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| Myocarditis | ||
| Etiology •Infections: viruses (e.g. CMV, HIV, coxsackie); chlamydia; rickettsia (e.g. typhus fever); bacteria; fungi (e.g. candida, aspergillus); protozoa (e.g. Chagas' disease (trypanosoma), toxoplasmosis; nematodes and cestodes: (e.g. filariasis (dirofilaria immitis), trichinosis). •Toxemias (diphtheritic myocarditis). •Immune mediated: postviral, poststrep. Rheumatic fever, systemic lupus erythematosus, drug hypersensitivity (sulfanomides, methyldopa). •Unknown: sarcoidosis, giant cell myocarditis. | ||
| Pathogenesis •Cardiotropic organisms, mostly viral, are blood borne. •Inflammatory response is to the organisms and necrotic muscle. •Postinfectious immunogenic cases may be due to complexing of antigenic products of organisms with tissues, or cross reacting determinants common to both organism and host tissues. •Diphtheria exotoxin causes necrosis of myocardial fibers., | ||
| Epidemiology •Epidemiology varies with cause. | ||
| General Gross Description •Heart may only be dilated and flabby with no obvious myocardial visible changes. •Dense interstitial inflammatory response may be seen as a gray diffuse or focal discoloration of the myocardium. •Valves not affected. •Mural thrombi may result. •Examples: | ||
| General Microscopic Description •Cellular infiltrate is usually mononuclear with dominance of lymphocytes. •Numerous evenly distributed giant cells are seen in giant cell type. •Examples: | ||
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 197-199, 562-564. This link will directly take you to the relevant new literature Myocarditis
| Synopsis by: J. Hasson, MD (T33010M40000)[340]
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