Myocarditis must be differentiated from an acute ST elevation myocardial infarction requiring immediate treatment and, on the other hand, from harmless ECG changes caused by increased sympathicotonia.
The diagnosis of myocarditis is based on the clinical picture, ECG and laboratory findings and ruling out of other reasons. In unclear cases and severe forms of the disease, cardiac imaging with MRI and taking a tissue sample (myocardial biopsy) may be needed.
Emergency assessment in specialized care is required if the patient has severe pains, tachycardias or loss of consciousness, bi- or trifascicular block, heart failure or signs of myocardial damage (TnT, TnI).
Symptomless patients as well as patients with only mild symptoms may be monitored on an outpatient basis.
Definition
Myocarditis and pericarditis are often concomitantly present, and the term myopericarditis or perimyocarditis is then used.
Myocarditis is usually associated with an acute microbial infection, its immediate sequela, other systemic disease, or the cause may also remain unknown. Possible causes include
viral infection (e.g. Coxsackie B4 or B5, influenza A or B, EBV, cytomegalovirus, parvovirus, adenovirus, herpesvirus 6 and coronavirus infection [COVID-19])
Myocarditis may be acute or chronic. Acute myocarditis may be part of an infection, or it may be the only manifestation of an infection. Chronic myocarditis may clinically manifest as dilated cardiomyopathy Dilated Cardiomyopathy.
Symptoms
Chest pain, arrhythmias, respiratory distress or acute cardiac insufficiency, especially in association with signs of a current infection or after an overcome infection
Reduced physical performance, tachycardia, arrhythmias (ventricular), loss of consciousness
Mild cases are not necessarily symptomatic.
Signs
Clinical examination
Clinical findings may be insignificant.
Premature beats and tachycardia may occur.
Heart failure is found in severe cases.
ECG
Sequential changes in the ST-T segment
Initially, extensive ST segment elevations are possible, followed after a few days by negative T wave inversions.
T wave changes only (T wave inversions)
The ECG changes may resemble acute myocardial infarction, but the ST changes usually do not follow the typical coronary supply regions. Differentiation between myocarditis and myocardial infarction on the basis of the ECG is not necessarily possible.
Disorders of the AV conduction (RBBB, LBBB, third-degree AV block)
In myocarditis, the ECG may also be completely normal.
Chest x-ray
In severe myocarditis, the size of the heart increases and vascular markings are increased.
May provide a clue to an infectious aetiology.
Laboratory tests
The concentrations of myocardial damage biomarkers (TnT, TnI) are often increased in the acute phase along with ECG changes, especially ST segment elevations. The concentrations of these markers usually normalize within one week. They are not necessarily increased at all in a number of patients.
If a myocardial damage biomarker remains increased, it suggests a more severe form of disease.
Full blood count (eosinophilia), proBNP or BNP (heart failure and tachycardia may increase the concentration), CRP; specific antibody analyses according to the possible aetiology in a systemic infection, virus isolation from body secretions
Echocardiography
Echocardiography findings may be completely normal in myocarditis.
Regional motion disorders, such as hypokinesia and myocardial swelling, are possible. In practice, detecting these may sometimes be difficult.
Systolic function may be normal, whereas diastolic function may be impaired.
Left ventricular dilatation and extensive decrease in contractility in severe forms
Pericardial effusion in case of simultaneous pericarditis
Other investigations
Contrast-enhanced MRI study
May reveal local inflammatory areas.
Oedema, increased T2 signal intensity, late enhancement
Intracardial thrombi
Biopsy of endomyocardium must be considered in a patient with
reduced left ventricular function, ventricular arrhythmias or a conduction disorder
local thinnings of the cardiac wall
MRI scan showing extensive myocardial damage
suggestion of progressive or ongoing myocardial damage (TnT or TnI clearly exceeding reference ranges)
systemic eosinophilia.
Differential diagnosis
Chest pain associated with myocarditis, increased cardiac marker concentrations and ST elevation may simulate myocardial infarction. Angiography provides a clear answer.
To differentiate myocarditis from infarction, in myocarditis
the patient is usually a young man
there is no history of ischaemic heart disease
Q waves are seldom present
ST changes may be found in several leads; these do not follow the typical coronary supply regions
ST elevations occur also in leads V4-V6
reciprocal depression of the ST segment is absent (except aVR and V1).
Sympathicotonia and dystonia are often associated with tachycardia and T wave changes in ECG. A beta-blocker abolishes these only if they are not caused by myocarditis or any other organic disease.
The athletic heart or early repolarization on the ECG may simulate the signs of myocarditis; echocardiography and follow-up of the ECG will confirm the diagnosis.
Immediate hospital observation is needed if the patient with symptoms has clear ECG changes, increased concentrations of myocardial damage markers (TnT, TnI), ventricular arrhythmias, conduction disorders or signs of heart failure. The risk of severe ventricular arrhythmias requiring treatment is highest in the first days of the disease.
Chest pain may be relieved by temporary use of an NSAID. Routine or continuous use of NSAIDs is, however, not justifiable.
Severe pain may be treated with opioidsin the hospital.
An infection is treated with antimicrobials, if the causative agent is known. Antimicrobial therapy is not a routine part of the treatment of myocarditis.
Possible indications for invasive investigations (coronary angiography, endomyocardial biopsy) are assessed.
A patient with no or only mild symptoms when there are no significant cardiac findings and the suspicion of myocarditis is primarily based on minor ECG changes may be followed in outpatient care. The condition is monitored, for example, every 1-2 weeks for 2 months, and always if cardiac symptoms appear.
Recovery phase
Vigorous physical exercise should be avoided until the resting ECG and troponin concentrations have normalized, which in a typical case of myocarditis takes 2-3 months. In athletes, an exercise test is recommended at this stage.
Competitive athlete's return to exercise and competition is assessed individually. The intensity and duration of myocarditis, imaging findings (echocardiography, cardiac MRI) as well as ECG, exercise test and 24-hour ambulatory ECG monitoring results are taken into account.
In case of infection myocarditis, recovery is usually complete.
According to the current view, the infectious agent (virus) may in some cases remain in the cardiac muscle and may lead to a clinical picture similar to dilated cardiomyopathy Dilated Cardiomyopathy months or years later.
References
Caforio AL, Pankuweit S, Arbustini E et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J 2013;34(33):2636-48, 2648a-2648d. [PubMed]
Ammirati E, Cipriani M, Moro C, et al. Clinical Presentation and Outcome in a Contemporary Cohort of Patients With Acute Myocarditis: Multicenter Lombardy Registry. Circulation 2018;138(11):1088-1099. [PubMed]
Pelliccia A, Sharma S, Gati S, et al. 2020 ESC Guidelines on sports cardiology and exercise in patients with cardiovascular disease. Eur Heart J 2021;42(1):17-96. [PubMed]