How is viral myocarditis diagnosed?

Updated: Mar 02, 2021
  • Author: Vinh Q Nguyen, MD, FACC; Chief Editor: Gyanendra K Sharma, MD, FACC, FASE  more...
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Viral myocarditis can produce variable degrees of illness, ranging from focal disease to diffuse pancarditis involving myocardium, pericardium, and valve structures. Viral myocarditis is usually a self-limited, acute-to-subacute disease of the heart muscle. Symptoms are similar to those of CHF and often are subclinical. Many patients experience a flulike prodrome.

Confirming the diagnosis can be difficult because symptoms of heart failure can occur several months after the initial infection. Patients with viral myocarditis (median age, 42 years) are generally healthy and have no systemic disease.

Acute viral myocarditis can mimic acute myocardial infarction, with patients sometimes presenting in the emergency department with chest pain; nonspecific electrocardiographic (ECG) changes; and abnormal, often highly elevated serum markers such as troponin, creatine kinase, and creatine kinase-MB.

The diagnosis of viral myocarditis is mainly indicated by a compatible history and the absence of other potential etiologies, particularly if it can be supported by acute or convalescent sera. An ECG demonstrates varying degrees of ST-T wave changes reflecting myocarditis and, sometimes, varying degrees of conduction disturbances. Echocardiography is a crucial aid in classifying this disease process, which manifests mostly as a dilated type of cardiomyopathy.

An important diagnostic tool in myocarditis is cardiac magnetic resonance imaging (MRI), which allows pertinent tissue characterization, specifically, myocardial edema, hyperemia and capillary leak, and necrosis/fibrosis. The classic finding in inflammatory injury is augmented permeability of cell membranes leading to tissue edema, which is detected using T2-weighted imaging. Intertwined with tissue edema is vasodilatation and increased blood tissue delivery to the site of inflammation. As gadolinium is rapidly distributed into the interstitium, using contrast-enhanced fast-spin echo T1-weighted MRI can facilitate myocardial early gadolinium enhancement to assess hyperemia and inflammation. Additionally, late gadolinium enhancement (LGE) can be used to assess necrosis/fibrosis as fibrocytes replace viable tissue in the natural evolution of the disease process. Characteristic distribution of LGE may aid in differentiation of the pathologic processes, such as ischemic versus nonischemic subtypes in which LGE distribution is located in the midwall whereas the subendocardium is involved in ischemia. [2]

Myocarditis is almost always a clinically presumed diagnosis because it is not associated with any pathognomonic sign or specific, acute diagnostic laboratory test result. In the past, percutaneous transvenous right ventricular endomyocardial biopsy has been used, but the Myocarditis Treatment Trial revealed no advantage for immunosuppressive therapy in biopsy-proven myocarditis, so biopsy is not routinely performed in most cases. The diagnostic sensitivity using endomyocardial biopsy is low due to the focal nature of the inflammatory process and to sampling error, leading to increased false negative rates. [3]

Tissue samples are conventionally analyzed by histologic means via light or electron microscopy (Dallas criteria) and modern immunohistochemical methods, but they are not universally assessed by molecular methods of viral genome analysis via polymerase chain reaction (PCR), which would significantly increase the diagnostic potential. Furthermore, on the basis of the combination of absence/scarcity of data on associations of viral loads with clinical outcomes and the uncertain sensitivity of viral genome data, routine testing for viral genome is not recommended outside centers with extensive experience in viral genome analysis. [4]

If a patient is thought to have viral myocarditis, the initial diagnostic strategies should be to evaluate cardiac troponin I or T levels and to perform antimyosin scintigraphy. Positive troponin I or T findings in the absence of myocardial infarction and the proper clinical setting confirm acute myocarditis. Negative antimyosin scintigraphy findings exclude active myocarditis.

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