Myocarditis is inflammation of the myocardium, the muscular tissue of the heart responsible for contraction. Inflammation can injure cardiac muscle cells and interfere with electrical conduction, contractile function or both. The condition ranges from mild disease discovered incidentally to fulminant myocarditis causing severe heart failure, cardiogenic shock or life-threatening arrhythmias. Myocarditis differs from Pericarditis because the principal affected tissue is cardiac muscle, although the two conditions can occur together. Myopericarditis and perimyocarditis are terms used in clinical contexts when both myocardial and pericardial inflammation are present, with terminology varying according to which component predominates.
Myocarditis has many possible causes. Viral infections have historically been prominent, but bacterial, fungal, parasitic and other infectious causes can occur, while immune-mediated disease, systemic inflammatory disorders, toxins and some medications can also produce myocardial inflammation. In some cases, the initiating trigger may no longer be detectable by the time the patient presents. The biological process can involve direct pathogen-mediated injury, immune responses against infected or damaged tissue, microvascular dysfunction and inflammatory cell infiltration. The exact mechanism varies according to the underlying cause, and identifying a cause can be difficult in individual patients.
Symptoms reflect the extent and location of myocardial injury. Patients may experience chest pain, breathlessness, fatigue, palpitations, reduced exercise tolerance, dizziness or syncope. Some have symptoms resembling an acute coronary syndrome, while others present predominantly with heart failure or arrhythmia. Severe myocardial inflammation can reduce ventricular contractility and cause pulmonary or systemic congestion. Electrical instability can produce atrial or ventricular arrhythmias, heart block or sudden cardiac death. Symptoms may occur during or after an infectious illness, but the presence of a preceding infection does not by itself establish myocarditis.
Diagnosis involves integrating history, examination, electrocardiography, cardiac biomarkers, echocardiography and cardiac magnetic resonance imaging. Troponin can be elevated because damaged cardiac muscle releases intracellular proteins into the circulation, but troponin elevation is not specific to myocarditis and occurs in myocardial infarction and other forms of cardiac injury. Cardiac magnetic resonance imaging can characterise myocardial oedema, inflammation and patterns of tissue injury and has become an important non-invasive diagnostic tool. Endomyocardial biopsy can provide direct tissue diagnosis in selected high-risk cases but is invasive and has limited sensitivity when disease is patchy.
Management depends on severity and cause. Patients with uncomplicated disease may require monitoring, treatment of symptoms and temporary restriction from strenuous physical activity while the heart recovers. Heart-failure therapies can be required when ventricular function is impaired, while specific antimicrobial or immunosuppressive treatment may be appropriate for particular identified causes. Severe or fulminant myocarditis can require intensive care, inotropes, mechanical circulatory support or other advanced interventions. Arrhythmias may require targeted treatment, and decisions about implantable devices depend on persistent risk and recovery rather than solely on the initial presentation.
Myocarditis can resolve completely, leave persistent ventricular dysfunction or progress to dilated cardiomyopathy. The prognosis varies according to the cause, severity, degree of myocardial injury and development of arrhythmias or heart failure. Fulminant myocarditis is characterised by severe acute haemodynamic compromise but some patients who survive the acute phase can experience substantial recovery. Persistent myocardial scar can remain after active inflammation has subsided and may provide a substrate for ventricular arrhythmias. Long-term follow-up may therefore include assessment of ventricular function, rhythm and exercise tolerance.
Myocarditis can be difficult to distinguish from other causes of chest pain and cardiac injury. A raised troponin does not prove myocarditis, and a normal early investigation does not necessarily exclude it. Exercise during active myocardial inflammation can increase the risk of serious arrhythmia, so return to strenuous activity is generally based on clinical recovery and specialist assessment. The condition also illustrates the distinction between inflammation and infection: inflammation can be triggered by an infectious process without the myocardium necessarily containing a persistent active infection. Accurate diagnosis is therefore essential before assuming that antimicrobial or immunosuppressive treatment is appropriate.
A common misconception is that Myocarditis is simply an infection of the heart. Infection can trigger myocarditis, but myocardial inflammation can also be immune-mediated, toxic or associated with systemic disease. Another misconception is that mild symptoms imply insignificant myocardial involvement; some patients can develop important arrhythmias with relatively modest symptoms. Conversely, severe biomarker abnormalities do not alone determine long-term prognosis. Myocarditis is best understood as a heterogeneous inflammatory myocardial syndrome requiring assessment of cardiac function, electrical stability, tissue characteristics and underlying cause.
