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  • New congestive heart failure with a history of an antecedent viral syndrome.
  • Elevated erythrocyte sedimentation rate, or cardiac markers.
  • ECG shows sinus tachycardia, nonspecific ST-T changes, atrial or ventricular arrhythmias, or conduction abnormalities.
  • Echocardiogram demonstrates chamber enlargement, wall motion abnormalities, systolic or diastolic dysfunction, or mural thrombi.
  • Endomyocardial biopsy reveals an inflammatory infiltrate with adjacent myocyte injury.

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Myocarditis is defined simply as an inflammatory process with necrosis that involves the myocardium. In the past, the myocardial injury was believed to be a direct result of the cytotoxic effects of the relevant organisms. Even as early as 1806, however, it was thought that a persistent inflammatory process following such an infection (eg, diphtheria) of the myocardium led to progressive cardiac damage and dysfunction. When the term “myocarditis” was first introduced in 1837 as inflammation or degeneration of the heart, the diagnosis could be made only postmortem. Fortunately, endomyocardial biopsy now allows the sampling of human myocardial tissue during life and thus the accurate antemortem diagnosis of myocarditis.

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The histologic hallmark of myocarditis is a focal patchy or diffuse inflammatory infiltrate with adjacent myocyte injury. The inflammation may not be restricted to the myocardium but may also involve the adjacent endocardium, pericardium, and valvular structures.

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Myocarditis is most commonly initiated by viral infection (Table 16–1). Initiation of the pathophysiologic abnormalities, however, may result from a variety of insults, including drugs, toxins, hypersensitivity reactions, collagen vascular diseases, and autoimmune reactions. The most common viruses associated with myocarditis in the United States and Western Europe in immunocompetent persons are adenoviruses, coxsackievirus B (enterovirus), parvovirus B19, herpes simplex, influenza A, and cytomegalovirus (CMV). Other viruses, bacteria, rickettsiae, spirochetes, fungi, protozoans, or metazoans can also produce myocarditis; such causes are uncommon, however (see Table 16–1). Successful identification of the most common offending pathogens depends on knowledge of the geographic region’s relevant endemic and epidemic infectious diseases, the person’s immunization status and immunocompetence, and the sophistication and availability of public health services.

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Table Graphic Jump Location
Table 16–1. Important Causes of Myocarditis. 
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Several mechanisms of myocardial damage have been proposed. (1) Direct injury of myocytes by the infectious agent. (2) Myocyte injury caused by a toxin such as that from Corynebacterium diphtheriae. (3) Myocyte injury as a result of infection-induced immune reaction or autoimmunity.

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