 1
• Do not use NSAIDs for symptom relief – they worsen outcomes 3
• Do not assume normal troponin rules out myocarditis – troponin can be normal in subacute or chronic presentations 2
• Do not delay CMR in hemodynamically stable patients – it has Class I indication and provides critical prognostic information 4, 2
• In severe renal dysfunction (eGFR <30 mL/min/1.73 m²), non-contrast CMR is reasonable but less useful for tissue characterization 4