Diagnosis myocarditis


Laboratory Studies

  • Complete blood count - Leukocytosis (may demonstrate eosinophilia)
  • Elevated erythrocyte sedimentation rate (and other acute phase reactants such as C-reactive protein)
  • Rheumatologic screening - To rule out systemic inflammatory diseases
  • Elevated cardiac enzymes (creatine kinase or cardiac troponins)
    • These are an indicator for cardiac myonecrosis. Cardiac troponin (troponin I or T), in particular, is elevated in at least 50% of patients with biopsy-proven myocarditis. They may also help identify those with resolution of viral myocarditis.
    • The test has 89% specificity and 34% sensitivity and increases more frequently than creatine kinase MB subunits (elevated in only 5.7% of patients with biopsy-proven myocarditis).
  • Serum viral antibody titers for viral myocarditis
    • Common viral antibody titers available for clinical evaluation include coxsackievirus group B, HIV, cytomegalovirus, Ebstein-Barr virus, hepatitis virus family, and influenza viruses. Titers increase 4-fold or more with gradual fall during convalescence (nonspecific), hence requiring serial testing.
    • Antibody titer test is rarely indicated in the diagnosis of viral myocarditis or any dilated cardiomyopathies, owing to its low specificity and the delay of rising viral titers, which would have no impact on therapeutic decisions.
    • The presence of viral genome in endomyocardial biopsy samples have been sought to be the criterion standard for viral persistence; however, it lacks specificity as the presence of viral genome can also be present in healthy controls. The most common viral genomes found include parvovirus and herpes simplex.

Imaging Studies

  • Echocardiography: This is performed to exclude other causes of heart failure (eg, valvular, amyloidosis, congenital) and to evaluate the degree of cardiac dysfunction (usually diffuse hypokinesis and diastolic dysfunction). It also may allow gross localization of the extent of inflammation (ie, wall motion abnormalities, wall thickening, pericardial effusion). In addition, echocardiography may distinguish between fulminant and acute myocarditis by identifying near-normal left ventricular diastolic dimensions and increased septal thickness in fulminant myocarditis (versus increased left ventricular diastolic dimensions and normal septal thickness in acute myocarditis), with marked improvement in systolic function in time.
  • Cardiac angiography: This is often indicated to rule out coronary ischemia as a cause of new-onset heart failure, especially when clinical presentation mimics acute myocardial infarction. It usually shows high filling pressures and reduced cardiac outputs.
  • Gadolinium-enhanced magnetic resonance imaging (MRI): This imaging technique is used for assessment of the extent of inflammation and cellular edema, although it is still nonspecific. Delayed-enhanced MRI has also been used to quantify the amount of scarring that occurred following acute myocarditis.
  • Nuclear imaging: Antimyosin scintigraphy (using antimyosin antibody injections) can identify myocardial inflammation with high sensitivity (91-100%) and negative predictive power (93-100%) but has low specificity (31-44%) and low positive predictive power (28-33%). In contrast, gallium scanning is used to reflect severe myocardial cellular infiltration and has a good negative predictive value, although specificity is low. Positron emission tomography (PET) scanning has been used in selected cases (eg, sarcoidosis) to assess the degree and location of inflammation.

Other Tests

  • Electrocardiogram - Often nonspecific (eg, sinus tachycardia, nonspecific ST or T-wave changes)
    • Occasionally, heart block (atrioventricular block or intraventricular conduction delay), ventricular arrhythmia, or injury patterns with ST- or T-wave changes mimicking myocardial ischemia or pericarditis (pseudoinfarction pattern) may indicate poorer prognosis.
    • Arrhythmia is common in Chagas heart disease. The following may be seen: right bundle-branch block with or without bifascicular block (50%), complete heart block (7-8%), atrial fibrillation (7-10%), and ventricular arrhythmia (39%).

Procedures

  • Endomyocardial biopsy (EMB): This is the criterion standard for diagnosis of myocarditis, although it still has limited sensitivity and specificity, as inflammation can be diffuse or focal. Routine EMB in establishing diagnosis of myocarditis rarely is helpful clinically, however, since histologic diagnosis seldom has an impact on therapeutic strategies, unless giant cell myocarditis is suspected.The risk of adverse events approaches 6% (including complications with 2.7% on sheath insertion and 3.3% on the biopsy procedure), including 0.5% probability of perforation.
  • Because of sampling technique, sensitivity may increase with multiple biopsies (50% for 1 biopsy, 90% for 7 biopsies). The standard is to obtain at least 4 or 5 biopsies, although false-negative rates still may be as high as 55%.
  • False-positive rates are also high, owing to small numbers of normally occurring lymphocytes in the myocardium and the difficulty in distinguishing between lymphocytes and other cells (such as eosinophils in hypersensitive/eosinophilic myocarditis).
  • Wide interobserver variability in histologic interpretations is also a factor.
  • Noncaseating granulomas for sarcoid myocarditis are found in only 5% of cases by biopsies, and in as many as 27% in autopsy series.
  • Persisting viral mRNA can be found in only 25-50% of patients with biopsy-proven acute myocarditis, and persistent viral mRNA often confers a poor prognosis. Recent epidemiological results from the European Study on the Epidemiology and Treatment of Cardiac Inflammatory Disease (ESETCID) database found that only 11.8% of patients with suspected acute or chronic myocarditis and reduced ejection fractions had detectable viral genomes in biopsy samples.

Histologic Findings

Biopsy specimens from EMB should reveal the simultaneous findings of lymphocyte infiltration and myocyte necrosis.

Staging

The Dallas classification (1987) and the World Health Organization (WHO) Marburg classification (1996) are commonly used.
  • Cell types - Lymphocytic, eosinophilic, neutrophilic, giant cell, granulomatous, or mixed
  • Amount - None (grade 0), mild (grade 1), moderate (grade 2), or severe (grade 3)
  • Distribution - Focal (outside vessel lumen), confluent, diffuse, or reparative (in fibrotic areas)
  • Dallas classification (1987)
    • Initial biopsy
      • Myocarditis - Myocardial necrosis, degeneration, or both, in the absence of significant coronary artery disease with adjacent inflammatory infiltrate with or without fibrosis
      • Borderline myocarditis - Inflammatory infiltrate too sparse or myocyte damage not apparent
      • No myocarditis
    • Subsequent biopsy
      • Ongoing (persistent) myocarditis with or without fibrosis
      • Resolving (healing) myocarditis with or without fibrosis
      • Resolved (healed) myocarditis with or without fibrosis
  • WHO Marburg criteria (1996) defines myocarditis as a minimum of 14 infiltrating leukocytes/mm2, preferably T cells (CD45RO), with as many as 4 macrophages possibly included.
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