Last Updated on by frcemuser

Myocarditis is clinically and pathologically defined as inflammation of the myocardium in the absence of the predominant acute or chronic ischaemia characteristic of coronary artery disease. It is a clinical syndrome of non-ischaemic myocardial inflammation resulting from a heterogeneous group of infectious, immune, and non-immune diseases. Histopathologically, it is characterised by an inflammatory cellular infiltrate with or without evidence of myocyte injury.


  • Fulminant myocarditis: presentation with acute illness following a distinct viral syndrome. Histological study reveals multiple foci of active myocarditis. Clinical presentation consists of severe cardiovascular compromise and ventricular dysfunction. This subgroup typically either resolves spontaneously or results in death.
  • Acute myocarditis: presentation with insidious onset of illness and evidence of established ventricular dysfunction. This subgroup may progress to dilated cardiomyopathy.
  • Chronic active myocarditis: presentation with insidious onset of illness with clinical and histological relapses with development of left ventricular dysfunction and associated chronic recurrent inflammatory changes.
  • Chronic persistent myocarditis: presentation with insidious onset of illness characterised by a persistent histological infiltrate frequently with foci of myocyte necrosis. Clinically, no ventricular dysfunction is present despite other cardiovascular symptoms (such as palpitations or chest pain).


  • Infectious causes:
    • Viral e.g. influenza A and B, adenovirus, coxsackie B virus, Dengue fever, hepatitis B and C virus, mumps, rubella, rubeola, HIV, echovirus, Epstein-Barr virus, cytomegalovirus, parvovirus, herpes simplex virus, poliomyelitis, rabies, varicella
    • Bacterial e.g. Mycobacterial, streptococcal species, mycoplasma pneumoniae, treponema pallidum, tuberculosis, staphylococcal species, clostridium species, neisseria gonorrhoeae
    • Spirochetal e.g. Lyme disease, leptospirosis, syphilis
    • Fungal e.g. Aspergillus species, candida species, coccidiomycosis, cryptococcus species, histoplasma species, sporotrichosis species, blastomycosis
    • Protozoal e.g. Trypanosoma cruzi (Chagas’ disease), African trypanosomiasis (sleeping sickness), toxoplasmosis, malaria, parasitic, schistosomiasis, larva migrans
    • Rickettsial e.g. Q fever, rocky mountain spotted fever
  • Non-infectious causes:
    • Toxins/drug related e.g. anthracyclines, arsenic, carbon monoxide, ethanol, iron, interleukin-2, cocaine, smallpox vaccination, catecholamines (e.g. adrenaline, noradrenaline, dopamine), cyclophosphamide, heavy metals (copper, iron, lead)
    • Hypersensitivity e.g. antibiotics (penicillins, cephalosporins, sulfonamides, amphotericin B), thiazide diuretics, antiepileptics (carbamazepine, phenytoin, phenobarbital), digoxin, lithium, amitriptyline, dobutamine, snake bites
    • Systemic disorders e.g. collagen-vascular diseases, inflammatory bowel disease, giant cell myocarditis, diabetes mellitus, sarcoidosis, thyrotoxicosis, granulomatosis with polyangiitis (formerly known as Wegener’s granulomatosis), Loeffler’s syndrome

Clinical features

Patients presenting with myocarditis are usually aged <50 years. A history of viral prodrome 2 to 3 weeks prior to the onset of myocarditis is commonly present. Symptoms may include chest pain, dyspnoea, orthopnoea, syncope, fatigue, and palpitations.

A thorough examination for both the cardiorespiratory findings and other general findings that may point to possible aetiology should be performed. Findings can include rales, elevated neck veins, S3 gallop, S3 and S4 summation gallop, pericardial friction rub, peripheral hypoperfusion, sinus tachycardia, atrial and ventricular arrhythmias, hypotension, altered sensorium, and lymphadenopathy.


  • Cardiac failure
  • Atrial fibrillation
  • Ventricular tachyarrhythmias
  • Dilated cardiomyopathy
  • Sudden cardiac death
  • Multisystem organ failure


  • 12-lead ECG
    • A 12-lead ECG should be ordered immediately on presentation in anyone with chest pain or cardiac symptoms. In myocarditis it most commonly displays non-specific ST-segment and T-wave abnormalities; however, ST-segment elevation and depression frequently occur.
  • Laboratory evaluation
    • Cardiac biomarkers should be ordered immediately in any patient with suspected myocarditis. Creatine kinase and creatine kinase-MB levels are often mildly elevated. Troponin (I or T) levels have shown to be a more reliable indicator of myocardial damage. Serum B-type natriuretic peptide may be helpful in distinguishing primary cardiac from primary pulmonary aetiologies of dyspnoea when the physical examination and initial work-up is unclear or non-specific. In myocarditis it is elevated in response to ventricular distention such as occurs in congestive heart failure.
  • Echocardiogram
    • This should be ordered in every patient suspected of having myocarditis. Myocarditis can cause global and regional left ventricular motion abnormalities and dilatation.
  • Endomyocardial biopsy (EMB)
    • The diagnostic standard for establishing the diagnosis of myocarditis is the endomyocardial biopsy. However, this test has a yield of 10% to 20% and is not indicated for most patients with suspected myocarditis. The potential risks and benefits of EMB should always be carefully assessed, particularly during the acute presentation, as the risk of arrhythmia or ventricular perforation is highest at this time.


The mainstay of therapy for myocarditis is supportive care and conventional heart failure therapy.

  • End-organ hypoperfusion or cardiogenic shock
    • A small proportion of patients with acute myocarditis will present with fulminant heart failure or cardiogenic shock requiring invasive haemodynamic monitoring and aggressive pharmacological therapy. This may include vasopressors such as norepinephrine (noradrenaline) or positive inotropes such as dobutamine. Rarely, mechanical assist devices are needed as a bridge to recovery, or heart transplantation is needed for patients who do not respond to treatment.
  • Supportive care and conventional heart failure therapy
    • An ACE inhibitor or angiotensin II receptor blocker (ARB) should be started as early as possible.
    • Oral arterial (hydralazine) and venous (nitrates) vasodilators acutely improve cardiac output and decrease pulmonary and LV filling pressures.
    • Beta-blockers should be started once the patient is no longer in acutely decompensated heart failure.
    • An aldosterone antagonist should be started in patients with New York Heart Association class III or IV heart failure.
    • Diuretics improve haemodynamics and patient comfort.
  • Immunosuppressive therapies and intravenous immunoglobulin (IVIG)
    • The routine use of immunosuppressive agents in patients with myocarditis is not recommended. The decision to use them or not should be determined on a case-by-case basis.


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