ECG criteria
- Sinus tachycardia is one of the most frequent yet non-specific findings; sometimes it is disproportionate to fever, pain, hypoxia, or the hemodynamic status
- Diffuse non-specific ST-T changes: T-wave flattening or inversion in multiple lead groups without strict localization to a single coronary territory
- ST-segment elevation, frequently accompanying myopericarditis: the shape (concave) and distribution (diffuse) only point toward inflammation but do not rule out acute coronary occlusion—if ACS is suspected, symptoms, serial ECGs, troponin dynamics, and urgent evaluation of indications for coronary angiography are decisive
- Decreased QRS amplitude (low QRS voltage: <5 mm in all limb leads or <10 mm in all precordial leads) is non-specific; it may occur with pericardial effusion, especially if significant, but its absence does not rule out effusion. Electrical alternans increases the likelihood of a hemodynamically significant effusion and warrants echocardiography
- Pathological Q wave and pseudoinfarct ST elevation in severe myocardial injury—the ECG does not reflect coronary artery patency, and coronary occlusion must be ruled out separately
- Conduction disorders: PR interval prolongation, AV block of any degree up to complete AV block (especially in giant cell myocarditis, sarcoidosis, Lyme disease)
- Prolongation of the corrected QT interval in severe injury is a risk factor for ventricular arrhythmias; evaluate taking into account the correction method, heart rate, electrolytes, and current medications, with Fridericia's formula preferred in tachycardia
- Ventricular extrasystoles, runs of ventricular tachycardia, and less commonly ventricular fibrillation in fulminant courses
What it looks like on ECG
The presentation is extremely variable—ranging from a normal ECG to life-threatening changes, and no single feature is specific for myocarditis.
One of the most frequent findings is sinus tachycardia; sometimes it is disproportionate to fever, pain, or the hemodynamic status, but this is neither an obligatory nor an early sign, rather a frequent and non-specific finding. Against this background, diffuse non-specific ST-T changes may be observed: a flattened T wave or inverted T wave in multiple leads across different walls (e.g., simultaneously in I, II, V2–V6), which does not conform to the blood supply territory of a single coronary artery.
With concomitant pericardial inflammation, an ECG pattern resembling acute pericarditis is typical: ST elevation predominantly in I, II, aVL, V2–V6 with ST depression in lead aVR and frequently in V1, sometimes with PR-segment depression. If the process is predominantly myocardial with pericardial involvement, it is termed myopericarditis; if pericarditis predominates with troponin elevation or signs of myocardial involvement, it is termed perimyocarditis. This pattern is not seen in all patients and may be incomplete; the shape and distribution of ST point toward inflammation but do not rule out acute coronary occlusion.
Myocarditis, including severe cases, can mimic STEMI—presenting with ST elevation, pathological Q wave, and a wide QRS complex. However, the presence of these changes does not prove the absence of coronary occlusion or concomitant coronary artery disease: coronary occlusion must be urgently ruled out, and given the appropriate clinical picture and ECG, the patient should be managed according to the ACS pathway until proven otherwise.
When the conduction system is involved—PR (PQ) interval prolongation, second- or third-degree AV block, bundle branch block. A new left bundle branch block and other intraventricular conduction delays may indicate significant myocardial injury and require risk stratification, but by themselves are non-specific and do not reflect the severity of myocarditis; management is determined by the clinical picture, hemodynamics, serial ECGs, and ACS criteria. Electrolyte- and inflammation-altered myocardium predisposes to ventricular extrasystoles and ventricular tachycardia, up to ventricular fibrillation.
| Finding | Leads | What it reflects |
|---|---|---|
| Sinus tachycardia | — | frequent non-specific finding |
| Diffuse ST-T changes | multiple walls simultaneously | non-specific myocardial injury |
| ST elevation, depression in aVR/V1 | diffuse | concomitant myopericarditis/perimyocarditis |
| AV block | — | conduction system involvement |
| Pathological Q, wide QRS | focal or diffuse | pseudoinfarct changes, require ruling out MI |
Mechanism
Inflammatory infiltration and myocardial edema impair impulse propagation and alter cardiomyocyte repolarization. Cell injury can be either diffuse, focal, or heterogeneous, resulting in multidirectional non-specific T-wave and ST-segment changes in one or more areas; the distribution of these changes merely reflects the probability of a particular etiology and does not replace imaging and ruling out ACS.
Inflammation and edema in the region of the conduction system (AV node, bundle of His, its branches) slow or block conduction—hence PR prolongation and AV blocks. Focal necrosis and fibrosis of cardiomyocytes can create electrically "silent" zones mimicking a pathological Q wave. The electrical instability of the inflamed myocardium provides a substrate for ventricular arrhythmias, including fatal ones.
Causes
- Viral infections (enteroviruses, parvovirus B19, influenza viruses, SARS-CoV-2, and others)
- Bacterial infections (including Lyme disease with typical AV blocks)
- Autoimmune and systemic diseases (cardiac sarcoidosis, giant cell myocarditis, systemic lupus erythematosus)
- Toxic and drug-induced injury (alcohol, cocaine, chemotherapy)
- Immune-mediated myocarditis secondary to immune checkpoint inhibitor therapy
- Idiopathic myocarditis with no established cause
Differential diagnosis
- STEMI: characteristically, ST elevation and reciprocal depression are localized in leads of a single coronary territory, whereas in myocarditis changes are more often diffuse and without clear reciprocity—yet this is a probabilistic rather than absolute distinction: a small MI may occur without prominent reciprocity, and myocarditis may produce regional ST elevation. Diffuseness of ST changes when STEMI is suspected should not delay the activation of a reperfusion strategy and the exclusion of coronary occlusion
- Pericarditis on ECG: isolated pericarditis produces a similar diffuse ST elevation with depression in aVR and frequently in V1, sometimes with PR-segment depression; differentiation from myopericarditis/perimyocarditis is often possible only based on clinical presentation, biomarkers, echocardiography, and MRI
- Early repolarization syndrome: ST elevation with a characteristic notch at the J point in young and healthy individuals, without dynamic evolution and without clinical signs of inflammation
- Takotsubo cardiomyopathy: a similar pattern of diffuse ST-T changes and LV dysfunction, but stress-induced and typical for a specific age and sex group
- Normal early repolarization variant in young athletes: a stable pattern without evolution on serial ECGs
Clinical significance and management
The ECG in myocarditis neither establishes nor rules out the diagnosis—it is used for initial risk stratification and detection of life-threatening rhythm and conduction disorders. High-degree AV block, ventricular tachycardia, syncope, hemodynamic instability, marked QT prolongation, or a newly developed significant intraventricular conduction block in a patient with suspected myocarditis warrant hospitalization and continuous monitoring (with readiness for temporary pacing in complete AV block); an isolated stable bundle branch block without symptoms and hemodynamic disturbances is assessed in the clinical context and does not always require emergency management.
In the presence of a pseudoinfarct pattern (ST elevation, pathological Q wave), true coronary occlusion must be ruled out—clinically and, if necessary, via coronary angiography, since the management of true STEMI (primary PCI) is fundamentally different. Misdiagnosing myocarditis as a myocardial infarction is more hazardous than performing an unwarranted coronary angiography; therefore, when acute coronary occlusion is clinically suspected, activation of the STEMI pathway must not be delayed.
The diagnosis of myocarditis is established based on a combination of findings: clinical presentation, myocardial injury biomarkers, echocardiography, contrast-enhanced cardiac MRI, and myocardial biopsy when indicated. Serial ECGs help monitor the progression or resolution of the process.
Common interpretation errors
- Automatically interpreting any diffuse ST elevation as "non-STEMI" without considering the clinical picture: when acute coronary occlusion is clinically suspected, the decision regarding urgent coronary angiography is made by the ACS team taking into account symptoms, dynamics, and biomarkers, rather than the ST morphology alone
- Disregarding a normal ECG as "ruling out" myocarditis—a normal ECG is not uncommon in myocarditis
- Missing occult AV block or QT prolongation due to a narrow focus on ST-T changes
- Dismissing non-specific ST-T changes in a young patient with an acute viral infection as "normal" without follow-up monitoring
- Confusing myopericarditis/perimyocarditis with isolated pericarditis without considering elevated cardiac biomarkers
1. Which finding is frequently encountered in acute myocarditis, although it is non-specific?
Myocarditis has no specific ECG sign; sinus tachycardia is one of the most frequent yet non-specific findings.
2. How should diffuse ST-segment elevation be properly evaluated when myocarditis/myopericarditis is suspected?
The shape and distribution of ST in myocarditis merely orient the diagnosis; acute coronary occlusion must be ruled out based on clinical presentation, ECG dynamics, troponin, and coronary angiography when indicated.
3. Which conduction disorder is particularly characteristic of myocarditis associated with Lyme disease or giant cell myocarditis?
Inflammatory involvement of the AV node and conduction system in Lyme disease and giant cell myocarditis typically manifests as progressive AV block, up to complete AV block.
Frequently asked questions
Can the ECG be normal in myocarditis?
Yes, a normal ECG does not rule out myocarditis, especially in mild to moderate cases. The diagnosis is confirmed clinically, via laboratory tests, and imaging methods (echocardiography, cardiac MRI), rather than by ECG alone.
How to differentiate myocarditis from myocardial infarction on the ECG?
The distribution of ST changes can help: in MI, ST elevation and reciprocal changes usually fit a single coronary territory, whereas in myocarditis, changes are more often diffuse. However, this is not an absolute criterion—it does not rule out either condition. Definitive differentiation is aided by the clinical picture, serial ECGs, troponin dynamics, echocardiography/MRI, and urgent coronary angiography when indicated.
Is myocarditis dangerous in terms of arrhythmias?
Yes, inflamed myocardium is electrically unstable and can produce ventricular premature beats, ventricular tachycardia, and even ventricular fibrillation, while involvement of the conduction system can lead to complete AV block; therefore, cardiac monitoring is required.
What finding is most commonly encountered in acute myocarditis?
Sinus tachycardia combined with non-specific ST-segment and T-wave changes is most commonly observed. This is a frequent but non-specific finding—there is no ECG sign specific solely to myocarditis.
Is coronary angiography necessary in pseudo-infarction patterns secondary to myocarditis?
If the clinical picture and ECG do not reliably differentiate myocarditis from true myocardial infarction, coronary angiography is performed to rule out coronary occlusion, since the management strategy for true STEMI is fundamentally different. Myocarditis should not be diagnosed based on a single ST pattern.
ECG Course
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Related terms
More in the «Channelopathies and Cardiomyopathies» section
Sources
- Hampton J. The ECG in Practice
- Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice
- Orlov V.N. Guide to Electrocardiography
- Russian Ministry of Health Clinical Guidelines for Myocarditis
Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.