Immune-Mediated Reactions

Postviral

Poststreptococcal (rheumatic fever)

Systemic lupus erythematosus

Drug hypersensitivity (e.g., methyldopa, sulfonamides)

Transplant rejection

Unknown

Sarcoidosis

Giant cell myocarditis

HIV, human immunodeficiency virus.

inflammation and myocyte damage without a clear etiologic agent and (2) myocarditis caused directly by HIV or by an opportunistic pathogen.

There are also noninfectious causes of myocarditis. Myocarditis can be related to allergic reactions (hypersensitivity myocarditis), often to a particular drug such as antibiotics, diuretics,

and antihypertensive agents. Myocarditis can also be associated with systemic diseases of immune origin, such as RF, SLE, and polymyositis. Cardiac sarcoidosis and rejection of a

transplanted heart are also considered forms of myocarditis.

Against this background we can turn to the anatomic changes seen in the major forms of myocarditis.

Morphology.

During the active phase of myocarditis, the heart may appear normal or dilated; some hypertrophy may be present. The lesions may be diffuse or patchy. The ventricular myocardium is

typically flabby and often mottled by either pale foci or minute hemorrhagic lesions. Mural thrombi may be present in any chamber.

During active disease, myocarditis is most frequently characterized by an interstitial inflammatory infiltrate and focal necrosis of myocytes adjacent to the inflammatory cells ( Fig. 12-36 ).

[74] Myocarditis in which the infiltrate is mononuclear and predominantly lymphocytic is most common (see Fig. 12-36A ). Although endomyocardial biopsies are diagnostic in some cases,

they can be spuriously negative because inflammatory involvement may be focal or patchy. If the patient survives the acute phase of myocarditis, the inflammatory lesions either resolve,

leaving no residual changes, or heal by progressive fibrosis, as mentioned earlier.

Hypersensitivity myocarditishas interstitial infiltrates, principally perivascular, composed of lymphocytes, macrophages, and a high proportion of eosinophils (see Fig. 12-36B ).

A morphologically distinctive form of myocarditis of uncertain cause, called giant cell myocarditis, is characterized by a widespread inflammatory cellular infiltrate containing

multinucleate giant cells interspersed with lymphocytes, eosinophils, plasma cells, and macrophages and having at least focal but frequently extensive necrosis ( Fig. 12-36C ). The giant

cells are of either macrophage or myocyte origin. This variant carries a poor prognosis.[117]

The myocarditis of Chagas diseaseis rendered distinctive by parasitization of scattered myofibers by trypanosomes accompanied by an inflammatory infiltrate of neutrophils,

lymphocytes, macrophages, and occasional eosinophils ( Fig. 12-36D ).

Clinical Features.

The clinical spectrum of myocarditis is broad; at one end the disease is entirely asymptomatic, and such patients recover completely without sequelae. At the other extreme is the

precipitous onset of heart failure or arrhythmias, occasionally with sudden death. A systolic murmur may appear, indicating functional mitral regurgitation related to dilation of the left

ventricle. Between these extremes are the many levels of involvement associated with such symptoms as fatigue, dyspnea, palpitations, precordial discomfort, and fever. The clinical

features of myocarditis can

Figure 12-36Myocarditis. A, Lymphocytic myocarditis, with mononuclear inflammatory cell infiltrate and associated myocyte injury. B, Hypersensitivity myocarditis, characterized by

interstitial inflammatory infiltrate composed largely of eosinophils and mononuclear inflammatory cells, predominantly localized to perivascular and large interstitial spaces. This form of

myocarditis is associated with drug hypersensitivity. C, Giant cell myocarditis, with mononuclear inflammatory infiltrate containing lymphocytes and macrophages, extensive loss of

muscle, and multinucleated giant cells. D, The myocarditis of Chagas disease. A myofiber is distended with trypanosomes (arrow). There is a surrounding inflammatory reaction and

individual myofiber necrosis.

TABLE 12-13-- Causes of Pericarditis

Infectious Agents

Viruses

Pyogenic bacteria

Tuberculosis

Fungi

Other parasites

Date: 2016-04-22; view: 684