These are the first European Society of Cardiology (ESC) integrated guidelines on myocarditis and pericarditis,1 recognizing their shared etiopathogenic basis and introducing the new concept of inflammatory myopericardial syndrome (IMPS). This umbrella term reflects the close interplay and frequent overlap between the two conditions in clinical practice (figure 1). This integrative approach offers several advantages, as it aims to enhance collaboration between expertise and research efforts in the fields of pericarditis and myocarditis, thereby paving the way for future therapeutic advances. However, merging the 2 entities has resulted in a substantially longer document, which reduces its conciseness. Given the limited available evidence, the guidelines rely largely on expert consensus-based recommendations for the contemporary management of myocarditis and pericarditis, highlighting the need for further research and more robust data.

Figure 1.

Central illustration. Main updates, concepts, and controversies in the 2025 ESC guidelines on myocarditis and pericarditis. CMR, cardiac magnetic resonance; EF, ejection fraction; EMB, endomyocardial biopsy; IL-I, interleukin-1; NSAID, nonsteroidal anti-inflammatory drug.

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The term inflammatory cardiomyopathy is formally introduced, referring to chronic myocarditis associated with cardiac dysfunction and ventricular remodeling with a hypokinetic phenotype, with or without ventricular dilation and an arrhythmogenic substrate. Notably, the document does not mention that IMPS is frequently diagnosed during the workup of myocardial infarction with nonobstructive coronary arteries (known as the MINOCA workup), missing the opportunity to refine the definition of this entity in which myocarditis is one of the most common final diagnoses.

The guidelines report incidences of 3 to 32 and 6.3 to 8.6 per 100,000 person-years for pericarditis and myocarditis, respectively, with higher rates observed in men and younger adults. They also acknowledge that asymptomatic or mild cases may lead to underestimation of the true disease burden. The causes of myocarditis and pericarditis are briefly discussed, emphasizing the predominance of viral infections in developed countries, whereas tuberculosis remains a frequent cause of pericarditis in endemic regions, particularly among individuals with HIV infection. Genetic background is increasingly recognized in IMPS, with variants in sarcomeric or desmosomal genes associated with myocarditis and autoinflammatory diseases linked to recurrent pericarditis

The term IMPS encompasses a spectrum of inflammatory conditions ranging from isolated myocarditis to isolated pericarditis, including mixed forms with features of both. The document provides clinical clues and red flags to facilitate timely recognition, as well as a practical table for risk assessment and stratification to guide diagnostic work-up. It also includes diagnostic algorithms and triage pathways for both inpatient and outpatient management.

From a temporal perspective, myocarditis is classified as acute (≤4 weeks, typically with chest pain, dyspnea, or fatigue and often following viral prodromes), subacute (weeks to months, characterized by progressive symptoms), and chronic (persistent low-grade inflammation with structural remodeling). Myocarditis is considered complicated when the left ventricular ejection fraction is <50% or when it is associated with acute heart failure, ventricular arrhythmias, or advanced atrioventricular block. The term fulminant is reserved for patients presenting with cardiogenic shock.

Pericarditis also progresses through acute, subacute, and chronic stages. Clinical forms include dry, effusive, effusive-constrictive, constrictive, transient constrictive, tamponade-associated, and polyserositis-related pericarditis. Timely differentiation between inflammatory and noninflammatory phenotypes is essential for appropriate diagnosis, management, and prognostic assessment.

An individualized diagnostic approach tailored to clinical presentation and risk stratification is recommended. Hospital admission is warranted for all patients with myocarditis and for those with high-risk pericarditis to allow appropriate monitoring, investigation, and treatment. Etiological evaluation is advised in complicated cases or when a specific cause with potential targeted therapy is suspected.

Diagnostic criteria have been substantially revised from previous documents,2,3 reflecting the guidelines’ recognition of the growing importance of CMR in IMPS. Diagnosis can now be established using the updated CMR Lake Louise criteria, which require the presence of both a T1-based and a T2-based abnormality.

Endomyocardial biopsy (EMB) remains reserved for high-risk presentations, with a strong recommendation for patients presenting with acute heart failure or cardiogenic shock. However, the indications for EMB have been expanded to include selected patients with malignant arrhythmias, conduction disorders, left ventricular ejection fraction <40%, or extensive late gadolinium enhancement (LGE) on acute-phase CMR. EMB is also recommended when a specific etiology is suspected (such as giant-cell myocarditis or cardiac sarcoidosis) or when there is no response to therapy. The guidelines update histopathological criteria, including immunohistology, and highlight the usefulness of biventricular and mapping-guided EMB to improve diagnostic yield. Molecular pathology (eg, viral polymerase chain reaction in EMB tissue) is mandatory when considering initiation of immunosuppression.

In summary, myocarditis is considered definite when a compatible clinical presentation is supported by confirmatory CMR or EMB findings. 18F-fluorodeoxyglucose positron emission tomography may be considered when CMR is inconclusive or contraindicated, particularly when cardiac sarcoidosis is suspected.

Although inflammatory markers, troponin, BNP/NT-proBNP, and echocardiography are recommended in all cases, the guidelines do not specify which laboratory tests are most informative, in contrast to the SEC-Working Group consensus.4 Routine viral or bacterial serologies are not recommended because of their low diagnostic yield. While viral polymerase chain reaction in blood may be useful in selected cases, only hepatitis C, HIV, and a limited number of bacterial serologies provide meaningful information. Computed tomography (CT) or invasive angiography is indicated only in patients with a moderate-to-high likelihood of coronary artery disease, whereas CMR is essential when coronary artery disease and myocarditis coexist.

In accordance with the recently published ACC consensus,5 a definite diagnosis of pericarditis requires a consistent clinical presentation (including typical chest pain) and at least 1 additional criterion: pericardial rub, electrocardiographic findings, C-reactive protein elevation, pericardial effusion or consistent CMR findings (pericardial edema or LGE), highlighting the diagnostic and prognostic value of CMR in pericardial disease. An interesting point is made regarding electrocardiographic changes in pericarditis: although ST-segment elevation suggests some myocardial involvement, it does not alter management, as patients with normal troponin levels and preserved left ventricular ejection fraction generally have a favorable prognosis.

Growing evidence links myocarditis with inherited cardiomyopathies, either as an initial manifestation or during follow-up. The diagnostic yield of genetic testing is particularly high in complicated myocarditis, where variants in sarcomeric and desmosomal genes have been identified. Accordingly, the guidelines recommend genetic testing (IIaB) in patients with the highest expected yield (ie, those with a family history, arrhythmic presentation, ring-like or septal LGE, persistent left ventricular systolic dysfunction, recurrent myocarditis, or sustained troponin elevation). This recommendation contrasts with the recent American College of Cardiology consensus,5 which advocates genetic testing for all patients with myocarditis.

In recurrent pericarditis, genetic testing should also be considered, as up to 15% of patients may have underlying autoinflammatory syndromes.

The treatment of myocarditis, and to a lesser extent, pericarditis, involves significant uncertainty that these guidelines do not fully resolve; however, they provide expert consensus on appropriate actions, contraindications, and areas for improvement.

In myocarditis, initial therapy should be guided by a comprehensive clinical assessment encompassing 3 elements: a) presentation type, b) severity and complications, and c) potential etiology. Unless myocarditis is fulminant or has a clearly defined etiology, initial management should be guided by symptoms, using paracetamol, aspirin, or nonsteroidal anti-inflammatory drugs (NSAID), with the addition of colchicine if symptoms of pericarditis are present to prevent recurrence (IIa). The Guidelines emphasize that immunosuppressants or corticosteroids should not be used as initial therapy but should be reserved for patients with fulminant noninfectious presentations (IIaC), refractory ventricular dysfunction (IIbC), or an autoimmune etiology. In such instances, EMB is prioritized to guide individualized treatment according to the etiologic phenotype. Similarly, antivirals should not be used as initial therapy in uncomplicated viral myocarditis, as viral replication is typically self-limited. Patients with heart failure or ventricular dysfunction should receive therapy and device management according to established heart failure guidelines. Notably, the guidelines support the withdrawal of neurohormonal therapy in patients with recovered ventricular function after 6 months (IIa C).

Surprisingly, in contrast to the ACC consensus,6 the guidelines recommend the use of beta-blockers for at least 6 months in patients with myocarditis (IIaC), regardless of ventricular function, to control symptoms and reduce arrhythmia risk. This controversial recommendation is based on a single observational study involving patients with reduced LVEF, raising reasonable doubts might about the benefit of these drugs in the broader myocarditis population.7

Rapid hemodynamic deterioration may necessitate short-term mechanical circulatory support (MCS). A timely discussion with a dedicated shock team is recommended to assess the need for escalation to MCS and determine a long-term management plan. An intra-aortic balloon pump may serve as a first-line bridge, but escalation to more advanced MCS should occur promptly if there is no improvement within a short time. Venoarterial extracorporeal membrane oxygenation is the most widely used and effective option, especially in advanced cardiogenic shock stages (SCAI stages D-E) or if biventricular dysfunction is present. In this scenario, this form of extracorporeal support offers high survival and recovery rates, making early initiation essential for optimal. Notably, in contrast to the ACC consensus,6 the document does not mention micro axial-flow left ventricular pumps, which have been successfully used in selected patients with fulminant myocarditis and predominant or exclusive left ventricular failure. Refractory cases may require long-term MCS or heart transplantation.

Arrhythmias are common in myocarditis, ranging from conduction disorders to ventricular arrhythmias. The risk of sudden cardiac death persists even after inflammation resolves. Wearable cardioverter-defibrillators are recommended for selected high-risk patients during the 3- to 6-month recovery period after acute myocarditis. Implantable cardioverter-defibrillators may be considered in persistent high-risk cases, particularly in giant-cell or cardiac sarcoid myocarditis. Catheter ablation, if needed, is best reserved for the postinflammatory phase.

For isolated pericarditis, first-line therapy consists of aspirin or NSAID combined with colchicine (IA) for at least 3 to 6 months, with colchicine being the last medication discontinued once sustained symptom remission is confirmed. Notably, the guidelines provide support for decision-making in patients with persistent or recurrent episodes. Low-to-moderate dose corticosteroids should be reserved for cases in which first-line therapy fails (IIaC). A novel recommendation is the introduction of interleukin-1 inhibitors for refractory cases (IIaC); moreover, if C-reactive protein is elevated in these patients, the recommendation is upgraded to class IA due to their effectiveness in reducing recurrences and minimizing corticosteroid use. Compared with the ACC consensus,6 which favors interleukin-1 inhibitors as the preferred strategy after NSAID-colchicine failure without prior corticosteroid therapy, these guidelines adopt a more conservative stance on these novel agents.

A specific section discusses pericardial effusion, cardiac tamponade, and constrictive pericarditis, presenting updates relative to the 2015 guidelines.2 However, the document provides 2 different algorithms for managing cardiac tamponade, which may cause confusion. Interventional strategies for pericarditis extend beyond fluid drainage to obtain samples for cytology. These procedures require high expertise and should ideally be performed at specialized centers. In constrictive pericarditis, the guidelines emphasize the diagnostic value of multimodal imaging in conjunction with inflammatory markers. In cases of newly diagnosed constriction with evidence of active inflammation, anti-inflammatory therapy is recommended to prevent progression to constriction and avoid pericardiectomy. A novel recommendation is tricuspid valve repair in patients with pericardial constriction and severe tricuspid regurgitation to improve symptoms and survival. Surgical interventions should be considered in selected conditions. Pericardiectomy, while potentially curative, carries considerable risk and should be limited to expert centers.

A dedicated chapter discusses myocardial and pericardial involvement in various systemic, predominantly immune-mediated, diseases. Emphasis is placed on interdisciplinary collaboration with specialists managing these systemic conditions to ensure diagnostic accuracy and optimize therapeutic strategies. A particularly novel contribution of the guidelines is the inclusion of a section on specific types of myocarditis, offering detailed recommendations for the diagnosis and management of these distinct etiological subtypes, including a comprehensive table outlining recommended treatment lines and dosages. The section on specific pericarditis updates the 2015 recommendations.2

Prognosis depends on the initial clinical presentation and underlying etiology, with certain multimodal imaging findings providing additional prognostic value. Biventricular dysfunction is the strongest predictor of adverse outcomes. An update in the guidelines includes the recommendation for comprehensive clinical follow-up during the first 6 months after hospitalization for myocarditis, encompassing biomarkers (C-reactive protein and troponin), electrocardiogram, Holter monitoring, exercise testing (if inflammation is absent), echocardiography, and CMR to identify persistent edema or fibrosis. For uncomplicated cases, follow-up at 6, 12, and 24 months is considered sufficient, whereas patients with complicated presentations require long-term monitoring.

Low-risk pericarditis can be managed on an outpatient basis. Clinical recovery after 4 to 6 weeks of treatment is common. Recurrence occurs in 15% to 30% of cases, while incessant pericarditis may develop in 10%. Progression to constrictive pericarditis or cardiac tamponade is rare in viral/idiopathic pericarditis (< 1%), intermediate in immune-mediated, posttraumatic, or oncologic etiologies (2%-5%), and high in bacterial pericarditis (20%-30%), particularly in purulent forms. Long-term follow-up is recommended for recurrent or incessant pericarditis.

The 2025 ESC guidelines represent a significant advance compared to the 2015 version, particularly in the sections on special considerations related to age and sex, as well as advice for patients. Pericarditis in the pediatric population shares diagnostic criteria and recurrence risk with adults, and the restriction on corticosteroid use due to its effects on growth is maintained. EMB for myocarditis in infants should be approached with caution, given its high complication rate (up to 30%). Regarding pregnancy and breastfeeding, while the previous guidelines contraindicated colchicine for pericarditis, the current document considers its use for the prevention of recurrences, although this is supported only by a class IIbC recommendation. Both guidelines advise caution with NSAID administration after the 20th week of pregnancy, as well as in elderly patients, in whom halving the colchicine dose, monitoring renal function, and assessing potential drug interactions is mandatory. In women with recurrent pericarditis or a history of myocarditis, a multidisciplinary preconception consensus (IC) is recommended.

The current document also reflects a paradigm shift in the prescription of physical activity, moving from a rigid model to an individualized approach. The duration of physical activity restrictions should initially be for 1 month and then individualized based on symptom resolution and the absence of ongoing inflammation or arrhythmias. Nevertheless, these recommendations pose challenges in our setting. Implementing flexible follow-up requires real access to biomarkers and imaging techniques, which may create inequities among different levels of care. The guidelines highlight the importance of patient counseling in IMPS, emphasizing clear, individualized education on treatment, complications, and warning signs. Special attention is given to young patients regarding activity restrictions and return to exercise or work, acknowledging the potential impact on quality of life and mental health.

Finally, consistent with the ACC consensus document,6 the guidelines highlight the need to establish multidisciplinary units in tertiary hospitals for complicated myocarditis. They also emphasize that the management of IMPS benefits from coordinated care across the healthcare system and from a structured referral network. Tertiary care centers of excellence serve as specialized hubs with advanced diagnostic tools, interventional and surgical capabilities, and expertise in complex myocarditis and pericarditis cases. These networks are essential for managing fulminant myocarditis, recurrent pericarditis, and cases requiring EMB with advanced immunohistology and molecular testing. Regional centers can manage uncomplicated diseases, but a hub-and-spoke model ensures seamless referral, communication, and continuity of care. This structure improves access to cutting-edge therapies, fosters multidisciplinary decision-making, and enhances overall outcomes. Although multidisciplinary teams are recommended for high-risk or complicated IMPS cases, it is surprising that there is no explicit mention of the advanced practice nurse in cardiology, despite their key role in symptom monitoring, early detection of complications, patient education, and care coordination while delivering cost-effective care.

Substantial gaps in evidence remain. Large-scale registries are needed to enhance understanding of the disease, particularly in specific populations and in chronic inflammatory forms. In this regard, the PREMYO project (NCT06898762) stands out in Spain, involving more than 70 centers nationwide. Furthermore, there is a need for clinical trials in complicated cases, although their low incidence hampers the achievement of adequate sample sizes. Patients with recurrent disease require particular attention to identify individual predisposition factors, including genetic testing; the management of these cases requires further research.

In summary, the 2025 ESC guidelines for the management of myocarditis and pericarditis represent an integrated framework for the care of IMPS and incorporate valuable tools to support decision-making in clinical practice. However, a significant number of recommendations rely on expert consensus, highlighting the urgent need for continued advancement of knowledge in this field through high-quality research, with the aim of improving the management of this complex disease and optimizing patient outcomes.

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No artificial intelligence was used to generate the content of this article.

The conflicts-of-interest declaration documents for all authors are available in the supplementary data.