Differentiating Myopericarditis from Pericarditis
Myopericarditis is distinguished from isolated pericarditis by the presence of elevated troponin levels (indicating myocardial involvement), ventricular wall motion abnormalities, or predominant heart failure symptoms, whereas pericarditis presents with characteristic chest pain and ECG changes without significant myocardial dysfunction. 1
Key Diagnostic Features
Clinical Presentation Differences
Pericarditis presents with sharp, pleuritic chest pain that improves with sitting up or leaning forward, and may be accompanied by a pericardial friction rub (audible in only one-third of cases). 1
Myopericarditis includes pericarditic features plus evidence of myocardial involvement: fatigue, exercise intolerance, and heart failure symptoms that distinguish it from isolated pericarditis. 1
The predominance of heart failure symptoms (dyspnea, fatigue) rather than positional chest pain suggests myocardial involvement. 1
Laboratory Markers
Troponin elevation occurs in up to 50% of acute pericarditis cases, and when present, defines myopericarditis rather than isolated pericarditis. 1
In pericarditis, minimally elevated troponin does not confer worse prognosis, but the presence of troponin elevation reflects myocardial involvement in the inflammatory process. 1
CRP/troponin ratio >500 has >85% specificity for myopericarditis over acute myocardial infarction, with ratios >1000 achieving >92% specificity. 2 Myopericarditis demonstrates median CRP/troponin ratios of 436 mg×ml/liter×ng compared to 84 for STEMI and 65 for NSTEMI. 2
Electrocardiographic Findings
Both conditions may show widespread ST-elevation with PR depression, which is the electrocardiographic hallmark of pericarditis. 1
Localized ST-elevation or regional changes suggest greater myocardial involvement (myopericarditis) or raise concern for acute coronary syndrome. 3
ECG changes in pericarditis are often nonspecific and may be transient. 1
Diagnostic Algorithm
Initial Assessment
Obtain transthoracic echocardiography (TTE) immediately to assess for:
Check troponin levels: Elevation indicates myocardial involvement and defines myopericarditis. 1
Calculate CRP/troponin ratio if acute coronary syndrome is in the differential: ratios >500 strongly favor myopericarditis over MI. 2
Advanced Imaging When Indicated
Cardiac MRI with gadolinium contrast is the gold standard when there is diagnostic uncertainty or to determine the extent of myocardial and pericardial inflammation. 1, 4
CMR has 94-100% sensitivity for detecting pericardial inflammation and can distinguish myopericarditis from myocardial infarction with nonobstructive coronary arteries (MINOCA). 1, 5
CMR should be performed within 2 weeks of presentation for optimal detection of acute changes, showing myocardial edema, thickening, and late gadolinium enhancement. 1
CMR features suggestive of myopericarditis include: pericardial enhancement or thickening, increased T2-weighted signal (indicating edema), and pericardial effusions. 1
When to Consider Coronary Angiography
If regional wall motion abnormalities are present on echocardiography, coronary angiography may be necessary to exclude acute coronary syndrome, particularly when clinical features overlap. 6, 7
In young patients without cardiovascular risk factors presenting with very high troponin levels (>15,000 ng/L), consider spontaneous coronary artery dissection in the differential. 4
Critical Pitfalls to Avoid
Normal echocardiography does not exclude pericarditis: pericardial effusion is detectable in only 60% of cases. 1
Elevated troponin in myopericarditis does not predict adverse outcomes when left ventricular function is preserved, unlike in acute coronary syndromes. 1, 7
Pericardial friction rubs are transient and intermittent: absence does not exclude the diagnosis, and multiple examinations may be necessary. 6
Focal ECG changes can occur in myopericarditis and may mimic acute myocardial infarction, requiring echocardiography or CMR to differentiate. 3
Prognostic Considerations
Despite markedly elevated cardiac enzymes, myopericarditis in young patients typically has a benign clinical evolution without myocardial dysfunction. 7
The inflammatory myocardial involvement appears self-limited without short-term overt sequelae. 7
However, long-term follow-up studies suggest higher cardiac mortality in myopericarditis compared to isolated pericarditis, though global complication rates are similar. 8
CMR may show myocardial sequelae (late gadolinium enhancement) that persist without clinical impact. 8