**1. Introduction**

308 Myocarditis

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Myocarditis is defined as myocardial inflammation allied with edema, cellular infiltration, apoptosis and necrosis of cardiomyocytes (Rosenstein et al., 2000). It is likely to be a complex disease and its etiology has been associated with various infections, systemic diseases, drugs, and toxins. Among them, a wide array of organisms, including viral, bacterial, rickettsial, fungal, and parasitic organisms have been implicated as causative agents (Feldman & McNamara, 2000). There are two types of myocarditis viz, lymphocytic and giant cell myocarditis.

Acute myocarditis must be considered in patients who present with recent onset of cardiac failure or arrhythmia, though the onset of clinical cardiac symptoms may be vague in many patients. Fulminant myocarditis is a distinct entity characterized by the sudden onset of severe congestive heart failure or cardiogenic shock, usually following a flu-like illness. Giant cell myocarditis is a rare, frequently fatal disorder of unknown origin characterized by the presence of giant cell inflammatory infiltrate in the myocardium with widespread necrosis and degeneration of myocardial fibers (Batra & Lewis, 2001). It may be associated with various systemic autoimmune diseases (Kuhl & Schultheiss, 2010).

Heart reactive autoantibodies are found in a high percentage of patients with myocarditis. Identified autoantigens include the β1 adrenoreceptor adenine dinucleotide translocator, branched-chain keto acid dehydrogenase, cardiac myosin, sarcolemmal and myolemmal proteins, connective tissue, and extracellular matrix proteins including laminin. Antigenic mimicry between the dominant self molecules and the infectious agents also contributes to the disease process (Caforio et al., 1997; Neumann et al., 1990; Maisch, 1989).
