Myocarditis

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

Because there are many cases which remain subclinical, and are therefore undiagnosed, the true number of cases is hard to estimate.
The male-to-female ratio is 1.5:1.
In the documented cases, the average age of patients is 42 years.¹

These are very variable:

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

Patients commonly complain of:

• Fatigue (>50% patients)
• Chest pain (35% of patients)
• Fever (20% of patients)
• Dyspnoea
• Palpitations
• There may be a tachycardia
• Soft S1
• S4 gallop
• Signs of heart failure

Post-mortem studies suggest myocarditis is a major cause of sudden unexpected death in adults, implicated in ~20% of those aged <40 years.²

ECG:

• ST segment elevation/depression
• T wave inversion
• Atrial arrhythmias
• Transient AV block

Bloods:

• FBC (Leucocytosis in 25%)
• U&E
• CK
• ESR or CRP ( Elevated in 60%)
• LFT

CXR:

• Normal cardiac silhouette, but pericarditis or overt clinical CHF is associated with cardiomegaly
• Vascular redistribution
• Interstitial and alveolar oedema
• Pleural effusion

Creatine kinase levels are often elevated, as are other markers of myocardial cell damage (troponin I and troponin T).
Viral or Chagas' serology may be helpful occasionally, as may autoantibodies (to screen for systemic autoimmune disease - eg scleroderma).
Endomyocardial biopsy (the gold-standard test) is sometimes performed - but has only limited sensitivity and specificity.
MRI is capable of showing abnormal signal intensity in the affected myocardium.
It has been shown to have sensitivities and specificities approaching 100% for diagnosis.³

• Treat 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.
• Supportive measures (see heart failure management). Patients may recover or progress to intractable heart failure (mechanical support devices may be needed as precipitous cardiac decompensation can occur).
• There are ongoing trials on the use of antiviral agents or viral specific vaccines.
• Immunomodulating agents. The most promising research addresses the immune response in myocarditis. It involves immune modulators that target particular steps in the immune cascade without eliminating the ability of the body's defenses to shed virus. The role of TNF appears to be central in these approaches. Although studies have failed to show any immediate improvement in left ventricular ejection fraction with immune globulin therapy,^4,5 there is some data showing more long-term benefit in patients with dilated cardiomyopathy and HLA upregulation on biopsy specimens.⁶

Recovering patients should have activity limitations for approximately 6 months, as animal models have shown permanent injury from a rapid return to activity.

• Congestive heart failure
• Pulmonary oedema
• Cardiogenic shock
• Cardiac failure
• Dilated cardiomyopathy
• Dysrhythmias
• Recurrent myositis

• Most cases are believed to be subclinical. They resolve spontaneously without sequelae.
• Patients presenting with CHF experience morbidity and mortality in proportion to the degree of left ventricular dysfunction.
• Elderly patients and patients with giant cell arteritis, who present with cardiogenic shock, have a poor prognosis.
• 50% of patients presenting with new-onset CHF, improve their cardiac function with treatment.
• 25% of patients presenting with CHF stabilise with compromised cardiac function.
• The condition of the remaining 25% of patients continues to deteriorate.
• Patients requiring transplantation have an increased risk of recurrent myocarditis and graft rejection.