01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Myocarditis is inflammatory injury of the myocardium. Its clinical range extends from self-limited chest pain with a troponin rise to biventricular failure, malignant arrhythmia and fulminant shock. The working diagnosis should describe the presentation and risk rather than assume a pathogen from a preceding illness.
The early task is parallel rather than sequential: support circulation and rhythm, exclude acute coronary and other time-critical diagnoses, document ventricular function, then obtain tissue characterisation. CMR and biopsy answer different questions and neither should delay life-saving care.
Most uncomplicated cases receive supportive care and treatment of ventricular dysfunction or arrhythmia. Immunosuppression and antimicrobial therapy are reserved for defined or strongly suspected subtypes in which the cause changes outcome. Persistent scar, dysfunction or arrhythmia determines the intensity of longer-term surveillance.
Key points
- Myocarditis may look like acute coronary syndrome, decompensated heart failure, an arrhythmia or an unexplained conduction disorder; a recent viral illness is neither required nor diagnostic.
- Use ECG, continuous rhythm observation when risk is significant, serial troponin, inflammatory markers, natriuretic peptide and transthoracic echo to establish injury and severity, not to assign a viral cause.
- Do not label a troponin-positive chest-pain presentation as myocarditis until acute coronary occlusion has been assessed according to the patient's age, risk, ECG, instability and clinical probability.
- CMR is the preferred non-invasive tissue test in a stable patient and should assess oedema, non-ischaemic injury, ventricular function, pericardial involvement and scar burden.
- Endomyocardial biopsy is most useful when haemodynamic or electrical risk is high, the diagnosis remains uncertain, or histology and myocardial pathogen testing would change urgent treatment.
- Shock, sustained VT or VF and advanced AV block require conventional resuscitation, pacing and advanced-heart-failure pathways alongside myocarditis investigation; consider temporary mechanical support early when shock is refractory.
- Routine empirical immunosuppression or antiviral treatment is not appropriate for uncomplicated presumed viral myocarditis. Treat giant-cell, eosinophilic, sarcoid, immune-checkpoint-inhibitor and proven infectious disease through a subtype-specific specialist pathway.
- Avoid vigorous exercise while inflammation or myocardial injury remains active. Return only after symptoms, biomarkers, ventricular function and clinically relevant rhythm risk have been reassessed.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Infection-associated inflammation
Viral and other infections may directly injure myocardium or trigger a damaging immune response. A preceding viral illness can support the history but neither proves nor excludes myocarditis.
Immune-mediated disease
Systemic inflammatory disease or myocarditis subtypes such as giant-cell, eosinophilic or sarcoid inflammation can target myocardium. Recognising the subtype matters because specialist treatment differs.
Medicines and cancer immunotherapy
Drug hypersensitivity can produce eosinophilic myocardial inflammation, while immune-checkpoint inhibitors may activate severe cardiac autoimmunity. Temporal exposure, rash, eosinophilia or conduction disease raises suspicion.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Myocardial injury begins
An infectious, toxic or immune trigger injures cardiomyocytes and activates innate and adaptive immune pathways locally within the myocardial interstitium.
- 2Oedema and cell death
Inflammatory cells and cytokines produce tissue oedema and myocyte necrosis. Troponin enters the circulation, while cardiac magnetic resonance may show non-ischaemic oedema and injury.
- 3Pump function deteriorates
Diffuse or focal inflammation impairs contraction and relaxation. Ventricular filling pressure rises and cardiac output may fall, producing heart failure or fulminant cardiogenic shock.
- 4Electrical instability develops
Patchy inflammation alters conduction and creates regions of slow or blocked activation. Ventricular arrhythmias, frequent ectopy, bundle-branch block or advanced atrioventricular block can result.
- 5Healing or chronic remodelling
Inflammation may resolve with functional recovery, but persistent injury can leave fibrosis, ventricular dilatation and scar. These changes sustain chronic heart failure and later arrhythmic risk.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Acute chest pain, ST-T change and troponin elevation may be indistinguishable from acute coronary syndrome at first contact. Pleuritic pain or a recent infection can support the history but cannot safely exclude coronary occlusion.
New exertional breathlessness, orthopnoea, oedema, raised JVP, gallop rhythm or ventricular dysfunction after an inflammatory illness suggests myocardial involvement. Hypotension, cool peripheries, oliguria, rising lactate or organ injury signals shock.
Palpitations, syncope, sustained ventricular tachycardia, ventricular fibrillation, frequent ventricular ectopy, new bundle-branch block or advanced AV block may be the dominant feature even when ventricular systolic function is preserved.
A patient receiving or recently exposed to immune-checkpoint inhibitor treatment who develops a troponin rise, weakness, arrhythmia, conduction disease or ventricular dysfunction needs urgent cardio-oncology assessment because deterioration can be rapid.
A new medicine, rash, fever, eosinophilia, systemic allergic features or an eosinophilic disorder raises suspicion but a normal peripheral eosinophil count does not exclude myocardial eosinophilic disease.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Immediate observations, ECG and rhythm monitoringFirst step - Why
- Identify ischaemia, ventricular arrhythmia, AV block and haemodynamic instability and establish whether a monitored setting is required.
- Interpretation and limitations
- ECG abnormalities are common but non-specific. Sustained ventricular arrhythmia, advanced AV block or worsening perfusion overrides a reassuring initial ventricular ejection fraction.
- 02
Serial blood tests - Why
- Use troponin to document myocardial injury; add CRP or ESR, FBC, U&E and eGFR, LFT, glucose, natriuretic peptide and lactate according to severity.
- Interpretation and limitations
- A normal troponin does not exclude every form of myocarditis, and an elevated troponin does not establish its cause. Trends help assess injury but must be read with symptoms, ECG and imaging.
- 03
Transthoracic echocardiography - Why
- Assess left- and right-ventricular function, regional or global wall-motion abnormality, filling, intracardiac thrombus, valve disease and pericardial effusion.
- Interpretation and limitations
- Regional abnormality does not by itself distinguish myocarditis from ischaemia. New severe dysfunction, right-ventricular failure or haemodynamic compromise increases urgency.
- 04
Coronary imaging - Why
- Exclude an acute coronary cause using invasive angiography or CT coronary angiography according to presentation, pre-test probability and stability.
- Interpretation and limitations
- A young age, viral prodrome or non-obstructive first test must not be used as a shortcut when the ECG or clinical course still suggests coronary occlusion, dissection, embolism or spasm.
- 05
Cardiac magnetic resonance - Why
- Characterise oedema and non-ischaemic myocardial injury, quantify biventricular function, map late enhancement and identify associated pericardial inflammation.
- Interpretation and limitations
- A compatible CMR supports a non-invasive diagnosis in a stable patient. Timing, prior treatment and focal disease affect sensitivity; a non-diagnostic study does not overrule a high-risk clinical picture.
- 06
Endomyocardial biopsy - Why
- Obtain histology, immunohistochemistry and targeted myocardial pathogen testing when a specific diagnosis will alter immunosuppression, antimicrobial treatment, device strategy or transplant planning.
- Interpretation and limitations
- Use an experienced centre, especially in shock, serious arrhythmia or conduction disease, suspected giant-cell or eosinophilic disease, or an immune-checkpoint-inhibitor presentation. Sampling error means a negative specimen must be interpreted in context.
- 07
Cause-directed testing - Why
- Use exposure-led tests for HIV, hepatitis, Lyme disease, autoimmune disease, eosinophilic disease, toxins or other infections and review medicines and cancer immunotherapy.
- Interpretation and limitations
- Routine broad viral serology does not identify myocardial infection and should not be used to select antiviral or immunosuppressive treatment.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Acute coronary syndrome
Coronary occlusion can produce identical chest pain, ECG change and troponin release. Coronary probability, territorial changes and angiographic findings should be assessed before assuming inflammatory injury.
Acute pericarditis
Pericarditis favours pleuritic positional pain, a rub and widespread ST or PR changes. Troponin evidence of myocardial injury or new ventricular dysfunction suggests concomitant myocardial involvement.
Takotsubo syndrome
Takotsubo often follows intense physical or emotional stress and produces a characteristic wall-motion pattern beyond one coronary territory. Cardiac magnetic resonance often shows oedema with little or no late enhancement rather than a typical myocarditis pattern, although findings can overlap.
Pulmonary embolism
Pulmonary embolism may cause chest pain, dyspnoea, troponin elevation and tachycardia. Disproportionate hypoxaemia, venous thromboembolic risk and right-ventricular strain point towards embolism.
Systemic illness-related myocardial injury
Sepsis, severe anaemia, hypoxia or sustained tachyarrhythmia may cause type 2 myocardial infarction when supply-demand imbalance produces acute ischaemia, or non-ischaemic myocardial injury when ischaemic evidence is absent. The systemic trigger and imaging pattern help discriminate.
Additional chapter-specific clues
Acute coronary syndrome, Takotsubo syndrome, pulmonary embolism, sepsis-related injury, tachycardia-mediated dysfunction, toxic injury and pericarditis can produce overlapping symptoms, ECG changes, troponin elevation or imaging findings.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01First contactRecognise risk and exclude coronary diseaseFirst stepChest pain, troponin elevation, new ventricular dysfunction, arrhythmia or conduction disease with suspected myocardial inflammation.+
- 1Perform ABCDE assessment, 12-lead ECG, serial observations and troponin, targeted bloods and urgent TTE; use telemetry when syncope, conduction disease, ventricular arrhythmia or significant dysfunction is present.
- 2Activate the acute coronary syndrome pathway when coronary occlusion remains plausible. Select invasive or CT coronary assessment from the patient's risk and stability rather than from the presence of a viral history.
- 3Classify the patient as uncomplicated, heart-failure predominant, arrhythmic, or fulminant/shock presentation and arrange care in a setting able to respond to that risk.
- 4Use CMR promptly in a stable patient once immediate coronary and other life-threatening alternatives have been addressed.
02High riskShock, malignant arrhythmia or advanced blockCardiogenic shock, cardiac arrest, sustained VT or VF, advanced AV block, rapidly progressive heart failure or severe new ventricular dysfunction.+
- 1Involve critical care, electrophysiology and a tertiary myocarditis, mechanical-support and transplant-capable service immediately; monitor rhythm, perfusion, lactate, urine output and organ function.
- 2Treat cardiac arrest and unstable tachyarrhythmia under current Resuscitation Council UK guidance and provide temporary pacing when clinically required for unstable advanced block.
- 3Use haemodynamic assessment to guide vasoactive support and discuss temporary mechanical circulatory support before irreversible organ injury when shock does not respond to initial treatment.
- 4Obtain urgent endomyocardial biopsy when the result can direct immediate subtype therapy. Do not postpone stabilisation, coronary exclusion or support while waiting for CMR or pathology.
03Cause specificTreat an actionable myocarditis subtypeBiopsy, microbiology or a high-confidence multidisciplinary diagnosis identifies a treatment-responsive cause.+
- 1Giant-cell myocarditis: start urgent combined immunosuppression through a tertiary service and plan early for temporary support and transplant assessment because electrical and haemodynamic deterioration may be rapid.
- 2Eosinophilic or hypersensitivity myocarditis: stop a suspected culprit when safe, assess for infection and systemic eosinophilic disease, and use specialist corticosteroid-based treatment when the diagnostic evidence supports it.
- 3Cardiac sarcoidosis or other systemic immune-mediated disease: coordinate cardiology and the relevant specialty for immunosuppression, ventricular-function treatment, rhythm surveillance and device-risk assessment.
- 4EscalationImmune-checkpoint-inhibitor myocarditis: withhold immunotherapy, admit for close rhythm and haemodynamic monitoring, and begin urgent guideline-directed corticosteroid treatment through cardio-oncology; escalate promptly if response is inadequate.
- 5Proven treatable infection: use pathogen-directed antimicrobial therapy with infection specialists. Do not infer myocardial viral replication from blood antibodies and do not prescribe empirical antiviral treatment for routine presumed viral disease.
04RecoveryProtect the ventricle and plan return to activityThe patient is haemodynamically stable and acute injury is resolving.+
- 1Treat persistent LV systolic dysfunction according to the dedicated NICE-aligned HFrEF chapter once haemodynamically stable; manage congestion, thromboembolism and clinically significant arrhythmia according to their own indications.
- 2Avoid vigorous exercise and competitive sport while symptoms, biomarkers, ventricular dysfunction, active imaging abnormalities or significant arrhythmia persist; give written safety-net advice for syncope, palpitations, chest pain or worsening breathlessness.
- 3Reassess symptoms, examination, ECG, troponin when clinically indicated, ventricular function and rhythm burden. Use repeat CMR when it will document resolution or scar and change return-to-activity or risk decisions.
- 4Make return to exercise individual and graded after clinical remission. Persistent ventricular dysfunction, complex ventricular arrhythmia or substantial residual scar requires specialist long-term follow-up rather than automatic discharge.
Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
Disease-modifying HFrEF treatment after myocarditis
There is no myocarditis-specific class dose. Once shock has resolved and the patient is haemodynamically stable, select and titrate each indicated medicine using NICE NG106, the current product SmPC and the dedicated HFrEF chapter.Do not initiate or up-titrate long-term vasodilating or rate-limiting treatment during active shock. Check blood pressure, rhythm, volume state, renal function, potassium, contraindications and pregnancy status for each selected medicine.
Immunosuppression for defined immune-mediated myocarditis
No single empirical adult regimen is safe. The tertiary team should use the subtype-specific 2025 ESC protocol, pathology and infection assessment, patient weight and organ function to prescribe and document the exact regimen.Do not extrapolate to uncomplicated presumed viral myocarditis. Screen for relevant infection, coordinate specialty care and monitor glucose, blood pressure, FBC, renal and liver function, infection, gastrointestinal and bone risk, and treatment response.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Acute heart failure and shock
Extensive inflammatory injury can sharply reduce biventricular function. Pulmonary congestion, impaired organ perfusion and refractory cardiogenic shock may require critical care and temporary mechanical support.
Malignant ventricular arrhythmia
Inflamed and electrically heterogeneous myocardium can trigger sustained ventricular tachycardia or fibrillation. Dangerous electrical disease may occur even when ventricular ejection fraction is near normal.
Advanced conduction block
Inflammation involving the conduction system can cause new bundle-branch or atrioventricular block. Severe block may produce syncope, haemodynamic compromise and a need for temporary pacing.
Chronic dilated cardiomyopathy
Incomplete recovery can leave scar, ventricular dilatation and persistent systolic dysfunction. The patient may develop chronic heart failure, recurrent arrhythmia and ongoing exercise restriction.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Use continuous ECG monitoring during high-risk acute disease and repeat a 12-lead ECG after clinically important rhythm or conduction change.
- Trend perfusion, lactate, renal and liver function, urine output and ventricular function in shock; reassess early for mechanical-support or transplant escalation when deterioration continues.
- Repeat troponin and inflammatory markers only when the trend will change acute risk assessment, treatment or return-to-activity planning; biomarkers are not a substitute for clinical review.
- Repeat TTE after a change in clinical state and during recovery to document left- and right-ventricular function and any effusion or thrombus.
- Use ambulatory ECG and, when recovery permits, supervised exercise assessment to evaluate symptoms and rhythm before higher-intensity activity in patients with an arrhythmic presentation or residual scar.
- Consider repeat CMR during follow-up when persistent symptoms, ventricular dysfunction, arrhythmia or an activity decision makes the extent of ongoing inflammation or scar clinically relevant.
- Give a named follow-up plan before discharge. Ongoing dysfunction, complex arrhythmia, recurrent injury or significant scar warrants specialist surveillance.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Troponin names injury, not cause
The same biomarker pattern can occur with coronary occlusion, myocarditis, pulmonary embolism, tachyarrhythmia and critical illness; the diagnostic pathway must remain open until urgent alternatives are addressed.
CMR and biopsy are complementary
CMR maps tissue and ventricular phenotype non-invasively; biopsy can identify a treatment-changing cell pattern or myocardial pathogen. Clinical risk determines which answer is needed and how quickly.
Electrical severity can exceed pump severity
Sustained ventricular arrhythmia or high-grade block may signal dangerous myocarditis even with a near-normal ejection fraction.
Blood viral serology is not myocardial virology
Prior exposure antibodies do not establish that a virus is present in myocardium and cannot safely justify antiviral treatment or decide whether immunosuppression is appropriate.
Recovery is multidimensional
Normal symptoms alone are insufficient for unrestricted activity; ECG, injury markers, ventricular function, rhythm burden and residual scar each contribute to the decision.
11Common pitfallsFrequent interpretation and management errors.
- 01
Diagnosing myocarditis from a viral prodrome and troponin rise without appropriately excluding acute coronary syndrome.
- 02
Waiting for CMR in a patient whose shock, sustained arrhythmia or advanced AV block already requires stabilisation and tertiary escalation.
- 03
Using routine viral serology to claim a myocardial pathogen or choose antiviral treatment.
- 04
Starting empirical immunosuppression for uncomplicated presumed viral myocarditis without a subtype-specific rationale and infection assessment.
- 05
Reassuring a patient because ventricular ejection fraction is preserved despite syncope, sustained ventricular arrhythmia or advanced conduction disease.
- 06
Allowing return to vigorous exercise on symptom resolution alone without reassessing myocardial injury, function and rhythm risk.