Myocarditis in Emergency Medicine Workup
- Author: David S Howes, MD; Chief Editor: David FM Brown, MD more...
Laboratory Studies
Positive cardiac troponin I results are seen in about 35% of patients with myocarditis.[13] Sensitivity of cardiac troponin I is approximately 35% but specificity is approximately 90%, with a positive predictive value of 82%.
Erythrocyte sedimentation rate (ESR) is elevated in many patients with acute myocarditis, but it has low sensitivity and specificity.[4]
Other serum biomarkers may have clinical utility, specifically cytokines, complement, and antiheart antibodies have been shown in studies to be routinely elevated in immune-mediated myocarditis. High serum levels of Fas ligand and interleukin 10 are associated with poor outcomes but have not been validated.[4]
Leukocytosis is present in 25% of cases.
Imaging Studies
Chest radiography
A chest radiograph often reveals a normal cardiac silhouette, but pericarditis or overt clinical CHF can be associated with cardiomegaly. Vascular redistribution and interstitial and alveolar edema and pleural effusion may be noted.
Echocardiography
- Impairment of left ventricular systolic and diastolic function
- Segmental wall motion abnormalities
- Impaired ejection fraction
- A pericardial effusion may be present, although findings of tamponade are rare.
Ventricular thrombus has been identified in 15% of patients studied with echocardiography.
MRI
MRI is capable of showing abnormal signal intensity in the affected myocardium.
With multiple sequences used for imaging, one study showed 76% sensitivity, 96% specificity, and overall 85% diagnostic accuracy.[14]
MRI can demonstrate nodular and patchy areas of inflammation, often seen first in the lateral and inferior wall and can be used to guide later biopsy. In one study, areas that showed delayed gadolinium enhancement led to positive biopsy findings in 19 of 21 patients and in only 1 of 7 patients that did not show enhancement.[15]
MRI should be considered in patients with suspected myocarditis in whom the diagnosis is unclear and in whom endocardial biopsy is being considered. Especially consider MRI in patients with chest pain and positive cardiac enzyme level results with normal coronary anatomy.[16]
Other Tests
On electrocardiography, sinus tachycardia is the most frequent finding. ST-segment elevation without reciprocal depression, particularly when diffuse, is helpful in differentiating myocarditis from acute myocardial infarction. Decreased QRS amplitude and transitory Q-wave development is very suggestive of myocarditis. As many as 20% of patients have a conduction delay, including Mobitz I, Mobitz II, or complete heart block. Left or right bundle-branch block is observed in approximately 20% of abnormal ECG findings and may persist for months.
Viral isolation from other body sites may be supportive of the diagnosis.
Polymerase chain reaction (PCR) identification of a viral infection from myocardial tissue, pericardial fluid, or other body fluid sites can be helpful. Persistent viral genome, as detected by PCR, has been identified as one marker of increased incidence of dilated cardiomyopathy and mortality.
If a systemic disorder (eg, SLE) is suspected, antinuclear antibody (ANA) and other collagen vascular disorder laboratory investigations may be useful.
Procedures
Cardiac catheterization usually reveals normal coronary vessels and regional wall motion abnormalities with diminished ejection fraction. It has no benefit over noninvasive echocardiography.
Endomyocardial biopsy continues to be of use in diagnosing myocarditis.[4] The use of MRI to target biopsy, immunohistochemical staining, and the ability to identify viral genome by PCR has allowed endomyocardial biopsy to remain a powerful tool. In one study of nearly 900 patients, biopsy altered diagnosis and treatment in 21% of patients.[17]
Endomyocardial biopsy should be performed in patients with unexplained acute-onset heart failure with hemodynamic compromise to identify fulminant myocarditis and in patients with heart failure of less than 3 months duration who do not respond to standard therapy and who exhibit dilated LV or new high-grade AV block or ventricular arrhythmia.[4]
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