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Pediatric Viral Myocarditis Workup

  • Author: Edwin Rodriguez-Cruz, MD; Chief Editor: Howard S Weber, MD, FSCAI  more...
 
Updated: Aug 26, 2015
 

Laboratory Studies

Perform a complete blood count (CBC) with differential. Acute anemia of any origin may cause heart failure, and chronic anemia exacerbates heart failure; both respond to blood transfusion. The presence of lymphocytosis or neutropenia supports diagnosis of a viral infection. In addition, perform blood cultures; ruling out any bacterial infection is important.[9]

Additional tests to perform are as follows:

  • Sedimentation rate and C-reactive protein – Nonspecific inflammation markers; they are usually elevated, but a normal value does not rule out myocarditis, particularly in the presence of congestive heart failure, which may lower the sedimentation rate
  • Nasopharyngeal and rectal swabs - May help to identify etiology
  • Viral titers - A 4-fold increase in a specific titer from the acute to convalescent phase is strong evidence of infection
  • In situ hybridization - Identifies viral ribonucleic acid (RNA) in myocardial tissue of patients believed to have myocarditis; the incidence of false-negative results is high
  • Polymerase chain reaction (PCR) assay [10]  - Used to find the viral genome in myocardial cells; it is rapid and sensitive, and it may become the test of choice for the diagnosis of viral myocarditis
  • Creatinine kinase–MB isoenzymes (CK-MB) - Markers of myocardial damage; they are elevated most commonly when an associated elevation of the ST segment on an electrocardiogram (ECG) is present
  • Lactate dehydrogenase isoenzyme 1 - May be elevated in idiopathic myocarditis
  • Troponin I - Another indicator of myocardial damage; it is usually elevated up to a month after infection, but it is not specific for this disease [11]

Other techniques are under investigation to determine a specific viral etiology of myocarditis, such as immunohistochemical stains, inflammatory mediators, and autoantibody measurements.

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Imaging Studies

Chest radiography and magnetic resonance imaging

On chest radiography, cardiomegaly and pulmonary edema may be depicted. Incidentally noted cardiomegaly on chest radiography may be the initial presentation.

Magnetic resonance imaging (MRI) with gadolinium can be used to evaluate the cardiac muscle inflammation via a special protocol for myopericarditis.

Echocardiography

Echocardiography is the most cost-effective test used for evaluation of myocardial function. It is sensitive but not specific. Findings include the following:

  • Global hypokinesis (the most common finding)
  • Increased left ventricular end diastolic and systolic dimensions
  • Left ventricular dysfunction, primarily systolic with decreased ejection fraction and shortening fraction
  • Segmental wall motion abnormalities
  • Pericardial effusion

Scintigraphy

Radionuclide imaging may be helpful as a screening tool. Gallium 67 (67 Ga) citrate myocardial scintigraphy is useful for revealing chronic inflammatory processes. It is a sensitive test but is limited by its low specificity and predictive value.

Indium 111 (111 In) antimyosin antibody imaging is highly sensitive for myocardial necrosis, but it has a high incidence of false-positive results. However, absence of antimyosin uptake is highly predictive of negative biopsy findings (92-98%).

Myocardial perfusion imaging with technetium 99m–labeled methoxyisobutyl isonitrile single-photon emission computed tomography (99m Tc-MIBI SPECT) scanning is usually a tool used to evaluate the severity of myocardial ischemia.[12]  Because the uptake and clearance of99m Tc-MIBI is affected by cell viability and membrane integrity, clinicians have also used it as a marker for the severity of myocardial necrosis and inflammation in patients with myocarditis, with results comparable to those obtained with enzymatic cell damage markers.

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Electrocardiography

In some patients with mild cardiac involvement, electrocardiographic changes may be the only abnormal findings suggestive of myocarditis. Low-voltage QRS (< 5 mm throughout the limb leads) is the classic pattern. Pseudoinfarction patterns with pathologic Q waves and poor progression of R waves in the precordial leads may also be present. T-wave flattening or inversion is a common finding associated with small or absent Q waves in V5 and V6.

Left ventricular hypertrophy with strain may be present. Other, nonspecific findings include prolonged PR segment and prolonged QT interval.[13]

Sinus tachycardia is the most common finding. Premature ventricular contractions and atrial tachycardias have been reported. Junctional tachycardia is common and may worsen congestive heart failure. Occasional second-degree and third-degree atrioventricular block may be present, requiring temporary pacing. Ventricular tachycardia may be associated with active myocardial inflammation early in the disease process or occur late in the course of the disease when myocardial fibrosis has developed.

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Biopsy

Right ventricular endomyocardial biopsy is the criterion standard for the diagnosis of myocarditis.[14] Myocardial biopsy findings establish diagnosis and classify disease stage. Biopsy is a relatively safe and effective way to sample heart muscle in older children; however, a risk of perforation in sick or younger infants is observed.

The use of endomyocardial biopsy is controversial because of the possibility of a high false-negative result rate and because no proven therapy is available, even when a positive biopsy finding is obtained. Some advocate using radionuclide imaging techniques as screening tools before considering endomyocardial biopsy.

Biopsy specimens may be useful for PCR assay diagnosis of viral etiology. Viral serology in adults has been shown to have poor sensitivity and specificity compared with endomyocardial biopsy with PCR assay detection of the viral genome under diagnostic testing.[15]

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Histologic Findings

Gross evaluation of the heart reveals flabby and pale muscle with petechiae. Ventricular muscle is usually thin and may be hypertrophied. Heart valves and the endocardium are not usually involved, but in cases of chronic myocarditis, they might appear as they appear in endocardial fibroelastosis. Some experts believe that endocardial fibroelastosis is a result of viral myocarditis that occurred much earlier.

The microscopic hallmark of acute myocarditis is focal or diffuse interstitial infiltrate of mononuclear cells, lymphocytes, plasma cells, and eosinophils. Viral particles are rarely seen unless searched for with special techniques (ie, PCR assay). Necrosis and disarrangement of the myocytes are typical and often are seen with coxsackievirus infection. In the chronic and healing stages, myocytes are replaced by fibroblasts (scar tissue).[16]

In adenoviral myocarditis, the infiltrate seen histologically is less severe than is seen in cases of enteroviral infection.

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Contributor Information and Disclosures
Author

Edwin Rodriguez-Cruz, MD Director, Section of Cardiology, Department of Pediatrics, San Jorge Children’s Hospital, Puerto Rico; Private Practice in Interventional Pediatric Cardiology and Internal Medicine, Centro Pedíatrico y Cardiovascular

Edwin Rodriguez-Cruz, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, American Society of Echocardiography, Society for Cardiovascular Angiography and Interventions, Society of Pediatric Echocardiography, American College of Physicians-American Society of Internal Medicine, American Medical Association, Puerto Rico Medical Association

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: St Jude's Medical Co.<br/>Received grant/research funds from NOVARTIS for investigator; Received consulting fee from St. Jude Medical Corp. for speaking and teaching.

Coauthor(s)

Robert D Ross, MD Director of Pediatric Cardiology Fellowship Program, Department of Pediatrics, Division of Pediatric Cardiology, Children's Hospital of Michigan; Professor of Pediatrics, Wayne State University School of Medicine

Robert D Ross, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Society of Pediatric Echocardiography

Disclosure: Nothing to disclose.

Chief Editor

Howard S Weber, MD, FSCAI Professor of Pediatrics, Section of Pediatric Cardiology, Pennsylvania State University College of Medicine; Director of Interventional Pediatric Cardiology, Penn State Hershey Children's Hospital

Howard S Weber, MD, FSCAI is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, Society for Cardiovascular Angiography and Interventions

Disclosure: Received income in an amount equal to or greater than $250 from: St. Jude Medical.

Acknowledgements

Ameeta Martin, MD Clinical Associate Professor, Department of Pediatric Cardiology, University of Nebraska College of Medicine

Ameeta Martin, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

References
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Hypersensitivity myocarditis. High magnification of myocardium with perivascular infiltrates rich in eosinophils. This patient had a clinical history compatible with drug-induced hypersensitivity myocarditis.
 
 
 
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