Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Myocarditis is acute or chronic inflammation of the myocardium - and may present similarly to myocardial infarction. Myocardial destruction may lead to dilated cardiomyopathy.

The exact incidence of myocarditis is unknown. One study suggested that myocarditis is the cause of sudden cardiac death in 8.6% of cases and is identified in up to 9% of routine post-mortem examinations[1].

This is very variable, from asymptomatic changes seen on ECG to fulminant heart failure, arrhythmias and sudden cardiac death[2]:

  • Patients may be asymptomatic with ECG abnormalities.
  • Others may have severe heart failure and left ventricular dysfunction (LVD).

Patients commonly complain of:

  • Fatigue (>50% of patients).
  • Chest pain (35% of patients).
  • Fever (20% of patients).
  • Dyspnoea.
  • Palpitations.
  • Tachycardia (may occur).
  • Heart sounds - soft S1 or S4 gallop rhythm.
  • Signs of heart failure.


  • Viral infection is the most common cause of acute myocarditis[2].
  • Coxsackievirus is the most common viral cause in Europe and the USA; however, most viruses are potential agents, including adenovirus, parvovirus B19, enteroviruses, HIV, Epstein-Barr virus and hepatitis A and hepatitis C[3].
  • Worldwide the most common bacterial cause is diphtheria.
  • There are also spirochetal, fungal, parasitic and rickettsial causes.
  • The protozoal Chagas' disease is a common entity worldwide[1].


  • Sarcoidosis.
  • Systemic lupus erythematosus.
  • Scleroderma.
  • Chlamydophila pneumoniae (chlamydial pneumonia).
  • Churg-Strauss syndrome.
  • Inflammatory bowel disease.
  • Giant cell myocarditis.
  • Type 1 diabetes mellitus.
  • Kawasaki disease.
  • Myasthenia gravis.
  • Polymyositis.
  • Thyrotoxicosis.
  • Granulomatosis with polyangiitis (Wegener's granulomatosis).
  • Heart transplant rejection.

Drugs causing hypersensitivity reactions
Clozapine, acetazolamide, amitriptyline, cefaclor, colchicine, furosemide, isoniazid, lidocaine, methyldopa, penicillin, phenytoin, streptomycin, tetracycline, thiazides and tetanus toxoid.

Eosinophilic myocarditis is a rare form of myocardial inflammation with variable aetiology. In developed countries, the most common causes are hypersensitivity or allergic reactions, as well as various conditions leading to eosinophilia[4].

Toxic myocarditis

  • Drugs: ethanol, cytotoxic antibiotics (anthracyclines - eg, doxorubicin), amfetamines, cocaine, cyclophosphamide, fluorouracil, lithium, interleukin-2 and trastuzumab may exert a direct cytotoxic effect.
  • Heavy metal poisoning: lead, copper, iron.
  • Others: arsenic, insect stings and bites, phosphorus, carbon monoxide and inhalants.

Physical agents

  • Electric shock
  • Hyperpyrexia
  • Radiation/radiotherapy
  • ECG: changes may include ST-segment elevation/depression, T-wave inversion, atrial arrhythmias, transient atrioventricular (AV) block.
  • Blood tests: FBC (leukocytosis in 25%), U&E, creatine kinase (often elevated, as are other markers of myocardial cell damage, including troponin I and troponin T), ESR or CRP (elevated in 60%), LFT.
  • CXR:
    • Normal cardiac silhouette but pericarditis or overt clinical congestive heart failure is associated with cardiomegaly.
    • Vascular redistribution.
    • Interstitial and alveolar oedema.
    • Pleural effusion.
  • Viral or Chagas' serology may be helpful occasionally, as may autoantibodies (to screen for systemic autoimmune disease - eg, scleroderma)[5].
  • Endomyocardial biopsy (the gold standard test) is sometimes performed - but has only limited sensitivity and specificity[6].
  • Cardiac MRI can differentiate transient and permanent tissue damage. Therefore, cardiac MRI is clinically useful to differentiate acute myocarditis from infarction[7].

Treat the underlying cause. Patients with signs of acute myocarditis (fever, WCC, flu-like illness and haemodynamic compromise) should be transferred to ITU, as ventricular support may become necessary. For an outline of appropriate supportive measures, see separate Heart Failure Management article.

Patients may recover or progress to intractable heart failure (mechanical support devices may be needed, as precipitous cardiac decompensation can occur).

  • Treatment of acute myocarditis is still mainly supportive, except for giant cell myocarditis where steroids have been shown to improve survival[2].
  • In patients with severe myocarditis and symptomatic hypotension, parenteral inotropes, including phosphodiesterase inhibitors (eg, milrinone) or adrenergic agonists (eg, dobutamine or dopamine) may be required[1].
  • The use of anticoagulation is similar to that in patients with non-ischaemic dilated cardiomyopathy; anticoagulation is usually indicated for patients with concomitant atrial fibrillation or arterial or venous thromboembolism[1].
  • Corticosteroids do not reduce mortality for people diagnosed with viral myocarditis and low left ventricular ejection fraction (LVEF). There is some evidence that corticosteroids may improve cardiac function but only from small, low-quality studies[8].
  • There is currently no evidence to support the routine use of intravenous immunoglobulin for presumed viral myocarditis in children or adults[9].

After recovery from acute myocarditis, patients should be advised to limit activity for several months[1].

The prognosis for patients with acute myocarditis can be very good but depends on clinical presentation, LVEF and pulmonary artery pressure[1].

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  1. Schultz JC, Hilliard AA, Cooper LT Jr, et al; Diagnosis and treatment of viral myocarditis. Mayo Clin Proc. 2009 Nov 84(11):1001-9. doi: 10.1016/S0025-6196(11)60670-8.
  2. Shauer A, Gotsman I, Keren A, et al; Acute viral myocarditis: current concepts in diagnosis and treatment. Isr Med Assoc J. 2013 Mar 15(3):180-5.
  3. Dennert R, Crijns HJ, Heymans S; Acute viral myocarditis. Eur Heart J. 2008 Jul 9.
  4. Kuchynka P, Palecek T, Masek M, et al; Current Diagnostic and Therapeutic Aspects of Eosinophilic Myocarditis. Biomed Res Int. 2016 2016:2829583. doi: 10.1155/2016/2829583. Epub 2016 Jan 17.
  5. Frishman WH, Zeidner J, Naseer N; Diagnosis and management of viral myocarditis. Curr Treat Options Cardiovasc Med. 2007 Dec 9(6):450-64.
  6. Greulich S, Ferreira VM, Dall'Armellina E, et al; Myocardial Inflammation - Are We There Yet? Curr Cardiovasc Imaging Rep. 2015 8(3):6.
  7. Wassmuth R; Cardiac magnetic resonance imaging for myocarditis and nonischemic cardiomyopathies. Minerva Cardioangiol. 2009 Aug 57(4):511-20.
  8. Chen HS, Wang W, Wu SN, et al; Corticosteroids for viral myocarditis. Cochrane Database Syst Rev. 2013 Oct 18 10:CD004471. doi: 10.1002/14651858.CD004471.pub3.
  9. Robinson J, Hartling L, Vandermeer B, et al; Intravenous immunoglobulin for presumed viral myocarditis in children and adults. Cochrane Database Syst Rev. 2015 May 20 (5):CD004370. doi: 10.1002/14651858.CD004370.pub3.
Dr Colin Tidy
Peer Reviewer:
Dr John Cox
Document ID:
1105 (v26)
Last Checked:
24 January 2017
Next Review:
23 January 2022

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. Patient Platform Limited has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.