What is the management for a patient with suspected myocarditis, indicated by elevated CRP and high hsTnI levels, after a negative CAD catheterization?

Management of Suspected Myocarditis with Elevated Troponin and Negative Coronary Angiography

In a patient with markedly elevated hsTnI (17,000 ng/L), elevated CRP (1.66 mg/dL), and non-obstructive coronary arteries on catheterization, the diagnosis is acute myocarditis until proven otherwise, and management should focus on cardiac magnetic resonance imaging for definitive diagnosis, supportive care with heart failure management if needed, and close monitoring for arrhythmias and hemodynamic instability. 1, 2

Diagnostic Confirmation

Cardiac Magnetic Resonance Imaging (CMR)

• CMR is required for definitive diagnosis of myocarditis when troponin elevation occurs with non-obstructive coronary arteries on angiography. 1
• The hsTnI level of 17,000 ng/L represents approximately 850-1700 times the upper reference limit (typical 99th percentile: 10-20 ng/L), which strongly suggests significant myocardial injury. 1
• This magnitude of troponin elevation can occur with both acute myocardial infarction and acute myocarditis, with overlapping distributions between the two conditions. 1
• Myocarditis is explicitly listed as a condition causing troponin elevation with this pattern when coronary angiography is normal. 1

Serial Troponin Monitoring

• Obtain serial troponin measurements at 3-6 hour intervals to document the dynamic pattern (rising/falling ≥20%) characteristic of acute myocardial injury. 1
• The rising/falling pattern differentiates acute myocardial damage from chronic cardiomyocyte injury. 1

Echocardiography

• Perform echocardiography immediately to assess for wall motion abnormalities, wall thickening, ejection fraction, and pericardial effusion. 2, 3
• Approximately 82-95% of adult patients with acute myocarditis present with chest pain, while 19-49% present with dyspnea. 2
• Echocardiographic findings may show regional wall motion abnormalities or reduced ejection fraction (as low as 35% in documented cases). 4

Inflammatory Markers

• The elevated CRP (1.66 mg/dL) supports an inflammatory process, as CRP levels are significantly elevated in myocarditis patients compared to controls (mean difference 6.03 mg/dL, p<0.00001). 5
• CRP measurement is valuable for identifying high-risk patients with myocarditis and selecting therapeutic strategies. 6

Risk Stratification

High-Risk Features Requiring Intensive Monitoring

• Approximately 75% of patients admitted with myocarditis have an uncomplicated course with 0% mortality. 2
• However, myocarditis complicated by acute heart failure or ventricular arrhythmias carries a 12% rate of in-hospital mortality or need for heart transplant. 2
• Patients with hemodynamic instability (2-9% of cases) requiring inotropic support or mechanical circulatory devices have approximately 28% mortality or heart transplant rate at 60 days. 2

Immediate Assessment Required

• Monitor for signs of acute heart failure: dyspnea, pulmonary edema, elevated jugular venous pressure, peripheral edema. 2
• Continuous telemetry monitoring for ventricular arrhythmias, which occur in a subset of patients and significantly worsen prognosis. 2, 3
• Assess hemodynamic stability: blood pressure, heart rate, end-organ perfusion (urine output, mental status, lactate). 2

Management Algorithm

Supportive Care (All Patients)

• First-line therapy depends on acuity, severity, clinical presentation, and etiology and includes supportive care. 2
• Standard heart failure management if left ventricular dysfunction is present: ACE inhibitors/ARBs, beta-blockers (once stabilized), diuretics for volume overload. 2
• Avoid NSAIDs, which may worsen myocardial inflammation. 3
• Activity restriction during the acute phase to reduce myocardial oxygen demand. 3

Etiology-Specific Considerations

• Identify potential causes: recent viral illness (influenza, coronavirus), systemic autoimmune disorders (systemic lupus erythematosus), drug exposures (immune checkpoint inhibitors), or recent vaccinations (smallpox, mRNA COVID-19 vaccines). 2
• Immunosuppression (corticosteroids) is appropriate for patients with eosinophilic or giant cell myocardial infiltrations or myocarditis due to systemic autoimmune disorders. 2
• However, routine corticosteroid use for viral myocarditis is not supported by randomized trial evidence and should be avoided unless specific indications exist. 2

Advanced Therapies for Complicated Cases

• For patients with acute heart failure: consider inotropic agents (dobutamine, milrinone) if inadequate end-organ perfusion despite standard therapy. 2
• For hemodynamically unstable patients: mechanical circulatory support devices such as extracorporeal life support may be required to facilitate functional recovery. 2
• Endomyocardial biopsy may be considered in nonresponders or when specific histologic diagnosis would change management (e.g., giant cell myocarditis, eosinophilic myocarditis). 2, 3

Follow-Up and Monitoring

Short-Term (Hospital Phase)

• Serial ECGs to monitor for evolving ST-segment changes or new conduction abnormalities. 4, 2
• Daily assessment of clinical status, vital signs, and symptoms. 2
• Repeat echocardiography before discharge to assess ventricular function recovery. 3

Long-Term Surveillance

• Arrhythmia monitoring should be titrated to refined risk assessments and includes consideration of ambulatory ECG monitoring or implantable loop recorders in high-risk patients. 3
• Repeat cardiac imaging (echocardiography or CMR) when results will likely impact management, particularly in patients with persistent symptoms or reduced ejection fraction. 3
• Genetic testing should be considered in selected cases, especially when family history suggests inherited cardiomyopathy or when disease chronicity is suspected. 3

Critical Pitfalls to Avoid

• Never dismiss markedly elevated troponin (>5-fold upper reference limit) as non-cardiac, as this magnitude has >90% positive predictive value for acute myocardial injury requiring urgent evaluation. 1
• Never attribute troponin elevation solely to a single cause without excluding competing diagnoses, particularly when coronary angiography is normal—consider myocarditis, Takotsubo syndrome, pulmonary embolism, and aortic dissection. 1
• Never delay CMR when clinically indicated, as it provides definitive diagnosis and prognostic information that guides management. 1, 3
• Never use routine immunosuppression without specific indications (eosinophilic, giant cell, or autoimmune myocarditis), as evidence for benefit in viral myocarditis is lacking. 2