Myocarditis
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Introduction

Myocarditis is an inflammation of the myocardial layer of heart muscle.

Myo=muscle, card=heart, itis=inflammation.

The heart wall is made of 3 layers:

  • Endocardium (layer of endothelium & connective tissue lining the inside of the heart wall)
  • Myocardium (middle layer composed of cardiac muscle responsible for heart contraction)
  • Epicardium (aka visceral pericardium; outer connective tissue/fat layer)

Inflammation of the middle muscular layer (myocardium) is termed myocarditis.

The inflammation can damage myocardial cells, weakening the heart’s pumping capacity and if severe, it can lead to acute-onset heart failure (fulminant myocarditis). Usually, the heart is able to recover once the inflammation subsides, however, it can very rarely cause dilated cardiomyopathy or sometimes end-stage heart failure (and death!).

Myocarditis is an important differential for an acute chest pain presentation. Myocarditis is a cause of sudden cardiac death in otherwise young fit well people (alongside hypertrophic cardiomyopathy).

 Epidemiology

  • All age groups can be affectedbut it commonly affects those <50
  • Slightly higher incidence in men than women
  • 5% of patients with acute viral illness may have myocardial involvement
  • Approximately 10% of all sudden cardiac deaths in people under 35 can be attributable to myocarditis aetiology

Causes

Infectious

  • Viral (main cause)
    • Coxsackie viruses are the commonest culprits in Europe and North America
    • Other common causes:
    • Diphtheria (commonest cause globally)
    • There are also (less common) bacterial and fungal causes

Non-infectious

  • Drugs/toxins
    • Cyclophosphamide, catecholamines (e.g. adrenaline, dopamine)
    • Amphetamines, ethanol, cocaine
    • Heavy metals (copper, iron, lead)
  • Hypersensitivity
    • Antibiotics (cephalosporins, penicillins, sulphonamides)
    • Clozapine
    • Diuretics
    • Lithium
    • Phenytoin
  • Inflammatory/immune disorders

Presentation

The presentation of myocarditis can be very variable – from asymptomatic, all the way up to life-threatening heart failure. Although it is important to consider in a differential of chest pain, only about 1/3 of patients will present with chest pain, and over half will have fatigue.

  • Usually age <50
  • 2-3 week history of viral symptoms (fever, myalgia, URTI)
  • Recent travel? (think infection)
  • Past medical history may include immune disorders
  • Medication list may reveal a precipitant
  • Symptoms
    • Fatigue
    • Chest pain (can be positional)
    • Dyspnoea/orthopnoea
    • Palpitations, syncope
  •  Examination
    • S3 and S4 gallops
    • Pericardial rub
    • Tachycardia (arrythmias)

Investigations

  • ECG: ST-segment and T-wave changes
    • ST depression or elevation
    • T-wave inversion
    • AV node block
  • Bloods: raised troponin and CK-MB
  • CXR: enlarged heart and / or signs of heart failure
  • Echo: ventricular dilatation and abnormal wall movement
  • Biopsy is the definitive test but very risky so not often done – it is only done if thought it will affect the management plan
  • Cardiac MRI: useful in differentiating between myocarditis and ischemia / infarction
Viral myocarditis on histology
Viral myocarditis on histology. This sample was taken at post-mortem, but occasionally biopsies will be taken from patients during the diagnostic work-up. This file is taken from wikimedia commons and is licensed under the Creative Commons Attribution-Share Alike 3.0 Unported license.

Differential Diagnoses

Can be almost anything that causes chest pain or shortness of breath

 

Management

The most important factor is to identify and treat the underlying cause

  • Acute + haemodynamically stable
    • Supportive care ± treat the underlying cause*
    • If there is also left ventricular dysfunction:
    • Acute + haemodynamically unstable
      • IV arterial vasodilator
      • Treat the underlying cause
    • Refractory/end-stage
      • 1stline: Heart transplant
      • 2ndline: Left ventricular assist device
    • *Underlying cause: viral (improves with time), bacterial (antibiotics), non-infectious (antidotes if appropriate) – for giant-cell & Chagas steroids or transplant will be needed

Prognosis

Although prognosis for many patients is good, where they have little or no residual loss of cardiac function, for some types of myocarditis (e.g. giant cell myocarditis), the prognosis can be very poor and result in death at <6 months post symptom onset.

References

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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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