The ECG may show sinus tachycardia, focal or generalised abnormality, ST segment elevation, fascicular blocks or atrioventricular conduction disturbances. Although the ECG abnormalities are non-specific, the ECG has the virtue of drawing attention to the heart and leading to echocardiographic and other investigations. Echocardiography may reveal segmental or generalised wall motion abnormalities or a pericardial effusion. Echocardiography allows other causes of heart failure to be excluded but pronounced focal changes in wall motion may lead to confusion with myocardial infarction, especially if the ECG changes also suggest this.5

The chest x ray may be normal, show cardiac enlargement, pulmonary venous congestion or pleural eVusions.

Evidence of myocyte necrosis may be found with an increase in creatine kinase or appearance of troponin, indicating myocytolysis. The highest enzyme concentrations occur early and will probably have returned to normal by about a week after onset.6 Cardiac autoantibodies can be demonstrated only later in the disease process.

A viral origin of myocarditis can only be proved if the virus is detected within an altered myocardium. This has become possible through molecular analyses of necropsy, transplant, and endomyocardial biopsy specimens using new techniques of viral gene amplification, which have shown persistence of viral mRNA.1 The histological diagnosis of myocarditis (fig 33.1) was clarified by the Dallas criteria,7 but these unfortunately did not include immunohistochemistry to demonstrate a T cell mediated immune response.

Figure 33.1. Acute myocarditis showing sheets of pale staining myocytes. Lymphocytes are seen which were identified as CD4 and CD8 cells on immunohistology.
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