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Myocarditis

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Description

Myocarditis is inflammation of heart muscle, which may be sudden or chronic, and may affect all, or parts of the heart.

Causes and risk factors

In 50% of cases, a cause is never found. In the rest, many possible causes have been identified, both infective and non-infective. The known agents are mainly viruses (the most common cause) such as coxsackie and enteroviruses and some parasites/protozoans. Myocarditis may be linked to polio and rubella viruses and to mass vaccination against smallpox.

Allergic reactions to drugs (sulfas, some diuretics or antibiotics) and exposure to direct toxins (e.g. arsenic) may also cause myocarditis, and there is an association with auto-immune diseases. Infection with parasites or other organisms are also implicated as in Chaga's disease.

Regardless of the cause, the heart muscle becomes inflamed, which leads to heart failure and often rhythm abnormalities. In young adults sudden death can occur.

Symptoms

Myocarditis nearly always causes noticeable symptoms, often quite severe. The main features of myocarditis are those of heart failure, sometimes with added features of viral infection, such as fever. Common presenting features are:

  • fatigue
  • breathing difficulties
  • abnormal heart rhythm - often with fainting spells
  • chest pain, which may mimic a heart attack
  • inability to lie flat because of shortness of breath
  • leg swelling
  • a history of a preceding viral illness
  • fever
  • joint pain and swelling, headache

A virulent form, Giant cell myocarditis, is often fatal.

Diagnosis and investigations

Myocarditis should be suspected when a young man in good health and with no known heart problems suddenly develops heart failure after a viral illness.

The diagnosis of heart failure is a clinical one. Extra findings on examination include rapid and irregular pulse, heart murmurs, a characteristic galloping sound,

fluid in the lungs and possible signs of a viral infection, such as rashes.

Supportive tests include:

  • ECG - this may be non-specific
  • chest x-ray - is also very variable
  • blood cardiac enzymes - elevated levels of troponin I or T reflect destruction of heart muscle
  • blood culture to detect bacterial infection
  • echocardiogram - this is the most useful investigation, showing decreased heart function, and typical changes in the shape of the ventricle, which tends to become more spherical. This can be used to monitor progress with treatment.
  • MRI may be useful in some cases.

The gold standard in diagnosis, though, remains the ENDOMYOCARDIAL BIOPSY, in which a sample of heart muscle is removed for analysis, to prove the diagnosis beyond doubt. This is an invasive procedure, with a risk of perforation of the heart and death, and is thus only done when absolutely necessary, and only by an experienced cardiologist.

Treatment

All patients benefit from standard anti-failure treatment. Management of rhythm disturbances, fluid overload and anti-coagulation are included here.

If a bacterial or other agent is found, specific treatment is given. In severe myocarditis, in newborn babies and outbreaks in institutions, anti-viral therapy may be tried.

Non-steroidal anti-inflammatories are not routinely used, as they are ineffective here, and may worsen the condition.

Intravenous immune globulin may be of use to children in whom no known cause can be found.

In myocarditis associated with Sarcoidosis (an auto-immune disorder), corticosteroids may help if given early, preventing fibrosis of the heart.

For severe Giant cell myocarditis, heart transplantation may be the only solution.

Outcome

There are no reliable predictors of outcome for myocarditis, with some patients recovering completely and others either dying during the illness or developing long-term complications.

Prevention

Myocarditis from some viruses such as polio, mumps, rubella and measles has been virtually eradicated with effective immunization. Future development of vaccine against viruses that cause myocarditis is possible. Increased awareness of parasitic agents and their transmission will reduce their role in this disease.

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