Myocarditis is inflammation of the myocardium — caused by viral infection (most common), immune-mediated conditions, toxins or drugs. Clinical presentation varies widely: subclinical (incidentally elevated troponin); acute chest pain mimicking ACS (young adults — myocarditis is a common young-adult cause of elevated troponin); heart failure (mild to fulminant cardiogenic shock); arrhythmias; sudden cardiac death. Most viral myocarditis is self-limiting and recovers completely — but GCM, ICI myocarditis and eosinophilic NEM carry very high mortality.

How is myocarditis diagnosed?

Clinical presentation (chest pain, dyspnoea, palpitations — often 1-2 weeks after viral illness); biochemical (elevated troponin + inflammatory markers); ECG (diffuse ST elevation without culprit artery distribution; PR depression; T-wave changes; conduction disease); echocardiography (LV dysfunction, wall motion, pericardial effusion); CMR: the gold standard — detects oedema (T2 mapping/STIR), inflammation and necrosis/fibrosis (LGE); 2022 Updated Lake Louise Criteria. EMB: reserved for haemodynamically unstable, suspected GCM or ICI myocarditis, or CMR non-diagnostic.

Why must athletes stop exercising with myocarditis?

Exercise during active myocarditis increases the risk of ventricular arrhythmias and sudden cardiac death. Inflamed myocardium creates electrical heterogeneity (oedema and necrosis) — a substrate for re-entrant VT/VF. Exercise (increased catecholamines, HR, wall stress) destabilises these areas. Multiple published sudden cardiac death cases from myocarditis during athletic exertion. The 3-6 month restriction allows complete resolution of inflammation and electrical remodelling. Return requires LVEF ≥50%, no arrhythmias, and CMR clearance.

How does GMJ News cover myocarditis?

GMJ News covers CMR gold standard (2022 Lake Louise Criteria), exercise restriction (3-6 months Class I), viral causes (Coxsackievirus B, SARS-CoV-2, parvovirus B19), GCM (EMB mandatory, triple IS), mRNA vaccine myocarditis (rare, self-limiting, lower than COVID disease rate), ICI myocarditis (25-50% mortality, steroids + infliximab), Chagas cardiomyopathy, fulminant myocarditis (VA-ECMO), and return-to-sport criteria.

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Myocarditis

Q: Can COVID vaccines cause myocarditis?

mRNA vaccine-associated myocarditis occurs predominantly in young males (16-30) within 1-5 days of the 2nd mRNA dose. Estimated incidence ~1-4 per 100,000 doses in the highest-risk group. Clinical course: almost always mild and self-limiting with >95% complete CMR recovery at 3-6 months. Crucially: COVID-19 disease itself causes myocarditis at substantially higher rates than the vaccine — the risk-benefit balance strongly favours vaccination. The rare vaccine-associated cases are predominantly mild; COVID disease myocarditis can be severe.

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

Summary Statistics Glossary GMJ news FAQ Documents Organizations Research

Myocarditis — inflammation of the myocardium — ranges from subclinical (detected only on CMR after sport-related chest pain) to fulminant (haemodynamic collapse requiring mechanical circulatory support) and is caused most commonly by viral infections (previously Coxsackievirus B; now SARS-CoV-2, influenza, parvovirus B19, adenovirus), immune-mediated conditions (giant cell myocarditis — the most aggressive form; eosinophilic myocarditis; immune checkpoint inhibitor-induced) and vaccines (mRNA COVID-19 vaccines — predominantly in young males, self-limiting; estimated 1-4 cases per 100,000 doses, with full recovery in the vast majority) (WHO/ESC). Cardiac MRI (CMR) with gadolinium is the non-invasive gold standard — detecting myocardial oedema (T2 mapping), hyperaemia and capillary leak (early gadolinium enhancement) and myocardial necrosis/fibrosis (late gadolinium enhancement/LGE) — and all patients with confirmed or suspected myocarditis should be restricted from competitive and strenuous sport for 3-6 months until complete clinical, biochemical and imaging recovery.

Key messages

CMR — the non-invasive gold standard — 2022 Updated Lake Louise Criteria

Cardiac MRI (CMR) with gadolinium is the non-invasive gold standard for myocarditis. 2022 Updated Lake Louise Criteria: ≥1 myocardial injury marker (T2-weighted oedema or non-ischaemic LGE) + ≥1 myocardial inflammation marker (elevated T1 mapping, elevated ECV, pericardial effusion, wall motion abnormality). T1/T2 parametric mapping added in 2022 update — more sensitive than original EGE/STIR alone. CMR replaces EMB as first-line in most cases.

Exercise restriction — 3-6 months — Class I recommendation

ALL patients with confirmed or suspected myocarditis: avoid competitive sport and strenuous exercise for a minimum of 3-6 months. Exercise during the inflammatory phase → electrical heterogeneity → ventricular arrhythmia and sudden cardiac death risk. Class I recommendation in both ESC 2022 and AHA guidelines. Return to sport requires ALL criteria met: symptoms resolved; troponin normalised; LVEF ≥50%; no significant arrhythmias on Holter; no significant LGE on CMR; normal ECG.

Viral — most common cause; SARS-CoV-2 now prominent

HICs: predominantly viral (historically Coxsackievirus B; now parvovirus B19 most common on biopsy in Europe; SARS-CoV-2; adenovirus; EBV; influenza). LMICs: Trypanosoma cruzi (Chagas disease — most common cause of non-ischaemic DCM in Latin America). Growing cause: immune checkpoint inhibitor myocarditis (pembrolizumab, nivolumab, ipilimumab — see below).

Giant cell myocarditis — the most aggressive form — EMB mandatory

Giant cell myocarditis (GCM): rare, rapidly progressive, fulminant. EMB diagnosis mandatory (histology: multinucleated giant cells + widespread myocyte necrosis). Young to middle-aged adults; rapid HF progression; high VT rate; high mortality without specific treatment. Treatment: high-dose corticosteroids + ciclosporin or tacrolimus + muromonab-CD3 (OKT3 — triple IS). ECMO/LVAD as bridge to recovery or transplantation. NEVER manage as presumed viral — if GCM suspected, proceed to EMB.

mRNA vaccine myocarditis — rare, self-limiting, lower rate than COVID disease

mRNA COVID-19 vaccine-associated myocarditis: predominantly young males (16-30 years); after 2nd mRNA dose (mRNA-1273/Moderna > BNT162b2/Pfizer). Estimated incidence: ~1-4 per 100,000 doses in highest-risk group. Clinical: chest pain 1-5 days post-vaccination; elevated troponin; mild-moderate LV dysfunction. Course: vast majority mild and self-limiting (>95% complete CMR recovery at 3-6 months). Crucially: COVID-19 disease itself causes myocarditis at substantially higher rates than the vaccine.

Immune checkpoint inhibitor myocarditis — up to 50% mortality

ICI myocarditis: increasingly prevalent as pembrolizumab, nivolumab, atezolizumab and ipilimumab become standard cancer therapy. Mechanism: T-cell disinhibition → autoreactive T-cell attack on myocardium. Incidence: ~0.5-1.5% on ICI; up to 27% with dual ICI. Mortality: 25-50% — far higher than viral myocarditis. Presentation: 1-3 months after ICI initiation; troponin ± ECG ± LV dysfunction ± cardiogenic shock. Treatment: stop ICI immediately; methylprednisolone 1g IV × 3-5 days; infliximab or abatacept for refractory.

Key statistics

CMR 2022

2022 Updated Lake Louise Criteria — non-invasive gold standard; T1/T2 mapping added

ESC 2022/JCMR

3-6 months

sport/exercise restriction for ALL confirmed/suspected myocarditis — Class I

ESC 2022/AHA

1-4/100K

mRNA vaccine myocarditis incidence in highest-risk group (young males after 2nd dose)

CDC/EMA

25-50%

ICI-associated myocarditis mortality — substantially higher than viral myocarditis

ESC/Oncology

COVID-19

disease causes myocarditis at substantially higher rates than the mRNA vaccine

CDC/ESC

GCM

giant cell myocarditis — EMB mandatory — triple IS therapy required — highest mortality

ESC/AHA

Myocarditis — causes by clinical setting and region (ESC 2022)

Source: ESC 2022. Viral dominant in HICs; Chagas disease in Latin America; ICI myocarditis rapidly increasing globally.

Glossary of key terms

2022 Updated Lake Louise Criteria
ESC/JCMR 2022CMR diagnosis of myocarditis requires: ≥1 myocardial injury marker: (a) Regional or global myocardial oedema on T2 mapping or T2-STIR; (b) Non-ischaemic (not subendocardial/transmural) LGE. AND ≥1 myocardial inflammation marker: (a) Elevated T1 mapping; (b) Elevated ECV (extracellular volume); (c) Pericardial effusion; (d) Wall motion abnormality. Supportive: EMB confirmation. The 2022 update adds T1/T2 parametric mapping — more sensitive than EGE/STIR criteria alone used in the original 2009 criteria.

Endomyocardial biopsy (EMB)
Cardiology/PathologyEMB indications (ESC 2022 Class I): haemodynamically unstable myocarditis; suspected GCM (must biopsy — treatment is specific); ICI myocarditis; new DCM with heart block or ventricular arrhythmias (sarcoidosis?); CMR contraindicated or non-diagnostic. Procedure: bioptome via femoral or jugular vein → RV free wall or IVS. Minimum 5 specimens, >50mg each. Risk: cardiac perforation <0.5% at experienced centres. Histological stains: H&E (inflammatory infiltrate); Masson trichrome (fibrosis); Prussian blue (iron — haemochromatosis); PAS (glycogen — storage diseases).

Fulminant myocarditis
Cardiology/Critical careFulminant myocarditis: rapid onset haemodynamic compromise (cardiogenic shock) requiring mechanical circulatory support. "Dickens paradox": most acutely ill but best long-term prognosis (among non-GCM/non-ICI forms). Mechanical support: IABP; Impella (LV assist); VA-ECMO (biventricular failure — most common support in fulminant myocarditis). Bridge to recovery (most recover fully) or bridge to transplant. ECMO allows myocardium to rest and recover from the inflammatory phase.

Chagas cardiomyopathy
Tropical/CardiologyT. cruzi (American trypanosomiasis): most common non-ischaemic DCM cause in Latin America (~6-7M infected; 30% develop cardiomyopathy). Acute phase: myocarditis + febrile illness (often unrecognised). Chronic phase (decades later): DCM + RBBB + left anterior hemiblock (classic ECG) + VT/VF risk + apical aneurysm + thromboembolism. Diagnosis: serology (ELISA). Treatment of cardiomyopathy: GDMT for HFrEF; ICD for VT/VF risk. Antiparasitic (benznidazole): effective in acute phase only. Global spread via immigration — clinicians worldwide must be aware.

ICI myocarditis
Oncology/CardiologyImmune checkpoint inhibitor myocarditis: rapidly growing cause — pembrolizumab, nivolumab (anti-PD-1); atezolizumab (anti-PD-L1); ipilimumab (anti-CTLA-4). Mechanism: T-cell disinhibition → autoreactive T-cells attack myocardial antigens (share antigens with tumour cells). Incidence: ~0.5-1.5% on ICI; up to 27% with dual ICI combination. Mortality: 25-50%. Clinical: troponin rise ± ECG ± LV dysfunction ± cardiogenic shock, 1-3 months post-initiation. Treatment: STOP ICI immediately; methylprednisolone 1g IV × 3-5 days; infliximab or abatacept for refractory (infliximab use in GCM may accelerate heart failure — use abatacept for GCM-histology ICI myocarditis). CMR + EMB to guide treatment.

Return-to-sport criteria
Cardiology/Sports medicineESC 2022 + AHA: minimum 3-6 months sport restriction from competitive/strenuous activity. Return criteria (ALL must be satisfied): clinical resolution (no chest pain, dyspnoea, palpitations); troponin normalised; LVEF ≥50% on echo or CMR; no significant arrhythmias (no VT/VF on 24-48h Holter or exercise test); no significant LGE on CMR (risk marker for future arrhythmias); normal ECG. CMR LGE persistence → further assessment required before high-intensity sport. Athletes: more stringent review — exercise testing + Holter + CMR.