Cardio · heart-failure
Myocarditis: presentation, biopsy criteria, management
Fellowship-level guide to myocarditis under the 2025 ESC myocarditis and pericarditis guideline, with the 2026 ESC heart failure, 2023 ESC cardiomyopathy and 2022 ESC ventricular arrhythmia guidelines, the 2024 ACC expert consensus decision pathway and AHA scientific statements: inflammatory myopericardial syndrome and stages, causes including immune checkpoint inhibitors and vaccines, the ESC 2025 diagnostic criteria, CMR with the updated Lake Louise criteria, endomyocardial biopsy indications, risk stratification, heart failure, arrhythmia and immunosuppression rows, return to sport and follow-up.
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Red flags
- ESC 2025 Table 7 high-risk myocarditis: acute HF/cardiogenic shock, dyspnoea NYHA III–IV refractory to medical therapy, cardiac arrest/syncope, ventricular fibrillation/sustained ventricular tachycardia, high-level AV block, newly reduced LVEF (<40%) or extensive LGE on CMR
- ESC 2025: EMB is recommended in high-risk myocarditis and/or haemodynamic instability, and/or in intermediate-risk myocarditis not responding to conventional therapy (Class I, Level C); Table 7 footnote a, printed on cardiac arrest/syncope, VF/sustained VT, high-level AV block, newly reduced LVEF (<40%) and extensive LGE, says these criteria do not lead directly towards EMB, which is then a case-by-case decision depending on the suspected underlying cause
- ESC 2025: in suspected ICI myocarditis, diagnostic triage within 24 h is recommended, and immediate disruption of ICI with high-dosage corticosteroids is recommended in ICI-associated myocarditis (both Class I, Level C)
- ESC 2025: in acute cardiac and systemic virus infection, immunosuppressive therapy must be avoided
- ESC 2025: patients with advanced AV block or sustained ventricular arrhythmia should be considered high risk even without LV dysfunction
This page follows a patient with suspected myocarditis from first contact to return to sport. It teaches the 2025 ESC criteria, how to stratify risk, and which formal rows govern heart failure, arrhythmia and immunosuppression.[1]
- Pericarditis-led presentations and colchicine: Acute pericarditis: diagnosis and colchicine.
- CMR sequences and LGE patterns in more depth: Cardiac MRI: LGE patterns and clinical questions.
- ICD and CRT rules in heart failure generally: ICD and CRT indications in heart failure.
The words you need: IMPS, stages and complicated myocarditis
Myocarditis and pericarditis are inflammatory diseases of the myocardium and pericardium, respectively, with potential overlap.[1] ESC 2025 is the first ESC guideline to cover myocarditis, and the first ESC guideline covering the whole spectrum of these diseases.[1] It groups the two under one starting label because they have similar aetiologies and are anatomically contiguous structures, with possible secondary involvement.[1]
IMPS is an entry label.[1] It should be used as an umbrella term during the initial diagnostic work-up until the final diagnosis is made.[1] For combined forms, the leading condition (myopericarditis or perimyocarditis) should guide therapy and follow-up.[1]
ESC 2025 Table 3: Terminology and stages
| Term | ESC 2025 definition |
|---|---|
| IMPS | Umbrella term for inflammatory myocardial and pericardial syndromes |
| Myopericarditis | Predominant pericarditis (footnote a) |
| Perimyocarditis | Predominant myocarditis (footnote b) |
| Acute myocarditis | Duration of symptoms ≤4 weeks; fulminant if acute onset and haemodynamically unstable patients requiring inotropes or mechanical circulatory support |
| Complicated myocarditis | Acute myocarditis and ≥1 of: LVEF <50% on echocardiogram; sustained ventricular arrhythmias; advanced heart block; heart failure; cardiogenic shock |
| Acute pericarditis | Duration of symptoms ≤4 weeks |
| Subacute/ongoing myocarditis | Duration of symptoms >4 weeks to ≤3 months |
| Subacute/incessant pericarditis (footnote c) | Duration of symptoms >4 weeks to ≤3 months |
| Chronic myocarditis/pericarditis | Duration of symptoms >3 months |
| Inflammatory cardiomyopathy | Chronic myocarditis in association with cardiac dysfunction and ventricular remodelling, with a clinical phenotype of hypokinetic, either dilated or non-dilated cardiomyopathy, with or without arrhythmogenic substrate |
| Recurrent myocarditis/pericarditis | New symptoms or disease activity after clinical remission |
| Remission without residuals | Regression/absence of symptoms, normalization of ECG, biomarkers, imaging abnormalities (echocardiography and CMR) |
| Remission with residuals | Regression/absence of symptoms, persistence of abnormalities on ECG, biomarkers and/or imaging (functional and/or structural abnormalities in echocardiography or CMR) |
- Footnote a (myopericarditis): definite criteria for pericarditis and elevated biomarkers of myocardial injury (high-sensitivity troponin I or T, CK-MB fraction) without newly developed regional or global impairment of left ventricular function in echocardiography or CMR.[1]
- Footnote b (perimyocarditis): the same, but with newly developed regional or global impairment of left ventricular function in echocardiography or CMR.[1]
- Footnote c (incessant pericarditis): persistent symptoms without a symptom-free interval of >4 weeks despite full-dose guideline-directed medical therapy (including corticosteroids), or relapse early during the tapering.[1]
The stages are not a fixed path.[1] ESC 2025 notes that a patient may recover completely without any residuals while others may develop complications, in some cases leading to death, and that complete remission can occur at every timepoint.[1] It is also not always possible to identify disease onset, for instance in subacute cases.[1]
[1]The ACC 2024 stages (consensus, no class)
The 2024 ACC expert consensus decision pathway (ECDP) proposes a different frame, applying the 4-stage model of heart failure to myocarditis.[5] It is an expert consensus document, and this page quotes it without any class of recommendation.[5]
ACC 2024 ECDP: proposed stages of myocarditis
| ACC 2024 stage | What it means in the ECDP |
|---|---|
| A (at-risk) | Risk factors listed in its Table 1, which include genetic variants, a personal or family history of myocarditis, cardiotoxins such as immune checkpoint inhibitors, doxorubicin, trastuzumab, clozapine, cocaine and methamphetamine, infectious agents and vaccines including smallpox and mRNA COVID-19 |
| B (asymptomatic) | Asymptomatic persons with CMR features of myocarditis or elevated hs-cTn, the latter in conjunction with additional supportive evidence |
| C (symptomatic myocarditis) | Symptomatic myocarditis without stage D features, with CMR findings meeting both T1 and T2 criteria, or an elevated troponin with supportive evidence, or an EMB consistent with myocarditis |
| D (advanced myocarditis) | Haemodynamic instability requiring inotropes/vasopressors or temporary circulatory support, or electrical instability requiring intervention, including high-grade AV block, frequent salvos of multifocal ventricular ectopy or non-sustained VT, VT or VF |
Unlike HFrEF staging, a patient with myocarditis can move from a higher to a lower stage in this scheme.[5] In the ECDP, for an asymptomatic person with elevated hs-cTn but no CMR, the level of supportive evidence depends on the clinical context, including which stage A risk factor is operative.[5] For example, if the person is receiving ICI therapy, an acute rise and markedly elevated troponin in the absence of coronary artery disease may suffice for the diagnosis.[5]
Who gets it
Population-based studies are limited, and hospital-based studies might underestimate the true disease burden.[1] In one example quoted by ESC 2025, the share of patients with angina-like symptoms and raised hs-TnT diagnosed with acute myocarditis rose from 5% to 13% once CMR was used.[1]
In children under 2 years the sex distribution is balanced; adolescents show a male predominance of about two-thirds, which persists in adults.[1] Myocarditis is probably more often drug-related in older patients, for example immune checkpoint inhibitors (ICIs) and clozapine (ESC 2025).[1]
Causes, as the guidelines list them
ESC 2025 divides the aetiology of IMPS into infectious and non-infectious causes, which can trigger disease in a genetically predisposed person through inflammatory or autoimmune mechanisms.[1]
- Viral (presumed most common infectious cause): enteroviruses, adenoviruses, parvovirus B19 (B19V), some herpesviruses (EBV, HHV-6), influenza and coronaviruses are the viruses most commonly associated with myocarditis.[1]
- Bacterial and parasitic: Borrelia species (Lyme carditis) and Trypanosoma cruzi (Chagas disease) are additional important aetiologies in specific regions of the globe.[1]
- Non-infectious: systemic diseases, autoimmune (or likely autoimmune) disorders (SLE, systemic sclerosis, rheumatoid arthritis, EGPA, hypereosinophilic syndrome), immune-mediated forms (lymphocytic, giant-cell and eosinophilic myocarditis, cardiac sarcoidosis), inflammatory bowel disorders, drugs and toxic reactions including ICI-associated myocarditis, chest radiation, and genetic conditions such as inherited cardiomyopathy.[1]
ESC 2025 notes that contemporary cohort studies suggest lymphocytic myocarditis is more commonly non-infectious or immune-mediated/autoimmune.[1]
Drugs and immune checkpoint inhibitors
ICI myocarditis is rare, affecting approximately 1% of treated patients, within the first weeks after starting therapy (ESC 2025).[1] ESC 2025 cites one of the largest case series (122 patients with ICI-associated myocarditis): onset was early after treatment initiation (median 30 days), with up to 50% mortality, and a systematic analysis of the WHO pharmacovigilance database confirmed a high mortality rate up to 33%.[1]
- Main risk factor: combination therapy with two types of ICI, such as an anti-CTLA-4 (ipilimumab) combined with an anti-PD-1 (nivolumab) (ESC 2025).[1]
- Who: mostly men and older patients (median age 65 years) with more comorbidities (ESC 2025).[1]
- Presentation: especially arrhythmogenic, including conduction disorders; HF with reduced EF occurs in about half; frequently associated with peripheral myositis, which with respiratory failure can negatively affect survival (ESC 2025).[1]
- Asymptomatic cases may exist with vaccine- or drug-related myocarditis, such as ICI-induced myocarditis, and are often underdiagnosed (ESC 2025).[1]
- Clozapine: among many drugs associated with myocarditis, ESC 2025 singles out clozapine, with a reported incidence of 0.1% to 5%.[1]
- DRESS: drug-induced myocarditis may be associated with drug reaction with eosinophilia and systemic symptoms; treatment is based on stopping the drug and corticosteroids (ESC 2025).[1]
Vaccines and COVID-19
- ESC 2025: apart from the SARS-CoV-2 vaccine, the main vaccine association is with smallpox vaccine, with data mainly from the US military population.[1]
- ESC 2025: a systematic review reported cardiac events including IMPS after influenza, pneumococcal and tetanus toxoid vaccination; few data report myocarditis after other vaccines (e.g. meningococcus, hepatitis A and B, diphtheria, poliovirus).[1]
- ESC 2025: a recent multicentre study reported good mid-term outcomes after COVID-19 vaccine-associated myocarditis, without death or need for heart transplantation.[1]
- The Brighton Collaboration, established in 2002, sets standards for defining adverse events after vaccination (ESC 2025); its myocarditis working group proposed 3 levels of certainty for vaccine-related myocarditis (as described in the ACC 2024 ECDP).[1][5]
- AHA/ACC 2025 sports statement: acute cardiopulmonary symptoms ≤1 week after SARS-CoV-2 vaccination warrant evaluation for vaccine-associated myocarditis, while flu-like symptoms immediately after vaccination do not require cardiac assessment.[7]
- ESC 2025: COVID-19-associated IMPS ranges from 0.1–4.5/1000 cases on CMR/EMB-derived diagnosis up to 2%–8% of symptomatic patients; for symptomatic complicated cases the predominant management is antiviral treatment plus supportive therapy.[1]
Genetic background
Gene variants predisposing to myocardial inflammation overlap with inherited cardiomyopathy (ARVC and NDLVC).[1] In the meta-analysis ESC 2025 cites, the pooled prevalence of pathogenic or likely pathogenic variants was 4.2% in uncomplicated myocarditis and 22% (adults) and 45% (children) in complicated myocarditis.[1] ESC 2023 cardiomyopathy reports disease-causing variants in DCM, NDLVC and ARVC genes in 8–22% of adults and children presenting with acute myocarditis.[3] ESC 2025 says different studies report that patients with myocarditis and pathogenic or likely pathogenic desmosomal variants (mostly DSP) have a higher incidence of adverse cardiovascular events, especially myocarditis recurrence and ventricular arrhythmia, than those without.[1] ESC 2023 reports a higher rate of myocarditis recurrence and ventricular arrhythmia in individuals with an acute myocarditis presentation and desmosomal variants than in myocarditis patients without one.[3]
Myocarditis, especially when recurrent, may represent the "hot phase" of some cardiomyopathies, such as DSP-related ARVC (ESC 2025).[1] ESC 2025 says it is important to consider additional features, such as a family history of myocarditis or pericarditis, cardiomyopathy or sudden cardiac death.[1]
What happens in the myocardium
- Cytolytic viruses such as enteroviruses destroy cardiomyocytes and induce severe infiltration by macrophages and lymphocytes (ESC 2025).[1]
- Vasculotropic B19V infects cardiac endothelial cells but not cardiomyocytes, yet can also induce severe lymphocytic myocarditis, especially in young children (ESC 2025).[1]
- Lymphotropic and other viruses (HHV-6, EBV, CMV, HCV, influenza, SARS-CoV-2) may trigger myocarditis indirectly by activating the immune system (ESC 2025).[1]
- Timing: the acute phase of viral myocarditis is characterised by intense virus replication and myocyte necrosis and usually lasts only a few days (ESC 2025).[1]
- Inflammasome: acute myocarditis shows significant activation of the NLRP3 inflammasome in the heart, which drives inflammation through IL-1β and IL-18 (ESC 2025).[1]
- Scar as substrate: resolution of inflammation does not necessarily mean absence of risk, because myocardial fibrosis may be an arrhythmogenic substrate long after the acute episode (ESC 2025).[1]
Scar-related ventricular arrhythmias can occur at any time during follow-up, even after inflammation has resolved (ESC 2025).[1] Polymorphic and irregular ventricular arrhythmias are more common in the active inflammatory phase, while monomorphic and regular ones are associated with healed myocarditis with residuals (ESC 2025).[1] VT ablation is more effective in the post-inflammatory stage than during acute myocarditis.[1]
How it presents
Most acute myocarditis presents with chest pain, but the presentation can vary from very mild symptoms to a life-threatening condition, including shock and sudden death.[1]
- ECG: normal in about 15%; ST-segment elevation most often (57.5%), other ST/T changes (23.5%), conduction blocks (10%) (ESC 2025).[1]
- Biomarkers and echo: cardiac enzymes are elevated in most acute presentations; echocardiography may show increased wall thickness and echogenicity from oedema, and pericardial effusion is seen in up to 25% (ESC 2025).[1]
- Fulminant myocarditis: cardiogenic shock at presentation needing haemodynamic support; biventricular failure occurs frequently, sustained ventricular arrhythmias may occur (46.9%) and some present with sudden cardiac death (25.8%) (ESC 2025).[1]
- Children with fulminant disease (usually <2 years) mostly have LV dilatation at presentation, whereas adults usually do not in the early phase (ESC 2025).[1]
Three presentations
Chest pain is the most common form of clinical presentation (about 75% of unselected cases) in adolescents and adults (ESC 2025).[1] It is commonly associated with a rise in necrosis biomarkers such as troponin, often with ECG alterations (especially ST-segment elevation) that may mimic ACS despite no significant obstructive coronary disease.[1] Patients with this presentation usually report a recent or concomitant viral infection, such as a respiratory infection or gastroenteritis, which often precedes myocarditis by several days to weeks (2–4 weeks).[1]
Acute HF, in particular with LVEF ≤40%, should be considered a high-risk group, and prognosis largely depends on the short-term response to therapy (ESC 2025).[1] Fulminant myocarditis presenting with HF carries a higher rate of cardiac death and transplantation, both in the short and long term, than LV dysfunction without fulminant myocarditis.[1] In this setting, giant-cell and eosinophilic myocarditis are independently associated with increased mortality.[1]
Arrhythmic presentations range from palpitations to syncope or aborted sudden death (ESC 2025).[1] Patients with advanced AV block or sustained ventricular arrhythmia should be considered high risk even without LV dysfunction.[1] ESC 2025 reports that VF or cardiac arrest occurs in about 2.5% of myocarditis-related hospitalisations, and that sustained VA during acute myocarditis carries a high risk of recurrence.[1] In patients with arrhythmic presentation, genetic testing for cardiomyopathy (ARVC, DCM, NDLVC) should be considered.[1]
ESC 2025 Table 6: Red flags for the clinical diagnosis of myocarditis and pericarditis (myocarditis column)
| Myocarditis column of ESC 2025 Table 6 |
|---|
| Recent or concomitant flu-like syndrome or gastroenteritis; infarct-like chest pain; palpitations; HF symptoms; ECG changes; ventricular arrhythmias (isolated, complex); syncope; haemodynamic instability; elevated markers of myocardial lesion (hs-Tn, CK-MB); elevated markers of HF (NT-proBNP); abnormal wall motion, increased wall thickness and/or impaired systolic function on imaging; CMR imaging with myocardial oedema and/or LGE |
The red flags raise awareness; ESC 2025 says they are not equivalent to the risk.[1] If IMPS is suspected, staging based on risk assessment follows.[1]
What else it could be
ACS is the main differential diagnosis, because chest pain, troponin, NT-proBNP and ECG changes overlap (ESC 2025).[1] ESC 2025 recommends invasive coronary angiography or coronary CT, depending on clinical likelihood, in patients with IMPS if ACS is suspected, to rule out obstructive coronary artery disease (Class I, Level C).[1] Coronary disease may coexist with myocarditis in particular scenarios, including eosinophilic and ICI-induced myocarditis.[1]
- Mimics listed in the ACC 2024 ECDP: acute coronary syndrome, arrhythmogenic cardiomyopathy, idiopathic or genetic arrhythmias, and non-inflammatory non-ischaemic DCM or infiltrative cardiomyopathies such as amyloidosis or haemochromatosis.[5]
- ACS-like presentations: CMR with tissue characterisation is useful for differentiating myocarditis from ischaemic injury (ACC 2024 ECDP).[5]
- Phenocopies such as ARVC: Dallas histology plus immunohistology for CD3+ T cells and CD68+ macrophages is required to identify histological subtypes and separate them (ESC 2025).[1]
- Conduction disease: AV block is common in myocarditis from non-viral infections (Chagas, Lyme, diphtheria) and can also be an initial presentation of cardiac sarcoidosis (ESC 2025); ESC 2025 cites a Finnish study in which 25% of people <55 years with clinically idiopathic heart block had giant-cell myocarditis or cardiac sarcoidosis on biopsy.[1]
- Sepsis: the AHA 2020 fulminant myocarditis statement notes that patients may present febrile from severe inflammation; although the more common diagnosis is infection and sepsis, this may also be severe myocarditis, discriminating sepsis from early cardiogenic shock secondary to myocarditis is challenging early in workup and treatment, and a high index of suspicion is warranted.[6]
Making the diagnosis: ESC 2025 criteria
ESC 2025 proposes new diagnostic criteria and a new classification (Table 4), with multimodality imaging, and CMR in particular, now a cornerstone of diagnosis.[1] Myocarditis can be diagnosed as definite or possible with an appropriate clinical presentation and additional criteria, including a CMR-proven or EMB-proven result; a clinical presentation with a CMR- or EMB-proven result makes it definite (Table 4).[1] Both EMB and CMR can provide a definitive clinical diagnosis, but with different indications.[1]
ESC 2025 Table 4: Diagnostic criteria and classification for inflammatory myopericardial syndrome (if diagnostic criteria for myocarditis and/or pericarditis are fulfilled, a)
| Myocarditis | Pericarditis | |
|---|---|---|
| Definite | Clinical presentation (b) and CMR- or EMB-proven | Clinical presentation (b) with >1 additional criterion |
| Possible | Clinical presentation (b) with at least 1 additional criterion; CMR- or EMB-uncertain or not available | Clinical presentation (b) with 1 additional criterion |
| Unlikely/rejected | Only clinical presentation (b) without additional criteria | Only clinical presentation (b) without additional criteria |
| Additional criteria: clinical (b) | Non-specific findings | Pericardial rubs |
| Additional criteria: ECG (c) | ST-T changes | PR depression, widespread ST-segment elevation |
| Additional criteria: biomarkers | Troponin elevation | C-reactive protein elevation |
| Additional criteria: imaging (d) | Abnormal strain, wall motion, reduced EF; myocardial oedema and/or LGE (CMR findings) | New or worsening pericardial effusion; pericardial oedema and/or LGE (CMR findings) |
- Clinical presentations include chest pain or infarct-like symptoms, arrhythmias, heart failure, aborted sudden cardiac death.[1]
- CMR categories: proven = 2 out of 2 updated Lake Louise criteria fulfilled; uncertain = only 1 out of 2; rejected = negative CMR.[1]
- EMB categories: proven, uncertain, rejected (according to pathologist consensus).[1]
- Footnote a: one condition may be leading.[1]
- Footnote b: rarely, asymptomatic cases may be detected (e.g. drug-related with a distinct history, such as immune checkpoint inhibitors).[1]
- Footnote c: if ECG changes, always consider/exclude myocarditis.[1]
- Footnote d: imaging findings are detailed in Sections 5.4–5.7 of the guideline.[1]
ESC 2025 Recommendation Table 1: Recommendations for clinical evaluation of myocarditis and pericarditis (selected rows)
| ESC 2025 row (Recommendation Table 1) | Class, Level |
|---|---|
| Complete clinical evaluation, including history, physical examination, chest X-ray, biomarkers, ECG, and echocardiography is recommended in all patients with a suspicion of myocarditis and/or pericarditis for the initial diagnostic assessment. | I, C |
| CMR is recommended in patients with the clinical suspicion of myocarditis (using updated Lake Louise criteria) and/or pericarditis for the non-invasive diagnosis of inflammatory reaction. | I, B |
| Hospital admission is recommended for patients with moderate- to high-risk myocarditis (Table 7) for monitoring and treatment. | I, C |
| EMB is recommended in patients with high-risk myocarditis (Table 7) and/or haemodynamic instability, and/or in patients with intermediate-risk myocarditis not responding to conventional therapy, in order to detect a specific histologic subtype and to assess the presence of viral genome for treatment. | I, C |
| Invasive coronary angiography or coronary CT, depending on clinical likelihood, is recommended in patients with IMPS if an acute coronary syndrome is suspected to rule out obstructive coronary artery disease. | I, C |
| Hospital admission should be considered for patients with low-risk myocarditis (Table 7) for monitoring and treatment. | IIa, C |
| Routine serology is not recommended in patients with myocarditis and/or pericarditis for the evaluation of viral aetiology except for hepatitis C, HIV, and Lyme disease. | III, C |
Two footnotes shape this table.[1] The biomarkers footnote names hs-TnT or hs-TnI, C-reactive protein and NT-proBNP.[1] The EMB footnote says contemporary evaluation should be based on histology, immunohistology and molecular pathology for viral infections in myocardial and blood samples.[1]
ECG and blood tests
- ECG: QRS amplitude may fall, especially with large effusions or extensive myocardial injury; QT lengthening might occur in acute myocarditis; and AV blocks and intraventricular conduction defects, particularly right bundle branch block, are not uncommon and may accompany more severe presentations (ESC 2025).[1]
- A normal ECG at presentation does not exclude IMPS (ESC 2025); the ACC 2024 ECDP puts ECG sensitivity at 47%.[1][5]
- ECG features that the ACC 2024 ECDP says are often associated with decreased LV function, LV scar and poor prognosis include pathological Q waves, LBBB, QRS ≥120 ms, prolonged QT, high-grade AV block, malignant tachyarrhythmias, fragmented QRS and T-wave inversion.[5]
- Troponin is elevated with myocardial involvement, usually indicating cardiomyocyte necrosis, and baseline troponin is crucial to grade severity (ESC 2025).[1]
- BNP or NT-proBNP: baseline assessment is recommended in suspected myocarditis and can be repeated at discharge and during outpatient follow-up to assess the risk of clinical events (ESC 2025).[1]
- C-reactive protein is often increased in acute myocarditis (up to 80%); a negative result does not exclude the diagnosis (ESC 2025).[1]
- Viral serology concurs with PCR results in a minority (∼4%) of patients with myocarditis, and routine serology is not recommended except for hepatitis C, HIV and Lyme disease (ESC 2025, Class III, Level C).[1]
CMR and the updated Lake Louise criteria
CMR detects the tissue changes of inflammation without a biopsy.[1] Oedema and inflammation increase tissue water, which can be detected as increased signal on T2-weighted imaging and/or T2 mapping; increased free water also increases signal in T1 mapping and ECV quantification (ESC 2025).[1] Necrosis and fibrosis can give non-ischaemic LGE (e.g. mid-wall, subepicardial, patchy) that does not typically follow a coronary distribution.[1]
ESC 2025: the updated Lake Louise criteria rest on at least one T2-based criterion plus ideally one T1-based criterion.[1] Both together increase specificity for acute myocarditis, but one alone can still support possible myocarditis in an appropriate clinical scenario, with less specificity.[1] Supportive criteria include pericardial abnormalities (which suggest concomitant pericarditis) and global or regional LV systolic dysfunction on cine imaging.[1]
- ACC 2024 ECDP wording: at least 1 T2-based criterion (global or regional increase of myocardial T2 relaxation time, or increased signal intensity on T2-weighted images) in addition to ≥1 T1-based criterion (increased myocardial T1, LGE, or ECV).[5]
- Sensitivity: high (>85%) for the updated criteria, per the ACC 2024 ECDP.[5]
- Timing: the diagnostic accuracy of CMR is higher if performed early in the time course of disease, best within the first 2 weeks (ESC 2025); the ECDP says the diagnostic yield of CMR in suspected myocarditis is typically highest when undertaken within the first 1 to 2 weeks of symptom onset.[1][5]
- Weak spots: diagnosis is less challenging with chest pain than in HF and arrhythmic presentations (ESC 2025), and imaging does not give the histotype.[1]
- LGE pattern (ACC 2024 ECDP): it tends to be mid-wall and/or subepicardial, predominantly lateral and inferior, although subendocardial involvement can occur with non-ischaemic patterns. Patterns are typically not pathognomonic for a specific aetiology of myocardial inflammation, but certain patterns may suggest one: diffuse subendocardial LGE beyond one coronary territory with LV thrombus is often seen in eosinophilic myocarditis, especially when multivessel obstructive CAD and a history of multiterritory myocardial infarction have been ruled out, and striking ring-like mid-wall/subepicardial LGE can be seen in desmoplakin and other genetic cardiomyopathies.[5]
- History: the original Lake Louise criteria took at least 2 of 3 CMR criteria (oedema on T2, LGE, early gadolinium enhancement), as the AHA 2020 fulminant myocarditis statement describes them.[6]
ESC 2025 imaging rows: Recommendation Table 3 (myocarditis rows) and Recommendation Table 5
| ESC 2025 row | Class, Level |
|---|---|
| CMR is recommended in patients with suspected myocarditis to reach a clinical diagnosis and to determine the cause of acute myocardial injury, including assessment of oedema, ischaemia, and necrosis/fibrosis/scarring. | I, B |
| CMR is recommended for follow-up at least within the first 6 months in patients with myocarditis to identify a healed or ongoing process, for risk stratification and personalized therapy, and to enable a return to exercise. | I, C |
| Carb-free ¹⁸F-FDG-PET or ¹⁸F-FDG-PET/CT should be considered for the diagnostic work-up in patients with suspected myocarditis and/or pericarditis in whom echocardiography and CMR are inconclusive, for the clinical diagnosis. | IIa, C |
FDG-PET can be considered as an alternative when CMR is unsuitable because of an irregular heartbeat or device-related artefacts, and appropriate fasting beforehand is a must (ESC 2025).[1]
[5] [1]Endomyocardial biopsy
Because CMR can now make the diagnosis, the role of EMB has changed (ESC 2025).[1] It remains important for high-risk patients and some intermediate cases where the histological subtype and a possible viral cause matter for targeted therapy.[1] When fulminant, giant-cell or eosinophilic myocarditis is suspected, early EMB is required to start immunosuppression rapidly and improve outcomes.[1]
Formal rows on endomyocardial biopsy
| Source | Row on EMB | Class, Level |
|---|---|---|
| ESC 2025 (Recommendation Table 1) | EMB is recommended in high-risk myocarditis and/or haemodynamic instability, and/or in intermediate-risk myocarditis not responding to conventional therapy, to detect a specific histologic subtype and assess viral genome for treatment. | I, C |
| ESC 2025 (Recommendation Table 16) | EMB is recommended in suspected giant-cell myocarditis due to unexplained new-onset HF of up to 2 weeks with a normal or dilated LV and new ventricular arrhythmias, second- or third-degree AV block, or failure to respond to usual care within 1 to 2 weeks, to initiate specific treatment. | I, C |
| ESC 2023 cardiomyopathies (Recommendation Table 7) | In suspected cardiomyopathy, EMB should be considered to aid in diagnosis and management when other clinical investigations suggest myocardial inflammation, infiltration, or storage that cannot be identified by other means. | IIa, C |
| ESC 2026 heart failure (Recommendation Table 4, established HF) | EMB should be considered to aid in diagnosis and management in patients with rapidly progressive HF despite standard therapy or when other clinical investigations suggest myocardial inflammation, infiltration, or storage that cannot be identified by other means. | IIa, C |
- Complications (perforation/tamponade, thromboembolism, valvular trauma, severe arrhythmias, death): rates depend on the setting and centre experience and range from 0.6% to 5%, rising up to 26% in fulminant cases on MCS; children may have higher rates (ESC 2025).[1]
- Yield: in giant-cell myocarditis, sensitivity 80%–93% and positive predictive value 71%, especially within 2–4 weeks of onset; in cardiac sarcoidosis EMB may have a low sensitivity (20%–30%), which can be improved by CMR or electro-anatomical mapping guidance (ESC 2025).[1]
- Immunohistology cut-off: ≥14 leucocytes/mm² with T lymphocytes ≥7 cells/mm² has been considered the cut-off for the diagnosis of myocarditis; in acute lymphocytic myocarditis T cells are generally higher (>25 cells/mm²) (ESC 2025), although ESC 2025 adds that these criteria have been questioned by cardiopathologists.[1]
- Viral PCR: a positive PCR on EMB must be paired with blood samples taken at the same time; in acute cardiac and systemic virus infection, immunosuppressive therapy must be avoided (ESC 2025).[1]
- Site: most often the RV septum, but occasionally LV or biventricular EMB may be needed (ESC 2025).[1]
- Sampling: a negative EMB does not necessarily rule out myocarditis; technical aspects that improve yield include earlier timing after symptom onset (e.g. within 2–4 weeks), ≥3 samples of 1 to 2 mm and voltage guidance to select biopsy sites (ACC 2024 ECDP).[5]
- Steroids first? In suspected giant-cell myocarditis, i.v. steroids before EMB may reduce its diagnostic yield (ESC 2025).[1]
ESC 2025 Table 5: Histopathological criteria for myocarditis
| Term | Predominant inflammatory cells | Myocyte necrosis | Infections PCR positive (viruses, etc.) |
|---|---|---|---|
| Active lymphocytic myocarditis | CD3+ T lymphocytes >7/mm², CD68+ macrophages | yes | yes/no |
| Persistent lymphocytic myocarditis | CD3+ T lymphocytes >7/mm², CD68+ macrophages | yes | yes/no |
| Resolved lymphocytic myocarditis | – | no | yes/no |
| Eosinophilic myocarditis (acute stage) | Eosinophils, CD3+ T lymphocytes, CD68+ macrophages | yes | yes/no |
| Giant-cell myocarditis (acute stage) | Eosinophils, CD68+ giant cells, CD3+ T lymphocytes, CD68+ macrophages | yes | no |
| Sarcoidosis | CD68+ giant cells, granuloma, CD3+ T lymphocytes, CD68+ macrophages | yes/no | no |
ESC 2025 Table 11: Parameters for reporting by endomyocardial biopsy
| Criteria | Parameters for reporting |
|---|---|
| Histology (paraffin-embedded EMB, at least 3 EMB) | Presence and extent of cardiomyocyte necrosis, inflammation, fibrosis |
| Immunohistology (paraffin-embedded EMB, at least 3 myocardial samples) | Presence, extent, localization and typing of immune cells: CD3+ T lymphocytes, CD68+ macrophages (≥14 leucocytes/mm² with T lymphocytes ≥7 cells/mm), HLA-DR expression in immune cells and endothelial cells |
| Molecular pathology for infections (RNAlater, snap-frozen tissue (1–2 EMB), paraffin-embedded EMB) and blood | Presence, typing and quantification of DNA/RNA from infectious agents by q(RT)-PCR (viruses: mainly enteroviruses, parvovirus B19, human herpesvirus 6, Epstein–Barr virus; Borrelia spp., Trypanosoma cruzi); q(RT)-PCR for detection of systemic infections |
| Molecular pathology for genetics (RNAlater, frozen tissue, paraffin-embedded EMB, blood) | NGS for pathogenic variants in cardiac genes traditionally associated with cardiomyopathies (especially desmosomal and sarcomeric/cytoskeletal genes) |
The ACC 2024 ECDP frames the same decision by stage, as consensus without class: select stage B patients (those attributed to ICI therapy), more stage C patients and most stage D patients should undergo biopsy.[5]
Genetic testing
ESC 2025 Recommendation Table 2: Recommendations for genetic testing
| ESC 2025 row (Recommendation Table 2) | Class, Level |
|---|---|
| It is recommended to obtain family history including pedigrees in cases of recurrent IMPS to provide clues to the underlying aetiology, determine inheritance pattern, and identify relatives at risk. | I, C |
| Genetic testing should be considered in patients with definite myocarditis/pericarditis in cases of: family history of IMPS, inherited or suspected cardiomyopathy; severe ventricular arrhythmia; significant left/right LGE (e.g. ring-like pattern or septal LGE) or persistent LVEF systolic dysfunction; recurrent myocarditis or persistent troponin elevation; recurrent pericarditis with an inflammatory phenotype, refractory to conventional treatment, with the aim to detect an underlying genetic cause. | IIa, B |
- Footnote c, printed on severe ventricular arrhythmia, points to Section 4; footnote d, printed on refractory to conventional treatment in the recurrent pericarditis case, reads: especially poor response to colchicine and anti-IL-1 agents.[1]
Cascade clinical and genetic screening of relatives, with familial counselling, should be offered (ESC 2025).[1] A variant also changes device thinking: myocarditis defers an ICD during the acute phase, but the primary-prevention threshold is lower in ARVC.[1] The ACC 2024 ECDP adds, as consensus, that genetic evaluation can wait until the acute phase has resolved, because results are unlikely to alter immediate management.[5]
Risk stratification: who goes where
Triage starts by assessing risk and ruling out ACS when the presentation suggests it, then asks whether first contact was inpatient or outpatient (ESC 2025).[1] Table 7 then stratifies clinical risk to guide work-up.[1]
ESC 2025 Table 7: Clinical risk stratification to guide work-up in inflammatory myopericardial syndrome (myocarditis rows)
| High risk | Intermediate risk | Low risk | |
|---|---|---|---|
| Clinical | Acute HF/cardiogenic shock; dyspnoea NYHA III–IV refractory to medical therapy; cardiac arrest/syncope; ventricular fibrillation/sustained ventricular tachycardia; high-level AV block | New/progressive dyspnoea; non-sustained ventricular arrhythmias; persistent release or relapsing troponin | Stable symptoms or oligosymptomatic |
| Imaging criteria | Newly reduced LVEF (<40%); extensive LGE on CMR | Newly mildly reduced LVEF (41%–49%) and/or WMA; preserved LVEF (≥50%) and LGE ≥2 segments on CMR | Preserved LVEF (≥50%) without LGE or limited LGE (<2 segments) on CMR |
Table 7 prints footnote a on cardiac arrest/syncope, ventricular fibrillation/sustained ventricular tachycardia, high-level AV block, newly reduced LVEF (<40%) and extensive LGE on CMR.[1] The footnote says these criteria do not lead directly towards EMB; in these scenarios it is a case-by-case decision depending on the suspected underlying cause (ESC 2025).[1] Hospital admission for monitoring and treatment is recommended for moderate- to high-risk myocarditis (Class I, Level C) and should be considered for low-risk myocarditis (Class IIa, Level C) (ESC 2025).[1]
ESC 2026 HF uses similar markers.[2] It says patients with myocarditis presenting with decompensated HF, LVEF <40%, life-threatening arrhythmias (VT/VF, third-degree AV block) and/or extensive LGE should be viewed as high risk.[2] In ESC 2026 HF, high-risk patients may require EMB to tailor treatment, whereas lower-risk patients may be examined with CMR.[2]
[1]Prognostic markers
- Presentation: low-risk myocarditis (about 75% of unselected cases) usually presents with chest pain and preserved biventricular function and has a benign short- and long-term prognosis; acute complicated myocarditis with arrhythmic, and especially HF, presentation has a worse prognosis (ESC 2025).[1]
- Troponin with preserved function: troponin release is usually not a negative prognostic marker when biventricular function is preserved (ESC 2025).[1]
- Mortality or transplant: factors associated with increased mortality or transplantation are giant-cell myocarditis, QRS >120 ms on the initial ECG and the need for temporary MCS other than IABP; biventricular dysfunction has been described as the main predictor of death or transplantation (ESC 2025).[1]
- CMR: patients with a normal CMR have a good prognosis; ESC 2025 reports that in a multicentre study of acute myocarditis with preserved EF, anteroseptal mid-wall LGE was the best independent predictor of the combined endpoint (cardiac death, appropriate ICD interventions, resuscitated cardiac arrest, HF hospitalisation; OR 2.73; 95% CI 1.2–5.9; median follow-up 4.3 years), and that anteroseptal LGE was the best independent predictor of SCD (HR 4.59; 95% CI 1.38–15.24).[1]
- After life-threatening arrhythmia: ESC 2025 reports that in a study of acute myocarditis with life-threatening arrhythmias, LGE in two or more segments and absence of oedema on the initial CMR were associated with recurrent major arrhythmic events including SCD (HR 4.51 and HR 2.59).[1]
- Other arrhythmic predictors: sustained VT or VF at onset, fibrosis on EMB and inducible major VA on PVS (ESC 2025).[1]
- Clinical predictors: ESC 2025 reports that young age and a previous myocarditis were independent relapse predictors, and that fulminant onset, lower LVEF at presentation, distinct autoimmune features (especially in women) and high-titre organ-specific anti-heart and antinuclear autoantibodies were independent predictors of death and transplantation.[1]
Management
Therapy rests on presentation, severity and aetiology (ESC 2025).[1] ESC 2025 says evidence in this field is very limited.[1] A multidisciplinary team discussion at a referral centre is recommended for high-risk or complicated IMPS to provide a patient-tailored approach (ESC 2025, Class I, Level C).[1]
Rest and chest pain
Restricting physical activity is an important non-drug measure.[1] ESC 2025 restricts physical activity beyond sedentary activities until symptoms resolve and clinical remission is reached with normal inflammatory markers; at least 1 month is needed to reach clinical remission, but it can last longer.[1]
Uncomplicated cases usually present with chest pain and can be treated empirically with aspirin or NSAIDs if needed; colchicine is safe in myopericarditis and prevents recurrences (ESC 2025).[1] The ACC 2024 ECDP adds, as consensus, that NSAIDs should be avoided in symptomatic HF or shock.[5] The AHA 2020 statement on fulminant myocarditis also advises avoiding NSAIDs, which may increase sodium retention, cause myocardial harm and worsen renal hypoperfusion.[6]
ESC 2025 Recommendation Table 9: medical therapy in myocarditis
ESC 2025 Recommendation Table 9: Recommendations for medical therapy in myocarditis
| Group (as printed) | ESC 2025 row | Class, Level |
|---|---|---|
| Management of symptoms | NSAIDs (together with proton pump inhibition) should be considered in patients with associated symptoms of pericarditis to reduce symptoms. | IIa, C |
| Management of symptoms | Colchicine should be considered in patients with myopericarditis to reduce recurrences. | IIa, B |
| Management of heart failure | Adherence to the ESC HF guidelines is recommended in cases of myocarditis with LV systolic dysfunction and/or HF to reduce symptoms and to improve LV function. | I, C |
| Management of heart failure | HF therapy should be considered in patients with myocarditis and LV systolic dysfunction for at least 6 months upon complete LV functional recovery to stabilize LV function. | IIa, C |
| Management of arrhythmias | β-Blockers, with a continuation for at least 6 months, should be considered in patients with acute myocarditis, especially those with troponin elevation, to control symptoms and prevent arrhythmias. | IIa, C |
| Management of arrhythmias | Anti-arrhythmic treatment should be considered in post-myocarditis patients with recurrent, symptomatic VT to reduce arrhythmic burden. | IIa, C |
| Immunosuppressive therapy | Corticosteroids should be considered in patients with fulminant, non-infectious forms of myocarditis to stabilize the patients. | IIa, C |
| Immunosuppressive therapy | Corticosteroids may be considered in patients with acute myocarditis with impaired LVEF if refractory to standard HF therapy to stabilize patients. | IIb, C |
| Immunosuppressive therapy | Routine use of immunosuppressive therapy is not recommended in acute myocarditis with preserved LV function because no outcome benefit has been shown. | III, C |
Heart failure and shock
ESC 2025 recommends adherence to the ESC HF guidelines in myocarditis with LV systolic dysfunction and/or HF, to reduce symptoms and to improve LV function (Class I, Level C).[1] ESC 2026 HF says patients with myocarditis and HFrEF should be treated empirically with foundational medical therapy (FMT) for HFrEF.[2] ESC 2025 adds that, in myocarditis with LV systolic dysfunction, HF therapy should be considered for at least 6 months upon complete LV functional recovery, to stabilize LV function (Class IIa, Level C).[1]
Stopping later is a separate decision. ESC 2026 HF lists myocarditis among causes of HF that might be reversible.[2] Where a completely reversible cause is suspected and LV function, volume and natriuretic peptides have completely normalised after treatment of that cause, a gradual trial of FMT withdrawal might be considered, but only with caution, in exceptional cases and at the patient's request.[2] Such withdrawal should only be done under frequent clinical, laboratory and imaging control to rule out relapse of HF.[2]
Fulminant myocarditis is a rare and severe presentation and a cause of cardiogenic shock, to be treated with inotropic or vasopressor support or, if needed, MCS (ESC 2025).[1] ESC 2025 advises referral, when needed, to tertiary centres able to provide temporary MCS and early EMB; early EMB has been independently associated with a lower rate of death or transplant/LVAD at 1 year.[1] ESC 2026 HF says such patients should be transferred to, or discussed with, a centre that can perform EMB and provide MCS.[2]
ESC 2025 Recommendation Table 11: interventional techniques including circulatory support in myocarditis
| ESC 2025 row (Recommendation Table 11) | Class, Level |
|---|---|
| A timely and dedicated Shock Team discussion is recommended in patients with myocarditis in the presence of haemodynamic compromise, to decide on the need for escalation to MCS and to determine a long-term management plan. | I, C |
| Temporary MCS should be considered in patients with myocarditis and cardiogenic shock or acute decompensation in chronic myocarditis to stabilize the patients. | IIa, C |
- Who responds best: patients with rapid haemodynamic deterioration and rapidly progressive myocardial dysfunction are among those who respond best to temporary MCS (ESC 2025).[1]
- Device choice: ESC 2025 reports that VA-ECMO is the most frequently applied or recommended temporary MCS, ranging from 75% to 85% of acute myocarditis cases, and that in patients on VA-ECMO for fulminant myocarditis, national and international multicentre studies showed in-hospital survival of 61% to 72%, but no freedom from heart transplantation in giant-cell fulminant myocarditis.[1]
- IABP: should be considered in cardiogenic shock as first-line MCS, with prompt escalation if haemodynamic and end-organ perfusion improvement is not seen within 1 h maximum; EMB should still be done as soon as possible on MCS (ESC 2025).[1]
- Rate control trap: the AHA 2020 statement advises against treating sinus tachycardia with rate-control agents (especially negatively inotropic ones such as metoprolol, diltiazem or verapamil) in fulminant myocarditis, because, in patients with systolic dysfunction, cardiac output may depend on a compensatory rise in heart rate.[6]
Arrhythmias and sudden death prevention
Sustained VA in acute myocarditis is rare, but it carries a substantial risk of recurrence, persisting even after the acute phase.[1] Recurrence rates of 28% to 60% are reported, and they appear higher with monomorphic VT, chronically active myocarditis, anteroseptal LGE and reduced LVEF (ESC 2025).[1] The risk of VA is independent of LVEF.[1]
ESC 2025 Recommendation Table 14: Recommendations for management of arrhythmias and prevention of sudden cardiac death in myocarditis
| Group (as printed) | ESC 2025 row | Class, Level |
|---|---|---|
| WCD in myocarditis | A WCD should be considered for 3–6 months in patients with sustained ventricular arrhythmia during the acute phase of myocarditis as a bridge to recovery. | IIa, C |
| Ablation in myocarditis | Catheter ablation, performed in specialized centres, should be considered in post-myocarditis patients with recurrent symptomatic SMVT or ICD shocks in whom AAD are ineffective, not tolerated, or not desired. | IIa, C |
| ICD in myocarditis: secondary prevention | ICD implantation is recommended in patients with non-active myocarditis (c) and haemodynamically not-tolerated sustained VT to prevent SCD. | I, C |
| ICD in myocarditis: secondary prevention | ICD implantation should be considered in patients with non-active myocarditis (c) and haemodynamically tolerated sustained VT to prevent SCD. | IIa, C |
| ICD in myocarditis: secondary prevention | ICD implantation may be considered in patients with acute myocarditis and sustained VA (VT/VF) in the acute phase to prevent SCD. | IIb, C |
| ICD in myocarditis: primary prevention | ICD implantation may be considered in patients with myocarditis after the acute phase (3–6 months) and persistent risk factors for VA (d) to prevent SCD. | IIb, C |
| Pacing in myocarditis | Temporary transvenous external pacing should be considered in patients with acute myocarditis and high-degree conduction disorders as a bridge to recovery. | IIa, C |
- Footnote c: non-active is based on CMR evidence of activity (T2) (ESC 2025).[1]
- Footnote d: NSVT, extensive LGE, unexplained syncope, positive PVS, reduced LVEF <50%; the Figure 17 legend lists the same risk factors and adds at least 1, with risk and indication increasing with more than 1 (ESC 2025).[1]
The ICD decision is usually deferred.[1] ESC 2025 says it is generally accepted to wait 3–6 months after an acute episode to evaluate the need for an ICD, with a WCD considered as a bridge in some high-risk patients.[1] Early ICD consideration is warranted with symptomatic VA, or heart block in giant-cell myocarditis or cardiac sarcoidosis.[1] Programmed ventricular stimulation should not be performed in the acute phase; it could help in selected non-active myocarditis with LGE and risk factors (ESC 2025).[1]
Pacing decisions also allow for recovery.[1] AV block in acute myocarditis may be reversible, and temporary pacing is often necessary with haemodynamic compromise as a bridge to recovery; a permanent pacemaker can be considered for persisting high-degree AV block despite medical therapy (ESC 2025).[1]
ESC 2022 ventricular arrhythmia rows, read against ESC 2025
ESC 2025 builds on the 2022 ESC VA/SCD guideline and adds focus on selected scenarios.[1] ESC 2025 writes in addition to the 2022 guideline, so 2022 rows it does not restate keep their 2022 attribution.[1]
ESC 2022 VA/SCD Recommendation Table 34 (selected rows)
| ESC 2022 row (Recommendation Table 34) | Class, Level | Status against ESC 2025 |
|---|---|---|
| In confirmed or clinically suspected acute myocarditis, it is recommended that patients who present with life-threatening VAs are referred to a specialized centre. | I, C | Not restated in 2025; consistent with the ESC 2025 referral advice for fulminant myocarditis; the nearest 2025 row is Recommendation Table 27, a multidisciplinary team discussion at a referral centre is recommended in high-risk/complicated IMPS to provide a patient-tailored approach (I, C) |
| In patients with haemodynamically not-tolerated SMVT occurring in the chronic phase of myocarditis, an ICD implantation is recommended. | I, C | Closest to the ESC 2025 Class I row for non-active myocarditis; ESC 2025 bases non-active on CMR evidence of activity (T2), whereas this 2022 row is worded by the chronic phase |
| AADs should be considered (preferably amiodarone and beta-blockers) in patients with symptomatic non-sustained or sustained VAs during the acute phase of myocarditis. | IIa, C | Not restated in 2025; the related ESC 2025 Recommendation Table 9 row says β-blockers, with a continuation for at least 6 months, should be considered in acute myocarditis, especially with troponin elevation, to control symptoms and prevent arrhythmias (IIa, C) |
| In patients with haemodynamically well-tolerated SMVT occurring in the chronic phase of myocarditis, preserved LV function and a limited scar amenable to ablation, catheter ablation may be considered as an alternative to ICD therapy, after discussion with the patient and provided that established endpoints (footnote c: VT non-inducibility and elimination of electrograms consistent with conduction delay) have been reached. | IIb, C | Not restated in 2025 |
One 2022 row is dated history only.[4][1] In 2022, ICD implantation before hospital discharge should be considered (Class IIa, Level C) for haemodynamically not-tolerated sustained VT or VF during the acute phase.[4] ESC 2025 now says ICD implantation may be considered (Class IIb, Level C) in acute myocarditis with sustained VA (VT/VF) in the acute phase to prevent SCD, so the 2025 row governs.[1]
[1]Immunosuppression
In general, corticosteroids for acute myocarditis are controversial, except in ICI-induced and eosinophilic myocarditis (ESC 2025).[1] The single RCT of combined immunosuppression (prednisone with cyclosporine or azathioprine) in biopsy-proven acute myocarditis of unspecified aetiology, as ESC 2025 reports it, found no survival difference (P = 0.96), with small size and histology-only EMB as limitations.[1] In specific histological forms such as giant-cell myocarditis, immunosuppressive drugs are recommended.[1]
- Before treating: positive viral PCR on EMB must be checked against blood; in acute cardiac and systemic virus infection, immunosuppression must be avoided (ESC 2025).[1]
- Fulminant myocarditis: specific subtypes, such as biopsy-proven non-infectious forms, may respond to immunosuppression on top of guideline-directed care; a trial of corticosteroids in fulminant myocarditis is ongoing (NCT05150704) (ESC 2025).[1]
- Anakinra: ESC 2025 reports that in the ARAMIS trial anakinra failed to demonstrate a benefit in suspected acute myocarditis without a specific aetiology, with limitations of small size, a low-risk population and short follow-up, but that it proved anakinra safe.[1]
- IVIG: further randomised studies are needed in adults; IVIG is commonly prescribed in children (ESC 2025).[1]
- Antivirals: evidence is limited, and antiviral treatment should be agreed with an infectious disease expert in the IMPS team (ESC 2025).[1]
- ACC 2024 ECDP (consensus): some members, without uniform consensus, felt the evidence supports immunosuppression of select patients with lymphocytic myocarditis if the EMB is viral PCR-negative; i.v. methylprednisolone 7 to 14 mg/kg/d for 3 days, then prednisone 1 mg/kg/d orally, then tapering with steroid-sparing drugs, has been associated with clinical benefit in case series.[5]
ESC 2025 Table 12: Therapy for specific forms of myocarditis (selected rows; Lyme and Chagas rows not shown)
| Form | 1st line therapy | 2nd line therapy | 3rd line therapy |
|---|---|---|---|
| Lymphocytic myocarditis (virus-negative) | Non-severe: prednisone 1 mg/kg/day p.o. then tapered. Severe: i.v. methylprednisolone 7–14 mg/kg/day for 3 days, then 1 mg/kg/day p.o. | Oral corticosteroids + azathioprine or mycophenolate mofetil, cyclosporine, methotrexate | IVIG or plasmapheresis |
| Eosinophilic myocarditis | Same as lymphocytic myocarditis + treat EM-associated condition if identified | Same as lymphocytic myocarditis + treat EM-associated condition if identified | – |
| Giant-cell myocarditis | Non-severe: prednisone 1 mg/kg/day p.o. then tapered. Severe: i.v. methylprednisolone 7–14 mg/kg/day for 3 days, then 1 mg/kg/day p.o. + immunosuppressive (azathioprine or mycophenolate mofetil, cyclosporine) | Antithymocyte globulin (ATG), cyclophosphamide, rituximab | – |
| Cardiac sarcoidosis | Non-severe: prednisone 1 mg/kg/day p.o., tapering from 40–60 mg daily. Severe: i.v. methylprednisolone 7–14 mg/kg/day for 3 days, then 1 mg/kg/day p.o. | Methotrexate (1st choice), or azathioprine, mycophenolate mofetil, cyclophosphamide | Infliximab or adalimumab, rituximab |
| ICI-induced myocarditis | Withdraw ICI, reassess. Non-severe: methylprednisolone 500–1000 mg/day × 3 days, then taper with oral prednisone. Severe: i.v. methylprednisolone 7–14 mg/kg/day × 3 days, then 1 mg/kg/day | If no response in 24–48 h: mycophenolate mofetil, ATG, abatacept, alemtuzumab | Infliximab or adalimumab, rituximab |
- Azathioprine: 1–2 mg/kg per day p.o. (typically 100–150 mg daily in 1–2 divided doses) (ESC 2025 Table 12 footnote).[1]
- Mycophenolate mofetil: 500–1000 mg p.o. b.i.d. (total 1–2 g/day).[1]
- Cyclosporine: ∼3–5 mg/kg/day p.o. (divided b.i.d.), adjusted to target trough levels ∼150–250 ng/mL.[1]
- Methotrexate: 15–20 mg/week p.o. or s.c. (low-dose weekly, with folic acid supplementation).[1]
- IVIG: standard dose off-label 2 g/kg total, typically over 1 to 2 days; alternative 0.4 g/kg/day for 5 consecutive days (less commonly used in myocarditis).[1]
- Plasmapheresis: 3–5 sessions in 5–10 days.[1]
- ATG: ∼1 mg/kg i.v., often daily for 3–5 days.[1]
- Cyclophosphamide: 600 mg/m² i.v. bolus on days 1, 15 and 30 (pulse therapy).[1]
- Rituximab: 375 mg/m² i.v. weekly × 4 doses (1 month).[1]
- Infliximab: 5 mg/kg i.v. at weeks 0, 2, 6, then every ∼8 weeks; adalimumab: 40 mg s.c. every week (or every 2 weeks, per clinical response).[1]
- Abatacept: 500 mg i.v. every 2 weeks × 5 doses (approximately 10 weeks); alemtuzumab: 30 mg i.v. once (alternative 15 mg i.v. daily for 2 days).[1]
Specific forms
- Giant-cell myocarditis: suspect it with treatment-resistant HF or shock, VA and AV block; ESC 2025 recommends combined immunosuppressive therapy once diagnosed (Class I, Level C); corticosteroid monotherapy does not prolong transplant-free survival.[1]
- Giant-cell survival: combined corticosteroids with cyclosporine, azathioprine or both improved transplant-free survival on average to 12 months, against 4 months with corticosteroids alone (ESC 2025).[1]
- Eosinophilic myocarditis is a rare form: look for hypersensitivity, EGPA, hypereosinophilic syndrome, parasites and cancer; it often presents fulminantly with thromboembolic risk, and peripheral eosinophilia is absent in up to 25% (ESC 2025).[1]
- Eosinophilic treatment: first-line i.v. corticosteroids, with caution if an infectious agent is the cause; anticoagulation could be considered in the acute phase, since endocavitary thrombi were reported in 12% (ESC 2025).[1]
- Hypersensitivity myocarditis, a subset of eosinophilic myocarditis, generally presents as fulminant myocarditis with peripheral eosinophilia (65%), rash or raised liver tests, per the AHA 2020 statement.[6]
- Cardiac sarcoidosis: in suspected CS, ESC 2025 recommends CMR using tissue characterisation techniques to assess cardiac inflammation and myocardial involvement (Class I, Level B), and ¹⁸F-FDG-PET for the diagnostic work-up, including detection of inflammation, and for follow-up and assessment of therapeutic response in CS (Class I, Level B).[1]
Inflammatory cardiomyopathy
Inflammatory cardiomyopathy is chronic myocarditis with cardiac dysfunction and remodelling, and can follow a prior myocarditis, treated or untreated (ESC 2025).[1] Suspect persistent or chronic myocardial inflammation with non-ischaemic ventricular dysfunction, low QRS voltages and persistently mildly raised troponin.[1]
ESC 2025 Recommendation Table 19: Recommendations for inflammatory cardiomyopathy
| ESC 2025 row (Recommendation Table 19) | Class, Level |
|---|---|
| Guideline-directed heart failure treatments are recommended in patients with inflammatory cardiomyopathy to improve and/or stabilize left ventricular function. | I, C |
| Specific medical therapy for the potentially underlying systemic disease is recommended in inflammatory cardiomyopathy. | I, C |
| Immunosuppressive therapy, guided by endomyocardial biopsy, should be considered in virus-negative inflammatory cardiomyopathies to suppress the autoimmune response. | IIa, B |
ESC 2025 notes that only one RCT showed improved cardiac function with immunosuppression in virus-negative inflammatory cardiomyopathy, so treatment should rest on biopsy histology, immunohistology and viral PCR.[1]
Population: 85 patients with myocarditis and chronic (>6 months) heart failure unresponsive to conventional therapy, with no myocardial viral genomes
Key finding
Primary outcome 6-month improvement in LV function; the treated group showed significant improvement of LVEF and decreases in LV dimensions and volumes from baseline
- HYPIC (2025): a multicentre randomised trial of 50 patients with chronic inflammatory cardiomyopathy after fulminant myocarditis; hydroxychloroquine plus prednisolone for 12 months, against prednisolone alone, reduced a composite of cardiovascular death or transplant, HF hospitalisation or myocarditis recurrence, pacemaker or ICD implantation (HR 0.28, 95% CI 0.11–0.71).[10]
- ARCHER (2026): a phase 2 double-blind trial randomised 109 patients within 10 days of CMR-confirmed acute myocarditis to oral cannabidiol or placebo for 12 weeks; in mild-to-moderate acute myocarditis, cannabidiol did not significantly change CMR ECV or GLS, although ECV trended lower.[9]
Immune checkpoint inhibitor myocarditis
ICI myocarditis needs speed.[1] When suspected, rapid diagnostic triage is needed, usually including laboratory tests and multimodality imaging; coexisting coronary disease in older patients should not stop the myocarditis work-up, and EMB can be necessary in inconclusive cases (ESC 2025).[1]
ESC 2025 Recommendation Table 18: Recommendations for immune checkpoint inhibitor-associated myocarditis
| ESC 2025 row (Recommendation Table 18) | Class, Level |
|---|---|
| Diagnostic triage within 24 h is recommended in patients with suspected myocarditis induced by ICI to initiate treatment rapidly (footnote: see Figure 5). | I, C |
| Immediate disruption of ICI and administration of high-dosage corticosteroids are recommended in patients with ICI-associated myocarditis in order to stop the inflammatory reaction and stabilize the patient. | I, C |
| Second-line immunosuppression treatment should be considered in patients with steroid-refractory ICI-associated myocarditis. | IIa, C |
| Second-line immunosuppression treatment may be considered in patients with fulminant/severe ICI-associated myocarditis. | IIb, C |
- Corticosteroids within 24 h: after diagnosis, immediate ICI discontinuation and early corticosteroids are warranted; up to 50% are steroid-refractory and need second-line drugs (ESC 2025).[1]
- Registry signal: in a prospective registry, ruxolitinib plus high-dose abatacept with screening for respiratory muscle failure was associated with improved survival (ESC 2025).[1]
- Rechallenge has to be considered after multidisciplinary discussion of myocarditis severity, cancer prognosis, oncology options and patient preference (ESC 2025).[1]
Return to exercise and sport
During the acute stage of myocarditis, patients are advised to rest completely, since exercise has been associated with arrhythmias and sudden cardiac death (ESC 2025).[1] ESC 2025 recommends restriction of physical exercise until remission, for at least 1 month, in athletes and non-athletes after IMPS, using an individualized approach (Class I, Level C).[1]
Clinical remission sets the point of return.[1] ESC 2025 defines it as full regression of symptoms plus normal laboratory results (e.g. C-reactive protein, troponin) and investigations (ECG, pericardial effusion, CMR evidence of active inflammation).[1] Additional testing (e.g. exercise testing and Holter monitoring) is recommended in myocarditis to detect clinical remission.[1] Earlier recommendations gave arbitrary abstention periods of 3 to 6 months; the ESC 2025 Task Force recommends an individualised approach based on remission times.[1]
ESC 2025 guideline
Recommendation Table 26 and Sections 6.1, 12.5
- Restriction of physical exercise until remission, for at least 1 month, is recommended in athletes and non-athletes after IMPS, using an individualized approach, to accelerate recovery (Class I, Level C).
- A complete clinical remission should be considered in athletes and non-athletes with normalization of symptoms, biomarkers and imaging.
- CMR is recommended for follow-up at least within the first 6 months, partly to enable a return to exercise (Class I, Level C).
- Personalised exercise prescription based on the patient (athletes, non-athletes) and type of exercise.
ACC 2024 ECDP
Consensus, no class
- Stage C and D: refrain from strenuous activity or competitive sport for 3 to 6 months.
- Although the literature is limited, the prevailing suggestion is to resume exercise 3 to 6 months after myocarditis, provided symptoms have resolved. At that time it is advisable to obtain CMR (stage D or at least medium-risk stage C) or transthoracic echocardiography (low-risk stage C), a 24-hour ECG and an exercise stress test for stress-induced arrhythmias. If all are unremarkable and the patient is asymptomatic, the ECDP considers it safe to resume exercise.
- Athletes: periodic reassessment, particularly within the first 2 years.
AHA/ACC 2025 statement
Competitive athletes; considerations, no class
- Independent of LV function, competitive athletes with myocarditis should not participate in competitive sports until both symptoms and active inflammation or oedema (T2 or elevated troponin levels, or both) have resolved.
- Preserved LV function: return can be considered 4 to 6 weeks after complete resolution of symptoms if all criteria are met: inflammation or oedema resolved (CMR T2 signal or serum biomarkers) and no clinically relevant arrhythmias on ambulatory ECG monitoring and exercise testing.
- Reduced LV function at diagnosis: resumption is reasonable if all criteria are met: ≥3 months without symptoms, LV systolic function back in the normal range, inflammation or oedema resolved (CMR T2 signal or serum biomarkers), and no clinically relevant arrhythmias on ambulatory ECG monitoring and exercise testing.
The AHA/ACC statement explains its shorter window.[7] Earlier 3 to 6 month bans were based solely on expert opinion, and data from athletes after SARS-CoV-2 suggest inflammation can resolve 4 to 6 weeks after diagnosis.[7] The statement also considers continued participation reasonable in asymptomatic competitive athletes with persistent LGE suggestive of previous myocarditis if all its criteria are met (LV systolic function within the normal range; clinically relevant arrhythmias absent on ambulatory ECG monitoring and exercise testing), with continued surveillance.[7]
ESC 2025 adds that exercise restriction can affect mental health, especially in children and young adults, and freedom to exercise should be a shared decision.[1]
[5] [1] [7]Follow-up
Low-risk chest-pain myocarditis can be discharged when cardiac enzymes trend towards normal (ESC 2025).[1] Relapses occur in about 10%, with a 1-year recurrence rate of around 5%.[1] Prognosis is determined by baseline and 6-month LV function, regardless of the initial presentation.[1]
ESC 2025 Recommendation Table 15: risk stratification, complications and outcomes (myocarditis rows)
| ESC 2025 row (Recommendation Table 15) | Class, Level |
|---|---|
| Follow-up with clinical assessment, biomarkers (at least troponin), ECG, exercise test, Holter-ECG monitoring, echocardiography, and CMR at least within 6 months after the index hospitalization is recommended in all patients with myocarditis to identify a potential progression or new risk factors. | I, C |
| Long-term follow-up is recommended for patients with complicated myocarditis (Table 3 definition) to identify a potential progression or new complications. | I, C |
ESC 2025 Table 15: Follow-up in inflammatory myopericardial syndrome after discharge (selected myocarditis rows; imaging rows below)
| Myocarditis | Within 1 month | Within 3–6 months | 12 months | >1 year and long-term follow-up (a) |
|---|---|---|---|---|
| Clinical evaluation and ECG | X | X | X | X |
| Biomarkers (TnI, C-reactive protein) | X | X | (X) | (X) |
| Rhythm (stress and/or Holter-ECG) | – | X | (X) | (X) |
- All follow-ups should be adapted to the clinical situation and severity; (X) means optional testing according to clinical presentation, a case-by-case decision.[1]
- Imaging rows (TTE and CMR for myocarditis) each carry one X marked b and two marked c, governed by footnotes b and c.[1]
- Footnote a: long-term follow-up, e.g. after 2 years, is suggested only for complicated cases of IMPS, usually myocarditis.[1]
- Footnote b: in complicated cases or if abnormal at 1 month, imaging should be repeated between 3 and 6 months.[1]
- Footnote c: if abnormal at 6 months, imaging should be repeated within the next 6 months and/or in the next 12 months.[1]
- Schedule: in uncomplicated cases, follow-up at 6, 12 and 24 months is sufficient, while it should be prolonged and lifelong in complicated cases or with residuals (ESC 2025).[1]
- Exercise test at 6 months: sustained or non-sustained VT was more common after an arrhythmic presentation and was associated with later adverse events, including malignant VA (ESC 2025).[1]
The ACC 2024 ECDP, as consensus, advises imaging at 2 time points: echocardiography early, e.g. at 2–4 weeks, to catch new or progressive LV deterioration, and a second study at 6 months, CMR if not low risk.[5] It suggests a CMR at 3 months may be preferable in athletes considering return to competitive sports.[5]
[1]Prognosis
- Biopsy-diagnosed acute myocarditis: up to 50% recover spontaneously, up to 25% may have persistent stable dysfunction, and 10%–25% have progressive ventricular dysfunction that could lead to end-stage DCM, transplantation or death (ESC 2025).[1]
- Registry data quoted by ESC 2025: complicated acute myocarditis 27% (fulminant 9%); in-hospital mortality 8.5% against 0% in uncomplicated cases; transplant or death in 18% of complicated cases after 5 years.[1]
- ESC registry (581 patients): at 1 year 2.7% died, 1.7% were transplanted, 0.7% had a VAD and 3.9% received an ICD (ESC 2025).[1]
- Viral type: B19V acute myocarditis most often presents infarct-like and may have a favourable long-term prognosis, but there is evidence describing cases with severe fatal outcomes; HHV-6 myocarditis (especially with B19V co-infection) usually presents with acute HF symptoms and frequently progresses to chronic HF (ESC 2025).[1]
- Stage D in the ACC 2024 ECDP (haemodynamic instability needing inotropes/vasopressors or temporary circulatory support, or electrical instability needing intervention): patients needing mechanical circulatory or inotropic support have a 27% to 35% rate of death or transplantation in the 6 months after presentation.[5]
Special populations
- Children: the adult diagnostic approach, including CMR, applies (ESC 2025); EMB needs particular care under 1 year and with LV biopsies, where complications reach up to 30%.[1]
- Children, treatment: therapy is not well defined; one meta-analysis found IVIG not associated with better survival, while another in fulminant myocarditis concluded IVIG (usually 1–2 g/kg over 24–48 h) reduced in-hospital mortality and improved LVEF (ESC 2025).[1]
- Children, AHA 2021 statement: presentation may vary from minimal symptoms to HF, life-threatening arrhythmias or cardiogenic shock, and outcomes span full resolution to chronic HF and the need for heart transplantation, with inadequate clues to predict the course.[8]
- Pregnancy: ESC 2025 recommends pre-conception counselling in women with recurrent pericarditis or myocarditis to assess disease activity and review therapy (Class I, Level C); azathioprine and IVIG are compatible with pregnancy and breastfeeding.[1]
- Pregnancy-associated myocarditis is rare, and its incidence and prognosis vary regionally (ESC 2025).[1]
- Older adults: myocarditis is probably more often drug-related (ICIs, clozapine), and in a Swedish study HF/DCM and deaths were more common above 50 years (ESC 2025).[1]
Guidelines and where they differ
- ESC 2025 myocarditis and pericarditis is the first ESC guideline to cover myocarditis and the core source among the guidelines checked for this topic.[1]
- ESC 2026 HF defers the treatment algorithm to the 2025 guideline and states that routine immunosuppression is not recommended with preserved LVEF and should be reserved for fulminant, non-infectious forms (narrative, no class or level given).[2]
- ESC 2023 cardiomyopathies adds that EMB should be considered in suspected cardiomyopathy when other investigations suggest inflammation, infiltration or storage that cannot be identified by other means (Class IIa, Level C), and reports disease-causing DCM, NDLVC or ARVC gene variants in 8–22% of adults and children presenting with acute myocarditis; the newer ESC 2026 HF row says EMB should be considered in established HF with rapidly progressive HF despite standard therapy, or when other investigations suggest inflammation, infiltration or storage that cannot be identified by other means (Class IIa, Level C).[3][2]
- ESC 2022 VA/SCD rows still stand where 2025 does not revise them; its pre-discharge ICD row for the acute phase is dated history.[1][4]
- ACC 2024 ECDP is consensus, without classes: it proposes stages A–D, recommends that patients with stage C and D myocarditis refrain from strenuous physical activity or competitive sports for 3 to 6 months, and notes that, although existing literature is limited, the prevailing suggestion is to resume exercise 3 to 6 months after myocarditis provided that symptoms have resolved; ESC 2025 notes the ECDP also supports personalising rest to clinical remission.[5][1]
- AHA scientific statements (2020 fulminant myocarditis; 2021 children; 2025 AHA/ACC competitive sports) are each titled as a scientific statement; this topic attributes them as statements and takes no classes from them.[6][8][7]
ESC 2025 is the newest dedicated ESC myocarditis guideline among the guidelines checked for this topic (census 2026-10-09); ESC 2026 HF defers the myocarditis treatment algorithm to it.[1][2] No Australian or New Zealand myocarditis guideline was found in the census for this topic. A 2026 clinical consensus statement covers the workup and management of rhythm disorders in myocarditis and inflammatory cardiomyopathy.[12] Its title names the European Heart Rhythm Association and the Heart Failure Association of the ESC, the ESC Working Group on Myocardial & Pericardial Diseases and the European Association of Preventive Cardiology of the ESC.[12] It also names the Heart Rhythm Society, the Asian Pacific Heart Rhythm Society and the Latin American Heart Rhythm Society.[12] It organizes its consensus advice in a phase-aware framework of hot, hot-to-cold and cold phases, with statements graded by opinion-, observational- or randomized trial-based evidence and supported by formal author voting.[12] Only its PubMed abstract is held; its full text was not checked for this topic, and no recommendation on this page is taken from it.
Pitfalls
Exam pearls
- IMPS: umbrella term until the final diagnosis; myopericarditis = predominant pericarditis, perimyocarditis = predominant myocarditis (ESC 2025 Table 3).[1]
- Complicated myocarditis: acute myocarditis and ≥1 of LVEF <50% on echocardiogram, sustained VA, advanced heart block, HF or cardiogenic shock (ESC 2025 Table 3).[1]
- Updated Lake Louise: at least one T2-based plus ideally one T1-based criterion; 2/2 proven, 1/2 uncertain (ESC 2025).[1]
- EMB immunohistology: ≥14 leucocytes/mm² with ≥7 T lymphocytes/mm² has been considered the cut-off, although these criteria have been questioned by cardiopathologists (ESC 2025).[1]
- ICI myocarditis: diagnostic triage within 24 h is recommended when suspected, and immediate ICI disruption with high-dosage corticosteroids is recommended once diagnosed (ESC 2025, both Class I, Level C).[1]
- β-blockers for at least 6 months should be considered in acute myocarditis, especially with troponin elevation (ESC 2025, Class IIa, Level C).[1]
- WCD for 3–6 months should be considered after sustained VA in the acute phase as a bridge to recovery (ESC 2025, Class IIa, Level C).[1]
References12ShowHide
- [1]Schulz-Menger J, et al. 2025 ESC Guidelines for the management of myocarditis and pericarditis. Eur Heart J, 2025.PMID 40878297
- [2]Køber L, et al. 2026 ESC Guidelines for the management of heart failure. Eur Heart J, 2026.PMID 42661420
- [3]Arbelo E, et al. 2023 ESC Guidelines for the management of cardiomyopathies. Eur Heart J, 2023.PMID 37622657
- [4]Zeppenfeld K, et al. 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J, 2022.PMID 36017572
- [5]Drazner MH, et al. 2024 ACC Expert Consensus Decision Pathway on Strategies and Criteria for the Diagnosis and Management of Myocarditis: A Report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol, 2025.PMID 39665703
- [6]Kociol RD, et al. Recognition and Initial Management of Fulminant Myocarditis: A Scientific Statement From the American Heart Association. Circulation, 2020.PMID 31902242
- [7]Kim JH, et al. Clinical Considerations for Competitive Sports Participation for Athletes With Cardiovascular Abnormalities: A Scientific Statement From the American Heart Association and American College of Cardiology. J Am Coll Cardiol, 2025.PMID 39976316
- [8]Law YM, et al. Diagnosis and Management of Myocarditis in Children: A Scientific Statement From the American Heart Association. Circulation, 2021.PMID 34229446
- [9]McNamara DM, et al. Impact of cannabidiol on myocardial recovery in patients with acute myocarditis: primary results of the ARCHER study. ESC Heart Fail, 2026.PMID 41711722
- [10]He W, et al. The efficacy and safety of hydroxychloroquine in patients with chronic inflammatory cardiomyopathy: a multicenter randomized study (HYPIC trial). BMC Med, 2025.PMID 40781621
- [11]Frustaci A, et al. Randomized study on the efficacy of immunosuppressive therapy in patients with virus-negative inflammatory cardiomyopathy: the TIMIC study. Eur Heart J, 2009.PMID 19556262
- [12]Peretto G, et al. Workup and management of rhythm disorders in myocarditis and inflammatory cardiomyopathy: a clinical consensus statement of the European Heart Rhythm Association and the Heart Failure Association of the ESC, the ESC Working Group on Myocardial & Pericardial Diseases, the European Association of Preventive Cardiology of the ESC, the Heart Rhythm Society, the Asian Pacific Heart Rhythm Society, and the Latin American Heart Rhythm Society. Europace, 2026.PMID 42669046