Myocarditis — Med2Date

🎧 Myocarditis — deep-dive podcast

📋 Key Information Summary

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Myocarditis is inflammation of the myocardium diagnosed by clinical presentation, cardiac MRI (Lake Louise 2018 criteria), and endomyocardial biopsy (gold standard); incidence in Australia is estimated at 4–14 per 100,000 persons annually, though the true burden is likely higher due to subclinical cases.
Presentations range from subclinical chest pain to fulminant cardiogenic shock requiring mechanical circulatory support (MCS); any patient presenting with troponin elevation, new ECG changes, and cardiac symptoms without ischaemic cause should be evaluated for myocarditis.
Viral aetiologies (Coxsackievirus B, adenovirus, parvovirus B19, HHV-6) remain the leading cause; COVID-19 infection and, rarely, mRNA COVID-19 vaccines (particularly in adolescent and young adult males) have emerged as important triggers since 2020.
Cardiovascular magnetic resonance (CMR) is the cornerstone non-invasive diagnostic tool, applying the updated 2018 Lake Louise Criteria (T1/T2 mapping, late gadolinium enhancement, and oedema ratio).
Endomyocardial biopsy (EMB) is indicated for fulminant presentations, suspected giant-cell or eosinophilic myocarditis, or when diagnosis remains uncertain after CMR — referral to a specialist centre with EMB capability is essential.
Management is predominantly supportive: ACE inhibitors (perindopril, ramipril), beta-blockers (carvedilol, metoprolol), and diuretics for heart failure; avoid NSAIDs in the acute phase.
Immunosuppression (corticosteroids, azathioprine, ciclosporin) is indicated only for biopsy-proven immune-mediated subtypes (giant-cell, eosinophilic, cardiac sarcoidosis) and should NOT be used empirically for viral myocarditis.
Fulminant myocarditis with refractory cardiogenic shock requires urgent escalation: intra-aortic balloon pump (IABP), extracorporeal membrane oxygenation (ECMO), or ventricular assist devices (VAD) — early retrieval to a transplant-capable centre (e.g., Alfred Hospital Melbourne, St Vincent's Sydney, Prince Charles Brisbane).
Exercise restriction: no competitive sport for a minimum of 3–6 months; return to activity only after normalisation of LV function, biomarkers, and absence of arrhythmias on ambulatory monitoring, guided by 2020 ESC sports cardiology criteria.
Long-term follow-up is essential: repeat CMR at 6 and 12 months, echocardiography every 3–6 months during recovery, Holter monitoring for arrhythmia surveillance, and screening for progression to dilated cardiomyopathy.
Aboriginal and Torres Strait Islander peoples have higher rates of rheumatic heart disease and may present with overlapping inflammatory myocarditis; culturally safe care, geographic access to specialist services, and early retrieval from remote communities are critical equity considerations.
Pregnant women with acute myocarditis should be managed in a tertiary centre with obstetric and cardiac ICU capability; early multidisciplinary team (MDT) involvement is essential for delivery planning if haemodynamic deterioration occurs.

Introduction & Australian Epidemiology

Myocarditis is defined as inflammation of the myocardium, most commonly triggered by infectious agents, immune-mediated processes, or cardiotoxic substances. The disease spectrum extends from subclinical, self-limiting inflammation to fulminant cardiogenic shock and sudden cardiac death. Histologically, myocarditis is characterised by inflammatory cell infiltrate with or without associated myocyte necrosis, as established by the Dallas criteria and refined by subsequent immunohistochemical and molecular classification systems.

In Australia, myocarditis accounts for an estimated 4–14 cases per 100,000 persons per year, though autopsy and CMR studies suggest the true incidence may be considerably higher. Myocarditis is responsible for approximately 5–12% of sudden cardiac death in young adults and up to 9% of unexplained dilated cardiomyopathy presentations nationally. The Cardiac Society of Australia and New Zealand (CSANZ) recognises myocarditis as a significant and under-recognised cause of cardiac morbidity, particularly in younger populations.

Since the onset of the COVID-19 pandemic, Australian data from the National Centre for Immunisation Research and Surveillance (NCIRS) have documented increased myocarditis incidence associated with both SARS-CoV-2 infection and, at lower rates, mRNA COVID-19 vaccination (particularly BNT162b2 [Comirnaty®] in males aged 12–30 years). The Australian Therapeutic Goods Administration (TGA) continues to monitor these events through active surveillance.

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Epidemiological note: Myocarditis is likely underdiagnosed in Australia due to reliance on clinical suspicion and the limited availability of CMR in regional and remote areas. Clinicians should maintain a low threshold for investigation in young patients presenting with chest pain, troponin elevation, and non-ischaemic ECG changes.

The median age at presentation is 30–40 years, with a male-to-female ratio of approximately 1.5–2:1. Males are disproportionately affected in both viral and immune-mediated forms. In paediatric populations, myocarditis presents at a median age of 5–7 years, with viral aetiology predominating.

Myocarditis clinical infographic — pathophysiology, clinical clues, diagnosis, imaging, and management — Tap or click image to enlarge — Myocarditis: pathophysiology, clinical clues, diagnosis, imaging, and management.

Clinical Presentation & Diagnosis

Myocarditis presents across a broad clinical spectrum. Accurate diagnosis requires integration of clinical features, biomarkers, ECG, echocardiography, and increasingly cardiovascular magnetic resonance (CMR). The diagnostic approach varies depending on whether the presentation is acute, chronic, or fulminant.

Clinical Spectrum: Acute, Chronic, and Fulminant Myocarditis

Mild

Acute Subclinical / Mild Myocarditis

Chest pain (pleuritic or atypical), mild troponin elevation, normal or mildly reduced LVEF (>50%), non-specific ECG changes (ST-T wave changes, T-wave inversions). Often preceded by a viral prodrome (fever, myalgia, malaise) 1–4 weeks prior.

Setting: Ward / cardiology outpatient

Moderate

Acute Symptomatic Myocarditis

Significant chest pain (may mimic ACS), dyspnoea, palpitations, sustained tachycardia, elevated troponin (often >5× upper limit of normal), BNP/NT-proBNP elevated, LVEF 30–50%, regional wall motion abnormalities, pericardial effusion present in up to 30%.

Setting: Cardiac monitoring ward / CCU

Severe

Fulminant Myocarditis

Rapid-onset cardiogenic shock (within days of symptom onset), severe biventricular failure, LVEF <30%, high-degree AV block, ventricular arrhythmias, multi-organ dysfunction. Histopathology typically shows giant-cell, eosinophilic, or lymphocytic myocarditis with extensive necrosis. High mortality without MCS (~50–70%).

Setting: ICU / transplant-capable centre with MCS

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Fulminant myocarditis is a medical emergency. Patients presenting with acute heart failure, haemodynamic instability, and suspected myocarditis require immediate escalation to a centre capable of mechanical circulatory support (ECMO, VAD) and potential cardiac transplantation. Early retrieval should not be delayed.

Diagnostic Approach

The initial evaluation of suspected myocarditis should include a systematic assessment combining clinical history, laboratory investigations, electrocardiography, and imaging. No single test is pathognomonic; diagnosis relies on the convergence of multiple findings.

Essential Investigations

Essential High-sensitivity Troponin I or T Elevated in >90% of acute myocarditis. Serial measurements at 0, 3, and 6 hours. Elevated beyond the expected rise/fall pattern for ACS supports myocarditis. MBS item 66504.

Essential 12-lead ECG Abnormal in up to 90% of cases: ST elevation (diffuse, concave-up, not following a single coronary territory), T-wave inversions, PR depression, low voltage QRS, QTc prolongation, new bundle branch block. Sinus tachycardia most common rhythm. High-degree AV block suggests giant-cell or cardiac sarcoidosis.

Essential BNP / NT-proBNP Elevated in myocarditis with associated ventricular dysfunction; useful for prognostication and monitoring treatment response. MBS item 66836.

Essential Transthoracic Echocardiography (TTE) Assess LVEF, regional wall motion abnormalities (RWMA — often non-coronary distribution), pericardial effusion, LV wall thickness (oedema may cause transient hypertrophy), and exclude differential diagnoses (valvular disease, aortic dissection). MBS item 55114.

Available Cardiovascular Magnetic Resonance (CMR) The gold-standard non-invasive investigation. Apply the 2018 Lake Louise Criteria (sensitivity 87%, specificity 91% when T1/T2 mapping is included). See criteria table below. Available at major tertiary centres (Royal Melbourne, Royal Prince Alfred, Princess Alexandra, Fiona Stanley).

Specialist Endomyocardial Biopsy (EMB) Histological gold standard. Dallas criteria: lymphocytic infiltrate ≥14 cells/mm² with myocyte necrosis. Immunohistochemistry (CD3, CD68) and PCR for viral genome (Enterovirus, Parvovirus B19, HHV-6, CMV, EBV) improve diagnostic yield. Available at select centres only. See indications below.

Available Viral Serology and PCR Panel Coxsackievirus B IgM/IgG, Parvovirus B19 IgM/PCR, HIV, Hepatitis B/C, CMV, EBV, SARS-CoV-2 PCR/serology. Blood PCR is lower yield than EMB tissue PCR but useful when biopsy is not performed.

Available Autoimmune / Inflammatory Markers ESR, CRP, complement (C3, C4), ANA, ANCA, anti-myosin antibodies, serum tryptase (eosinophilic myocarditis), ACE level (cardiac sarcoidosis). Consider when immune-mediated aetiology is suspected.

2018 Lake Louise CMR Diagnostic Criteria

The updated Lake Louise Criteria require at least ONE T2-based criterion AND at least ONE T1-based criterion (or one from each category) for a CMR-based diagnosis of myocarditis. Native T1 mapping, T2 mapping, and extracellular volume fraction (ECV) significantly improve sensitivity compared to the original 2009 criteria.

Criterion Category	Parameter	Technique	Suggested Threshold
T2-based (Oedema)	Regional or global myocardial oedema	T2-weighted STIR / T2 mapping	T2 ratio >1.9 (STIR); Native T2 >52 ms (1.5T) or >54 ms (3T)
T2-based (Oedema)	Elevated T2 signal	T2 mapping	≥2 SD above normal mean
T1-based (Injury/Fibrosis)	Regional or global myocardial injury	Native T1 mapping	Native T1 >1010 ms (1.5T) or >1080 ms (3T); ≥2 SD above normal mean
	Elevated extracellular volume	ECV quantification	ECV >27%
	Late gadolinium enhancement (LGE)	Post-gadolinium IR-GRE	Non-ischaemic pattern (epicardial/mid-wall, non-coronary territory)

CMR diagnosis is positive when: ≥1 T2-based criterion AND ≥1 T1-based criterion are met. A CMR study is considered negative for acute myocarditis if neither T2 oedema nor T1-based criteria are present.

Indications for Endomyocardial Biopsy

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EMB is recommended by CSANZ, AHA, and ESC in the following circumstances:

Fulminant heart failure with haemodynamic instability (suspected giant-cell or eosinophilic myocarditis where specific therapy would change management)
Heart failure with progressive LV dysfunction refractory to standard therapy for ≥2 weeks
Suspected cardiac sarcoidosis or eosinophilic myocarditis where CMR is non-diagnostic
New-onset heart failure of <2 weeks' duration with LV dilation and new ventricular arrhythmias or high-degree AV block
Heart failure associated with cutaneous drug rash, peripheral eosinophilia, or suspected immune checkpoint inhibitor toxicity

Differential Diagnosis

The following conditions should be systematically excluded before confirming a diagnosis of myocarditis:

Acute coronary syndrome (ACS): Coronary angiography should be performed if clinical features suggest ischaemic aetiology, particularly in patients >40 years or with cardiovascular risk factors.
Acute pericarditis: Distinguished by predominant pleuritic chest pain, pericardial rub, diffuse ST elevation with PR depression, and normal troponin/pericardial effusion without ventricular dysfunction.
Stress cardiomyopathy (Takotsubo): Apical ballooning pattern on echocardiography/CMR, often triggered by emotional or physical stress, typically reversible within weeks.
Pulmonary embolism: Acute right heart strain, D-dimer elevation, CT pulmonary angiogram diagnostic.
Acute decompensated cardiomyopathy: Pre-existing dilated cardiomyopathy with new decompensation — CMR features of chronicity (fibrosis pattern) aid differentiation.

Etiology

Myocarditis aetiology is diverse and often multifactorial. Identifying the underlying cause is essential because treatment strategies differ significantly between viral, immune-mediated, and drug-induced forms. In approximately 30–50% of cases, a specific aetiology cannot be identified despite comprehensive evaluation.

Viral Causes

Viral infection remains the most common identifiable cause of myocarditis in Australia. The pathogenesis involves direct viral cytopathic effects during the acute phase (days to weeks) followed by an immune-mediated inflammatory response (weeks to months). Molecular diagnosis via EMB tissue PCR has improved viral identification.

Virus	Prevalence in Viral Myocarditis	Key Clinical Features	Australian Relevance
Parvovirus B19	Most common (30–50% of viral cases by PCR)	Endothelial tropism; may cause microvascular dysfunction; often detected in EMB but causality debated	Endemic; common childhood infection
Coxsackievirus B (Enterovirus)	15–25%	Classic viral myocarditis; direct myocyte lysis; linked to dilated cardiomyopathy progression	Summer/autumn seasonality; paediatric predominance
Human Herpesvirus 6 (HHV-6)	10–20%	Latent reactivation; often co-detected with Parvovirus B19; significance debated	Common latent infection; reactivation in immunocompromised
Adenovirus	5–10%	Paediatric predominance; often with concurrent respiratory illness	Common cause of paediatric viral myocarditis
SARS-CoV-2	Emerging (see below)	Direct myocardial invasion via ACE2 receptors; cytokine-mediated injury; up to 20–30% of hospitalised COVID-19 patients show myocardial injury biomarkers	Significant pandemic burden; ongoing surveillance
Influenza A/B	5–10%	Seasonal; may present with concurrent pneumonia and myocarditis	Annual influenza season (April–October); vaccination recommended
CMV, EBV, HIV	Individual: 2–5% each	Consider in immunocompromised patients; HIV-related cardiomyopathy has improved with ART	HIV: higher prevalence in priority populations

Immune-Mediated Myocarditis

Immune-mediated myocarditis involves aberrant immune activation against cardiac tissue without active viral replication. These subtypes often require targeted immunosuppression and carry distinct prognoses. Diagnosis typically requires EMB with immunohistochemistry.

Subtype	Histopathology	Clinical Features	Prognosis / Key Points
Giant-Cell Myocarditis (GCM)	Multinucleated giant cells + eosinophils + myocardial necrosis	Fulminant presentation in 75%; rapidly progressive HF, ventricular arrhythmias, high-degree AV block; often affects young–middle-aged adults	Poor prognosis without treatment (median transplant-free survival ~5.5 months); aggressive immunosuppression + early transplant listing essential
Eosinophilic Myocarditis	Eosinophilic infiltrate + myocyte necrosis; degranulation pattern	Associated with hypereosinophilic syndrome, drug reactions (antibiotics, anticonvulsants), parasitic infections, eosinophilic granulomatosis with polyangiitis (EGPA)	Treat underlying cause; corticosteroids first-line; mepolizumab for EGPA-related cases
Cardiac Sarcoidosis	Non-caseating granulomas with lymphocytic infiltrate	Conduction abnormalities, ventricular arrhythmias, HF; may present with syncope; 5–10% of systemic sarcoidosis patients have cardiac involvement	CMR (LGE in basal inferolateral wall) + PET (FDG uptake) for diagnosis; corticosteroids + steroid-sparing agents
Autoimmune Myocarditis	Lymphocytic infiltrate; no viral genome on PCR	Associated with SLE, rheumatoid arthritis, systemic sclerosis, inflammatory bowel disease; cardiac involvement may be the presenting feature	Treat underlying autoimmune disease; corticosteroids + disease-modifying agents

Drug-Induced Myocarditis

Drug-induced myocarditis is an increasingly recognised entity. The most important categories in Australian clinical practice include:

Immune checkpoint inhibitors (ICIs): Nivolumab, pembrolizumab, ipilimumab — ICI-related myocarditis occurs in 0.3–1.5% of treated patients, with mortality rates of 25–50%. Onset typically within 6 weeks of commencing therapy. Presentation is often fulminant with concurrent myositis and myasthenia gravis overlap. Key emerging cause
Antimicrobials: Clofazimine, penicillins, cephalosporins, sulfonamides (eosinophilic pattern), dapsone.
Antipsychotics: Clozapine (1–2% risk; requires baseline and serial troponin monitoring per TGA guidance), chlorpromazine.
Recreational substances: Methamphetamine (increasingly prevalent in Australia), cocaine, synthetic cannabinoids.
Other: Interferon-alpha, lithium (rare), TNF-alpha inhibitors (paradoxical).

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Clozapine monitoring: Per TGA requirements in Australia, patients on clozapine must have troponin measured at baseline, at 4 weeks, and at 12 weeks after initiation, then annually. Any new cardiac symptoms or troponin elevation should prompt urgent cardiology review.

COVID-19 and Vaccine-Related Myocarditis

Since 2020, SARS-CoV-2 infection and mRNA COVID-19 vaccination have emerged as important considerations in the differential diagnosis of myocarditis.

COVID-19 Infection-Associated Myocarditis

Mechanism: direct viral invasion via myocardial ACE2 receptors, cytokine storm, microvascular thrombosis, and autoimmune cross-reactivity
Incidence: myocardial injury (troponin elevation) in 20–30% of hospitalised COVID-19 patients; clinical myocarditis diagnosed in approximately 2–5%
Higher risk in older patients, those with pre-existing CVD, and severe COVID-19 pneumonia
CMR studies in post-COVID patients (including athletes) demonstrate myocardial oedema/fibrosis in 30–60% even after mild infection

mRNA COVID-19 Vaccine-Related Myocarditis

Predominantly affects males aged 12–30 years; highest risk after dose 2 of BNT162b2 (Comirnaty®) or mRNA-1273 (Spikevax®)
Onset typically 1–7 days post-vaccination (median 2–3 days)
Australian TGA data: ~30 cases per 100,000 doses in males 12–17 years; ~15 per 100,000 in males 18–29 years
Typically mild (LVEF >50% in >90%) with excellent prognosis; resolution of symptoms in 1–7 days; recovery of LV function in >95% at 3–6 months
ACIP/ATAGI recommendation: benefit–risk favours vaccination; consider extended dosing interval (8 weeks) for those at higher risk of myocarditis

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Clinical guidance (CSANZ/TGA): Patients with confirmed vaccine-related myocarditis should avoid further doses of the same mRNA vaccine platform. Alternative vaccines (Novavax, protein subunit) may be considered after cardiology consultation. Routine cardiac follow-up (echocardiography at 3–6 months) is recommended for all cases.

Management Strategies

Management of myocarditis depends on the clinical severity, aetiology (viral vs immune-mediated), and haemodynamic status. The majority of patients with acute lymphocytic myocarditis are managed supportively, while specific subtypes (giant-cell, eosinophilic, sarcoidosis) require targeted immunosuppression or immunomodulation.

Supportive Care (First-Line for All Patients)

Haemodynamic Support

IV diuretics (frusemide 20–80 mg IV) for congestion; vasopressors (noradrenaline) for hypotension; inotropes (dobutamine, milrinone) for cardiogenic shock. Fluid restriction (1.5 L/day) in decompensated heart failure.

Guideline-Directed Heart Failure Therapy

ACE inhibitor or ARB, beta-blocker (once haemodynamically stable), and mineralocorticoid receptor antagonist (MRA) for those with LVEF <40%. Initiate at low doses and titrate cautiously. ARNI (sacubitril/valsartan) may be considered after stabilisation.

Avoid Harmful Agents

NSAIDs should be avoided in the acute phase (increased risk of myocardial injury and fluid retention). Alcohol cessation is mandatory. Exercise restriction during the acute phase.

Anticoagulation

Systemic anticoagulation (heparin bridge to warfarin or DOAC) if LVEF <30%, intracardiac thrombus, or atrial fibrillation. Not routine in all myocarditis patients.

Arrhythmia Management

Amiodarone for sustained VT (avoid in pregnancy); temporary pacing for high-degree AV block; avoid class IC antiarrhythmics in structural heart disease. ICD implantation deferred until recovery phase (≥3–6 months) unless recurrent VT/VF despite medical therapy.

Pharmacotherapy — Heart Failure Management

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Perindopril

Coversyl® · ACE inhibitor

Adult dose 2 mg PO daily, titrate to 5–10 mg daily (maximum 10 mg/day)

Paediatric dose 0.07 mg/kg PO daily (max 0.1 mg/kg/day for children >6 years)

Renal adjustment Start 2 mg every other day if eGFR <30 mL/min; titrate with monitoring

PBS status ✔ PBS General Benefit

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Carvedilol

Dilatrend® · Non-selective β/α₁ blocker

Adult dose 3.125 mg PO BD, titrate every 2 weeks to target 25 mg BD (≤85 kg) or 50 mg BD (>85 kg)

Paediatric dose 0.05 mg/kg PO BD, titrate to 0.4 mg/kg BD (max 12.5 mg BD)

Renal adjustment No specific adjustment; monitor closely in severe renal impairment

PBS status ✔ PBS General Benefit

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Spironolactone

Aldactone® · Mineralocorticoid receptor antagonist

Adult dose 12.5–25 mg PO daily, titrate to 25–50 mg daily

Paediatric dose 1 mg/kg PO daily (max 25 mg/day)

Renal adjustment Contraindicated if eGFR <30 mL/min or K⁺ >5.0 mmol/L

PBS status ✔ PBS General Benefit

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Frusemide (Furosemide)

Lasix® · Loop diuretic

Adult dose 20–80 mg IV/PO daily or BD; continuous infusion 5–20 mg/hr in severe HF

Paediatric dose 1–2 mg/kg IV/PO every 6–12 hours (max 6 mg/kg/day)

Renal adjustment Higher doses required in renal impairment (eGFR <30); consider bumetanide if diuretic resistance

PBS status ✔ PBS General Benefit

Immunosuppression — Indications and Regimens

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Critical safety principle: Immunosuppression is CONTRAINDICATED in active viral myocarditis (PCR-positive for virus on EMB). Immunosuppression in viral myocarditis may worsen outcomes by impairing viral clearance. Immunosuppression is indicated ONLY for biopsy-proven immune-mediated subtypes: giant-cell myocarditis, eosinophilic myocarditis, cardiac sarcoidosis, and autoimmune myocarditis (PCR-negative for viral genome).

Myocarditis Subtype	First-Line Immunosuppression	Second-Line / Steroid-Sparing	Duration
Giant-Cell Myocarditis	Methylprednisolone 1 g IV daily × 3 days → Prednisolone 1 mg/kg/day PO (max 60 mg) taper over 6 months	Ciclosporin 3–5 mg/kg/day (trough 150–300 ng/mL) OR azathioprine 2 mg/kg/day + anti-thymocyte globulin (ATG) for refractory cases	Lifelong immunosuppression required; early transplant evaluation
Eosinophilic Myocarditis	Methylprednisolone 500–1000 mg IV daily × 3 days → Prednisolone 1 mg/kg/day taper over 2–3 months	Mepolizumab 300 mg SC every 4 weeks (for EGPA); azathioprine; ciclosporin	6–12 months minimum; lifelong if underlying eosinophilic disorder
Cardiac Sarcoidosis	Prednisolone 0.5–1 mg/kg/day (max 40 mg) for 4–8 weeks, then taper to 5–10 mg/day over 6–12 months	Methotrexate 10–20 mg/week, azathioprine 2 mg/kg/day, mycophenolate 1–1.5 g BD; consider infliximab for refractory disease	Minimum 12–24 months; often lifelong steroid-sparing therapy
ICI-Related Myocarditis	Stop ICI immediately; Methylprednisolone 1–2 g IV daily × 3–5 days → Prednisolone 1–2 mg/kg/day taper over 4–6 weeks	Abatacept (for fulminant cases), mycophenolate, infliximab, anti-thymocyte globulin	Corticosteroids for minimum 4–6 weeks; may require longer taper

Immunomodulation — Adjunctive Therapies

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Intravenous Immunoglobulin (IVIG)

Intragam® P / Flebogamma® · Immunomodulator

Adult dose 0.4 g/kg/day IV for 5 days (total 2 g/kg) or 1 g/kg/day for 2 days

Paediatric dose 1–2 g/kg IV over 2–5 days

Indication Paediatric myocarditis (evidence base limited); autoimmune myocarditis; giant-cell myocarditis adjunct; ICI-related myocarditis refractory to steroids

Renal adjustment Use low osmolality formulation; monitor renal function; rate-related renal impairment risk

PBS status ⚠ PBS Authority Required

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Colchicine

Colgout® / Colcrys® · Anti-inflammatory

Adult dose 0.5 mg PO BD for 1–3 days, then 0.5 mg daily for 3 months (for perimyocarditis)

Paediatric dose Not routinely recommended in children <12 years

Renal adjustment 0.5 mg daily if eGFR 10–30 mL/min; contraindicated if eGFR <10 mL/min

PBS status ✔ PBS General Benefit

Mechanical Circulatory Support (MCS)

Fulminant myocarditis with refractory cardiogenic shock may require mechanical circulatory support as a bridge to recovery or to transplantation. Early recognition and transfer to a transplant-capable centre are critical. Australian ECMO-capable centres include The Alfred (Melbourne), Royal Prince Alfred (Sydney), St Vincent's (Sydney), Prince Charles Hospital (Brisbane), Fiona Stanley Hospital (Perth), and Royal Adelaide Hospital.

MCS Modality	Indication	Key Features	Australian Availability
IABP (Intra-Aortic Balloon Pump)	Cardiogenic shock with adequate but depressed LV function	Provides counterpulsation; improves coronary perfusion; limited in severe biventricular failure; reduces afterload	Widely available at tertiary centres
VA-ECMO (Veno-arterial ECMO)	Refractory cardiogenic shock; biventricular failure; cardiac arrest	Full circulatory and respiratory support; femoral or central cannulation; complications include limb ischaemia, bleeding, thromboembolism	Major cardiac transplant centres; retrieval services via state ambulance ECMO programs
Impella® / pVAD	Isolated LV failure; bridge to decision	Percutaneous axial flow pump; provides up to 5.5 L/min LV unloading; limited availability in Australia	Select centres only
Ventricular Assist Device (VAD)	Prolonged cardiogenic shock; bridge to transplant	Durable LVAD or BiVAD; requires sternotomy; complications include device thrombosis, stroke, infection, bleeding	Cardiac transplant centres (Alfred, St Vincent's, Prince Charles)

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Fulminant myocarditis prognosis: Paradoxically, fulminant myocarditis has better long-term survival than acute non-fulminant myocarditis in patients who survive the acute phase with MCS support. In-hospital mortality is approximately 40–50%, but among survivors, ventricular recovery occurs in the majority (70–90%) and long-term prognosis is favourable. This is a key distinction from other forms of acute heart failure.

Myocarditis visual summary infographic — 🖼️ Myocarditis — visual summary

Long-term Follow-up

Myocarditis requires structured long-term follow-up to detect incomplete recovery, progression to dilated cardiomyopathy, arrhythmic complications, and relapse. The duration and intensity of surveillance depend on the initial severity, aetiology, and LV function trajectory.

Recovery Monitoring Timeline

2–4 weeks

Repeat echocardiography to assess LVEF trajectory; repeat troponin and BNP/NT-proBNP; clinical review for persistent symptoms; medication optimisation and uptitration of heart failure therapy.

3 months

Repeat echocardiography; 24-hour Holter monitor for arrhythmia surveillance; consider repeat CMR if LVEF not normalising or if initial diagnosis was uncertain; review exercise restriction status with cardiologist.

6 months

Repeat CMR to assess for residual oedema, fibrosis (LGE), and LV function; if LVEF has normalised and no LGE, consider graduated return to activity (not competitive sport yet); repeat Holter; continue heart failure therapy for minimum 12 months.

12 months

Comprehensive review: CMR, echocardiography, Holter, cardiopulmonary exercise testing (CPET) if considering return to sport. If fully recovered (LVEF ≥55%, no LGE, no arrhythmias on Holter, normal CPET), consider discontinuation of heart failure therapy under specialist guidance. If persistent LV dysfunction, continue guideline-directed medical therapy indefinitely and consider ICD evaluation.

Annually thereafter

Annual cardiology review with echocardiography and clinical assessment for at least 5 years; earlier review if new symptoms develop. Patients with persistent LVEF <50% require lifelong cardiology follow-up.

Exercise Restriction

Exercise restriction is a critical component of myocarditis management. Myocardial inflammation renders the myocardium electrically unstable and susceptible to catecholamine-mediated arrhythmias. The 2020 ESC Guidelines on Sports Cardiology and Exercise in Patients with Cardiovascular Disease provide the framework for return-to-activity decisions.

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Exercise restriction periods (per ESC 2020 / CSANZ):

Acute phase (first 3–6 months): Complete avoidance of all competitive sport and moderate-to-vigorous recreational exercise. Light daily activities (walking) are permissible once haemodynamically stable.
3–6 months: Re-assessment with CMR, echocardiography, Holter, and biomarkers. If LVEF has normalised, no arrhythmias, no LGE, and biomarkers are normal, graduated return to recreational exercise may begin under cardiologist guidance.
Return to competitive sport: Requires normalisation of ALL parameters: LVEF ≥55%, no residual oedema on CMR, no significant LGE, no ventricular arrhythmias on 24–48 hour Holter, normal BNP, and satisfactory CPET. This typically occurs at 6–12 months in recovered patients.
Persistent LV dysfunction: No competitive sport indefinitely; recreational exercise per heart failure guidelines (moderate-intensity aerobic, avoid isometric heavy lifting).

Arrhythmia Surveillance

Ventricular arrhythmias are a significant cause of morbidity and mortality in myocarditis survivors. Arrhythmia surveillance is essential throughout the recovery period and beyond.

24–48 hour Holter monitoring: At 3, 6, and 12 months post-diagnosis; annually thereafter for 5 years if LGE is present on CMR.
Implantable loop recorder (ILR): Consider for patients with recurrent unexplained syncope, non-sustained VT on Holter, or suspected arrhythmia with negative standard monitoring.
Electrophysiology study (EPS): May be considered for risk stratification in patients with LGE on CMR and non-sustained VT; positive programmed ventricular stimulation predicts future sustained arrhythmic events.
ICD implantation: Indicated for survivors of cardiac arrest, sustained VT despite medical therapy, or LVEF ≤35% persisting beyond 3–6 months (per AHA/ACC/HRS 2017 guidelines). Primary prevention ICD in patients with LVEF 30–35% and LGE on CMR remains an individualised decision.

Chronic Sequelae

Myocarditis may lead to several long-term complications that require ongoing surveillance:

Dilated cardiomyopathy (DCM): 20–30% of biopsy-proven myocarditis progresses to DCM over 5–10 years; ongoing guideline-directed heart failure therapy is essential; genetic testing should be considered as 30–50% of DCM has a genetic basis.
Restrictive cardiomyopathy: Rare; more common in eosinophilic myocarditis (Löffler endocarditis) and cardiac amyloidosis (important differential).
Recurrent myocarditis: Relapse rate approximately 10–15% for lymphocytic myocarditis; higher for giant-cell myocarditis (>50% without maintenance immunosuppression).
Chronic pericarditis: Perimyocarditis may evolve into chronic relapsing pericarditis; colchicine prophylaxis may be beneficial.
Stroke and thromboembolism: In patients with severe LV dysfunction (LVEF <30%) or atrial fibrillation; anticoagulation considerations per current guidelines.
Psychological impact: Anxiety, depression, and reduced quality of life are common after myocarditis; screening with PHQ-9 and GAD-7 is recommended; referral to cardiac rehabilitation programs improves outcomes.

Special Populations

🤰 Pregnancy

Peripartum cardiomyopathy overlap Myocarditis diagnosed in pregnancy or the first 5 postpartum months may overlap with peripartum cardiomyopathy (PPCM); EMB may show lymphocytic infiltrate. Differentiation affects prognosis and treatment.

Medication safety ACE inhibitors/ARBs are CONTRAINDICATED in pregnancy (teratogenic — fetopathy). Use hydralazine + nitrates for afterload reduction. Beta-blockers: metoprolol is preferred (Category C). Spironolactone: avoid (anti-androgenic). Frusemide: use cautiously.

Delivery planning LVEF <40% in pregnancy requires MDT (cardiology, obstetrics, anaesthesia, neonatology) at a tertiary centre. Vaginal delivery preferred with epidural and shortened second stage. Caesarean section for haemodynamic instability or obstetric indications.

Breastfeeding Enalapril and metoprolol are compatible with breastfeeding. Corticosteroids at doses ≤20 mg/day prednisolone are considered safe during breastfeeding.

🧒 Paediatrics

Age-specific presentation Neonates: fulminant course with 50–70% in-hospital mortality if presenting with cardiogenic shock. Children: more commonly presents as acute HF rather than chest pain. Adolescents: viral myocarditis is most common; consider COVID-19 vaccine-related myocarditis in males 12–17 years.

IVIG use Commonly used empirically in paediatric myocarditis in Australia despite limited RCT evidence; 1–2 g/kg over 2–5 days. May improve outcomes in immune-mediated paediatric myocarditis.

MCS in children ECMO is the primary MCS modality in children; VAD (Berlin Heart EXCOR) for prolonged support. Referral to specialised paediatric cardiac centres (Royal Children's Melbourne, Children's Hospital Westmead, Queensland Children's Hospital).

Exercise restriction No competitive sport for minimum 6 months (per AHA/ACC paediatric guidelines). Return requires normalisation of LVEF, biomarkers, and Holter monitoring.

👴 Elderly (≥65 years)

Diagnostic challenge Presentation often mimics ACS or decompensated HF in the context of pre-existing cardiac disease. Maintain high index of suspicion for myocarditis superimposed on ischaemic or valvular heart disease.

Medication caution Start ACE inhibitors and beta-blockers at lower doses; increased risk of hypotension, renal impairment, and hyperkalaemia. More conservative diuretic dosing. Avoid NSAIDs absolutely.

Cardiac sarcoidosis Bimodal age distribution with second peak in patients 50–60+ years. Consider in elderly with unexplained AV block and LV dysfunction.

🫘 Renal Impairment

CMR considerations Gadolinium-based contrast agents: risk of nephrogenic systemic fibrosis (NSF) if eGFR <30 mL/min. Use macrocyclic agents only (gadoterate, gadobutrol) if CMR essential. EMB can proceed without gadolinium.

Drug adjustments ACE inhibitors: start low, monitor potassium and creatinine at 1–2 weeks. Spironolactone: contraindicated if eGFR <30 or K⁺ >5.0. Colchicine: halve dose if eGFR 10–30; contraindicated if eGFR <10. IVIG: use low osmolality preparation; rate-limit to reduce renal risk.

🫁 Hepatic Impairment

Drug metabolism Prednisolone: risk of fluid retention and hepatotoxicity in cirrhosis; use lowest effective dose. Ciclosporin: hepatically metabolised; requires drug-level monitoring with dose adjustment. Amiodarone: avoid in severe hepatic impairment (hepatotoxicity risk).

Biomarker interpretation BNP clearance is hepatically dependent; NT-proBNP may be more reliable. Troponin may be elevated in acute liver injury (hepatocyte release).

🛡️ Immunocompromised

Expanded differential Consider CMV, EBV, adenovirus, toxoplasmosis, aspergillosis, and mycobacterial infection as aetiologies. HIV-related cardiomyopathy remains relevant despite ART.

ICI-related myocarditis Patients on immune checkpoint inhibitors represent a specific immunocompromised-adjacent population with iatrogenic immune dysregulation. See etiology and management sections for ICI-specific protocols.

Transplant patients Cardiac allograft rejection can mimic myocarditis; endomyocardial biopsy is standard surveillance in the post-transplant setting. Acute cellular rejection (ISHLT grade ≥2R) requires augmented immunosuppression.

Aboriginal and Torres Strait Islander Health Considerations

Rheumatic Heart Disease Overlap

Aboriginal and Torres Strait Islander peoples have significantly higher rates of acute rheumatic fever (ARF) and rheumatic heart disease (RHD), which can coexist with or mimic myocarditis. ARF-related carditis involves valvulitis and myocarditis; the overlap between RHD and viral myocarditis may lead to diagnostic confusion in remote communities. ARF/RHD registers exist in NT, QLD, and WA to facilitate case management.

Geographic Access to CMR and EMB

CMR is available only at major tertiary centres (Adelaide, Darwin — limited, Perth, Brisbane). Patients in remote NT, WA, QLD, and SA communities face significant logistical barriers to accessing CMR and EMB. Point-of-care echocardiography by trained remote area nurses and fly-in-fly-out (FIFO) cardiologists is the primary diagnostic modality in many communities. Retrieval to tertiary centres should be initiated early for suspected fulminant myocarditis.

Higher Burden of Comorbidity

Aboriginal and Torres Strait Islander peoples have higher prevalence of cardiovascular risk factors (diabetes, hypertension, chronic kidney disease, smoking), rheumatic heart disease, and lower average age of cardiovascular disease onset. Myocarditis occurring in the context of pre-existing cardiac disease may present later and with worse prognosis.

Cultural Safety and Communication

Culturally safe care requires acknowledgment of the social determinants of health, use of interpreters when English is not the first language, family-inclusive consultation models, and culturally appropriate health education materials. Aboriginal Health Workers (AHWs) and Aboriginal Community Controlled Health Organisations (ACCHOs) play a vital role in follow-up and medication adherence. Yarning-based approaches to explaining heart inflammation and the need for rest and medication are recommended.

Medication Access and PBS Co-payment

Aboriginal and Torres Strait Islander peoples with a Concession Card or living in remote areas are eligible for PBS Close the Gap (CTG) programs, providing medicines at reduced or no co-payment cost. This is critical for ensuring access to long-term heart failure medications (ACE inhibitors, beta-blockers) in remote communities. Pharmacy support through Remote Area Aboriginal Health Services is essential.

Exercise and Community Life

Exercise restriction advice must be culturally contextualised. Many Aboriginal and Torres Strait Islander communities have strong engagement in community sport and physical activities integral to social wellbeing. Clear, culturally appropriate communication about activity restrictions and graduated return to activity is essential, with involvement of family and community in supporting the patient during recovery.

📊 Myocarditis — slide deck

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📚 References

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