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Wednesday 2 July 2008

Myocarditis, viral


DESCRIPTION Inflammatory disease of the myocardium caused by a virus. There are more than 20 viruses implicated in viral myocarditis. Myocarditis typically occurs several weeks after an acute systemic infection, suggesting an associated immunological component. The most frequent cause of viral myocarditis is Coxsackie B virus, which is estimated to be the causative agent in more than 50% of cases. The agent is particularly virulent in children. It may cause concurrent pericarditis.
Other causative agents are: Coxsackie A, cytomegalovirus, dengue virus, hepatitis virus, acquired immunodeficiency (AIDS) virus, influenza virus, poliomyelitis, respiratory syncytial virus, rubella, rubeola, varicella, variola and vaccinia. Myocardial involvement is subclinical in many acute viral diseases. Consequently, the chest X-ray is usually normal. In severe myocarditis, there is cardiomegaly and pulmonary venous hypertension or oedema.
Echocardiography may disclose increase of left ventricular volumes, regional or global hypokinesis and mural thrombus. Nuclear scans after gallium 67, indium 111 antimyosin antibody, or technetium 99m pyrophosphate may indicate inflammatory or necrotic foci in the myocardium. Spin echo MRI after gadolinium chelates has also shown focal hyperenhancement of the myocardium. Endomyocardial biopsy is sometimes used to confirm myocarditis.
Myocarditis generally results in a decrease in myocardial function, with concomitant enlargement of the heart and an increase in the end-diastolic volume caused by increased preload. Normally, the heart compensates for dilation with an increase in contractility (Starling law), but because of inflammation and muscle damage, a heart affected with myocarditis is unable to respond to the increase in volume. In addition, inflammatory mediators, such as cytokines and adhesion molecules, as well as apoptotic mechanisms are activated. The progressive increase in left ventricular end-diastolic volume increases left atrial, pulmonary venous, and arterial pressures, resulting in increasing hydrostatic forces. These increased forces lead to both pulmonary edema and congestive heart failure. Without treatment, this process may progress to end-stage cardiac failure and death.


SYNONYMS

• Inflammation - heart muscle
• Cardiomyopathy; VM
SYMPTOMS

• Fever
• Cough
• Nausea
• Vomiting
• Myalgia
• Arthralgia
• Palpitation
• Heart failure (in severe cases)

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