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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Myocarditis = inflammation of the myocardium — most commonly viral (Coxsackie B, parvovirus B19, adenovirus, SARS-CoV-2)
- Suspect in a young person with recent viral illness + chest pain + troponin rise + normal coronary arteries
- Cardiac MRI is the gold standard non-invasive investigation (Lake Louise criteria: oedema + necrosis/scar on late gadolinium)
- Management is supportive: heart failure therapy if LVEF reduced, avoid exercise for 3–6 months, treat arrhythmias
- Most viral myocarditis resolves; ~20–30% progress to dilated cardiomyopathy
Overview
Myocarditis is an inflammatory disease of the myocardium that may present with chest pain mimicking ACS, new-onset heart failure, or life-threatening arrhythmias. Viral infection is the most common cause in the UK (Coxsackie B, parvovirus B19, adenovirus, EBV, CMV, HIV, SARS-CoV-2). Non-viral causes include autoimmune conditions (SLE, sarcoidosis, giant cell myocarditis), drugs (checkpoint inhibitors, doxorubicin), and hypersensitivity reactions. Definitive diagnosis historically required endomyocardial biopsy (Dallas criteria), but cardiac MRI has largely supplanted this in clinical practice.
Epidemiology
True incidence is difficult to establish due to subclinical cases, but estimated at 1–10 per 100,000 per year. It predominantly affects young, otherwise healthy adults (20–40 years). It is an important cause of sudden cardiac death in young athletes. Male predominance (2:1). Most cases of acute viral myocarditis are self-limiting with full recovery. However, approximately 20–30% develop chronic dilated cardiomyopathy. Giant cell myocarditis and eosinophilic myocarditis carry a much worse prognosis.
Clinical Features
Symptoms
Chest pain (may mimic ACS — sharp or dull, often pleuritic if pericardial involvement)
Recent viral prodrome (1–4 weeks prior): fever, myalgia, sore throat, diarrhoea
Dyspnoea and exercise intolerance (heart failure)
Palpitations (arrhythmias)
Syncope or presyncope
Sudden cardiac death (rare presentation, especially in young athletes)
Signs
Tachycardia (out of proportion to fever)
Soft S1, S3 gallop (LV dysfunction)
Signs of heart failure (raised JVP, bibasal crackles, oedema) if LVEF reduced
Pericardial friction rub (if myopericarditis)
Arrhythmias on monitoring
Investigations
First-line
High-sensitivity troponinElevated in acute myocarditis — may mimic NSTEMI. Serial troponins show rise and fall
ECGNon-specific ST/T-wave changes, sinus tachycardia, widespread ST elevation (if pericarditis component), new conduction abnormalities, arrhythmias (VT, complete heart block)
TTEMay show regional or global wall motion abnormalities, reduced LVEF, pericardial effusion
BloodsCRP/ESR elevated, FBC, U&Es, BNP/NT-proBNP (if HF), viral serology
Second-line
Cardiac MRI (gold standard)Lake Louise criteria: T2-weighted oedema (acute inflammation) + late gadolinium enhancement (necrosis/fibrosis, typically mid-wall or epicardial — NOT subendocardial which suggests MI)
Coronary angiographyTo exclude CAD in patients presenting like ACS with troponin rise — typically shows normal coronaries in myocarditis
Specialist
Endomyocardial biopsyDefinitive diagnosis (Dallas criteria) — reserved for suspected giant cell myocarditis, fulminant myocarditis not responding to treatment, or unexplained new-onset HF with haemodynamic compromise
1
Supportive care
- Bed rest and activity restriction — avoid exercise for 3–6 months (risk of arrhythmia and sudden death)
- Cardiopulmonary monitoring, especially in acute phase
- Treat heart failure with standard therapy if LVEF reduced: ACEi, beta-blocker (cautiously), diuretics
- Treat arrhythmias as per standard protocols
2
Fulminant myocarditis
- ICU admission with inotropic support
- Mechanical circulatory support (IABP, ECMO, VAD) if cardiogenic shock
- Consider urgent endomyocardial biopsy to exclude giant cell myocarditis
3
Specific causes
- Giant cell myocarditis: immunosuppression (corticosteroids + ciclosporin)
- Autoimmune myocarditis: corticosteroids + steroid-sparing agents
- Checkpoint inhibitor myocarditis: stop immunotherapy, high-dose corticosteroids
- Viral myocarditis: no specific antiviral therapy for most causes; supportive
4
Follow-up
- Repeat echo at 1–3 months to assess LV recovery
- Cardiac MRI to assess residual inflammation and fibrosis
- If persistent LV dysfunction → manage as dilated cardiomyopathy
- Return to sport: only after complete resolution of symptoms, normal echo/MRI, and no arrhythmias (minimum 3–6 months)
Complications
- Dilated cardiomyopathy: 20–30% develop chronic DCM after viral myocarditis
- Arrhythmias: VT/VF (risk of sudden death), heart block
- Cardiogenic shock: Fulminant myocarditis — requires mechanical support
- Thromboembolism: Mural thrombus formation in dilated, hypokinetic ventricles
- Recurrence: Can recur, especially autoimmune causes
UKMLA Exam Tips
- 1Young patient + recent viral illness + troponin rise + normal coronary arteries = think myocarditis
- 2Cardiac MRI is the key diagnostic test — late gadolinium enhancement in a mid-wall or epicardial pattern (NOT subendocardial, which is MI)
- 3Absolute exercise restriction for 3–6 months — risk of sudden death in athletes with myocarditis
- 4Fulminant myocarditis has a paradoxically BETTER long-term prognosis than acute myocarditis (if the patient survives the acute phase)
- 5Giant cell myocarditis = rapidly progressive, high mortality → requires immunosuppression and often transplant
practicetest your knowledge on myocarditisApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — cardiovascular and beyond.
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