Myocarditis
Myocarditis refers to inflammation of the myocardium. It has a wide range of presentations, anywhere from acute and fulminant to chronic.
As the cardiac conduction system is in the myocardium, myocarditis predisposes to arrhythmias. It also affects the myocardium’s ability to contract. It may mimic ACS.
Myocarditis is mostly a disorder of younger adults. It may occur together with pericarditis as part of "perimyocarditis" or "myopericarditis". Myocarditis is usually self-limiting and patients usually achieve complete remission, but some may develop chronic heart failure.
Etiology
- Viral (most common)
- Coxsackie group B
- Adenoviruses
- Enteroviruses
- Bacterial (rheumatic fever)
- Protozoa (Chagas disease, due to Trypanosoma cruzi, which is endemic in Latin America)
- Autoimmune disorders (including Giant cell myocarditis)
- COVID-19
- COVID-19 vaccines (rare)
- Immune checkpoint inhibitors
Determining the exact etiology is rarely possible in clinical practice but it's assumed that most cases are viral.
Pathology
The first phase of the disease involves virus-mediated cellular injury. If the immune response is strong enough, the virus will be eliminated but there will be significant myocardial injury as a complications. This is the cause of fulminant myocarditis.
If the immune response is milder, there won't be significant myocardial injury initially, but the virus also won't be eliminated. This causes a more subacute or chronic course, with low-grade myocardial injury over many weeks.
The latter course may progress to a second phase, where progressive myocardial injury, and the myocardial remodellation that follows, causes dilated cardiomyopathy.
Clinical features
Many are asymptomatic, and symptoms are highly variable. Some have preceding symptoms of viral infection (myalgia, fever, upper respiratory symptoms). The cardiac symptoms may range from asymptomatic to:
- New onset or worsening heart failure or even cardiogenic shock
- Acute coronary syndrome-like symptoms (chest pain, dyspnoea)
- Arrhythmias, both supraventricular and ventricular
Cardiac symptoms may progress slowly or rapidly.
Diagnosis and evaluation
Troponins and NT-proBNP are elevated, as are inflammatory markers. ECG is often abnormal, but no findings are specific for myocarditis. ST-elevations and heart blocks are probably the most common. Echocardiography is important to determine the myocardial contractility and to exclude differential diagnoses like myocardial infarction. There may be regional hypokinesia (like in myocardial infarction) but these regions often do not correspond with the area which is supplied by a single coronary artery (which is the case for myocardial infarction).
MRI with gadolinium contrast is usually sufficient to diagnose myocarditis and can show oedema and necrosis of the myocardium. Unlike in myocardial infarction, the necrosis is usually localised epicardially rather than subendocardially. In doubtful cases, endomyocardial biopsy (which is the gold standard) can be performed, which may also provide information on the etiology, although this is rarely necessary.
There is no role for viral serology, as studies have shown that serology does not correlate with findings on biopsy PCR.
Treatment
Due to the variable course, myocarditis is an indication for hospital admission.
There is no specific treatment, except if there’s a treatable underlying cause. Most cases are self-limiting. Patients should be continuously monitored for arrhythmias by telemetry. The patient may require antiarrhythmics or treatment for heart failure. Unlike in pericarditis, NSAIDs cannot be used as they are not helpful and might even worsen outcomes.
Patients should avoid strenous physical activity for at least 3-6 months after myocarditis to decrease the risk of fatal arrhythmia.