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Patients may present several days to a few weeks after the onset of an acute febrile illness or a respiratory infection or with heart failure without antecedent symptoms The onset of heart failure may be gradual or may be abrupt and fulminant Emboli may occur due to the procoagulant effect of cytokines combined with decreased myocardial contractility and blood pooling Pleural-pericardial chest pain is common Examination reveals tachycardia, gallop rhythm, and other evidence of heart failure or conduction defect Many acute infections are subclinical, though they may present later as idiopathic cardiomyopathy or with ventricular arrhythmias At times, the presentation may mimic an acute myocardial infarction with ST changes, positive cardiac markers, and regional wall motion abnormalities despite normal coronaries Microaneurysms may also occur and may be associated with serious ventricular arrhythmias Patients may present in a variety of ways with fulminant, subacute, or chronic myocarditis

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Nonspecific ST T changes and conduction disturbances are common Ventricular ectopy may be the initial and only clinical finding Chest radiograph is nonspecific, but cardiomegaly is frequent, though not universal Evidence for pulmonary venous hypertension is common and frank pulmonary edema may be present

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Viral Adenovirus, arbovirus (dengue fever, yellow fever), arenavirus (Lassa fever), coxsackie virus, cytomegalovirus, echovirus, encephalomyocarditis virus, Epstein Barr virus, hepatitis B, herpesvirus, HIV-1, influenza virus, mumps virus, poliomyelitis virus, rabies, respiratory syncytial virus, rubella and rubeola virus, vaccinia virus, varicella virus, variola virus Bacterial Brucellosis, clostridia, diphtheria, Francisella (tularemia), gonococcus, Haemophilus, Legionella, meningococcus, Mycobacterium, Mycoplasma, Pneumococcus, psittacosis, Salmonella, Staphylococcus, Streptococcus, Whipple s disease Fungal Actinomyces, Aspergillus, Blastomyces, Candida, Cryptococcus, Histoplasma, Nocardia, Sporothrix Rickettsial Rocky Mountain spotted fever, Q fever, scrub typhus, typhus Spirochetal Borrelia (Lyme disease and relapsing fever), Leptospira, syphilis Helminthic Cysticercus, Echinococcus, Schistosoma, Toxocara (visceral larva migrans), Trichinella Protozoal Entamoeba, Leishmania, Tryponosoma (Chagas disease), toxoplasmosis Modified, with permission, from Pisani B et al Inflammatory myocardial disease and cardiomyopathies Am J Med 1997 May;102(5):459 69

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There is no specific laboratory study that is consistently present, though the white blood cell count is usually elevated and the sedimentation rate may increase Troponin I levels are elevated in about one-third of patients, but CK-MB is elevated in only 10% Echocardiography provides the most convenient way of evaluating cardiac function and can exclude many other processes Gallium-67 scintigraphy may reveal increased cardiac uptake in acute or subacute myocarditis, but it is not very sensitive MRI with gadolinium enhancement reveals spotty areas of injury throughout the myocardium Paired serum viral titers and serologic tests for other agents may indicate the cause

Pathologic examinations may reveal a lymphocytic inflammatory response with necrosis, but the patchy distribution of abnormalities makes this relatively insensitive By biopsy, the diagnosis of myocarditis has been established by the 1986 Dallas criteria The diagnosis is dependent on describing the severity of an inflammatory infiltrate with necrosis and degeneration of adjacent myocytes The

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type of infiltrate is dependent on the causal agent; usually this is lymphocytic in viral disease, but it may be neutrophilic, eosinophilic, giant cell, granulomatous, or mixed

Patients with fulminant myocarditis may present with acute cardiogenic shock Their ventricles are usually not dilated, but thickened (possibly due to myoedema) There is a high death rate, but if the patients recover, they are usually left with no residual cardiomyopathy Patients who present with subacute disease have a dilated cardiomyopathy and generally make an incomplete recovery Those who present with chronic disease tend to have only mild dilation of the LV and eventually present with a more restrictive cardiomyopathy Specific antimicrobial therapy is indicated when an infecting agent is identified All patients should receive standard heart failure therapy and have arrhythmias suppressed Exercise should be limited during the recovery phase Some believe digoxin should be avoided Immunosuppressive therapy with corticosteroids and intravenous immunoglobulins may improve the outcome when the process is acute (< 6 months) and if the biopsy suggests ongoing inflammation However, controlled trials have not been positive, so the value of routine myocardial biopsies in patients presenting with an acute myocarditic picture is uncertain; immunosuppressive therapy without histologic confirmation is clearly unwise, and there are few data to support its use Patients with fulminant myocarditis require aggressive short-term support including an intra-aortic balloon pump or an LV assist device Ongoing studies are addressing whether patients with giant cell myocarditis may be responsive to immunosuppressive agents, as a special case Overall, if improvement does not occur, many patients may be eventual candidates for cardiac transplantation

Barbaro G Cardiovascular manifestations of HIV infection Circulation 2002 Sep 10;106(11):1420 5 [PMID: 12221062] Brady WJ et al Myocarditis: emergency department recognition and management Emerg Med Clin North Am 2004 Nov;22 (4):865 85 [PMID: 15474774] Magnani JW et al Myocarditis: current trends in diagnosis and treatment Circulation 2006 Feb 14;113(6):876 90 [PMID: 16476862]

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