Myocarditis
Overview
Inflammatory condition of the myocardium - most common in young adult males; a key reversible cause of dilated cardiomyopathy and accounts for up to 12% of sudden cardiac deaths in young adults.
Aetiology
•Most common cause: viral infection - classic culprit is coxsackievirus B (enterovirus)
•Other viral causes: parvovirus B19, HIV, EBV, CMV, adenovirus
•Non-infectious: autoimmune, drugs (e.g. clozapine, immune checkpoint inhibitors), sarcoidosis, giant cell myocarditis
•Lyme carditis (Borrelia burgdorferi) - important cause of complete heart block
Presentation
•Prodrome - URTI or gastroenteritis 1-2 weeks prior is a critical contextual clue
•Chest pain - sharp, pleuritic (worse with inspiration/lying flat); reflects concurrent pericardial involvement
•Dyspnoea - due to impaired LV systolic function and elevated filling pressures
•Palpitations/syncope - ventricular ectopy or VT; risk of sudden cardiac death
•Fatigue and fever - systemic inflammation
•Signs of heart failure - tachycardia, raised JVP, S3 gallop, pulmonary crackles, oedema in severe cases
•Fulminant myocarditis - cardiogenic shock (hypotension, cool peripheries, oliguria)
Investigations
🥇 First-line
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•ECG - sinus tachycardia, diffuse ST elevation, PR depression, T-wave changes, ventricular ectopy/VT; new LBBB or heart block is a red flag for severity
•Troponin (hs-cTnI/hs-cTnT) - elevated due to myocyte injury; rise-and-fall pattern
•CRP/ESR - elevated; BNP/NT-proBNP - elevated proportionally to LV dysfunction
•Echocardiogram - LV/RV function, wall motion abnormalities, pericardial effusion
•Coronary angiography or CT coronary angiogram - essential to exclude ACS, particularly in patients >35 years or with risk factors
🏆 Gold standard
•Cardiac MRI (CMR) with gadolinium - T2-weighted sequences show myocardial oedema; late gadolinium enhancement (LGE) in non-ischaemic pattern (mid-wall or epicardial); Lake Louise criteria applied
🥈 Second-line
•Endomyocardial biopsy (EMB) - reserved for haemodynamically unstable patients, suspected giant cell or eosinophilic/autoimmune myocarditis where histology will guide immunosuppression
Management
•Activity restriction - mandatory; competitive sport must be avoided for at least 3-6 months pending reassessment
•Heart failure therapy - ACE inhibitor + beta-blocker for LV dysfunction
•Arrhythmia management - antiarrhythmics or electrical cardioversion as needed; temporary pacing for complete heart block (e.g. Lyme carditis)
•Fulminant myocarditis - mechanical circulatory support (IABP, VA-ECMO) as bridge to recovery or transplant
•Giant cell / eosinophilic myocarditis - immunosuppression directed by endomyocardial biopsy histology
Complications
•Dilated cardiomyopathy - most important long-term complication; ~10-20% of cases; myocyte loss and fibrosis
•Sudden cardiac death - ventricular arrhythmias (VT/VF) during acute phase; major cause of SCD in young athletes
•Complete heart block - particularly Lyme carditis and giant cell myocarditis
•Cardiogenic shock - fulminant myocarditis
•Intracardiac thrombus and systemic embolisation - from severely impaired LV function
Prognosis
•Most lymphocytic (viral) myocarditis with haemodynamic stability resolves completely within weeks to months
•Fulminant myocarditis - paradoxically better long-term prognosis than non-fulminant disease if the patient survives the acute phase
•Giant cell myocarditis - worst prognosis; median survival <6 months without cardiac transplantation
•Persistent LGE on CMR after recovery - associated with increased risk of VT, heart failure, and SCD
•Lyme carditis and eosinophilic myocarditis (drug withdrawn) - excellent prognosis with appropriate treatment