Myocarditis and pericarditis, though distinct in pathology, frequently overlap in clinical presentation. Chest pain, arrhythmias, new-onset heart failure or tamponade may represent either disease, or a mixed picture. For decades, their management relied on tradition, observational studies and fragmented society statements.
Myocarditis remains a leading cause of sudden cardiac death in young adults and athletes, while pericarditis accounts for a large share of chest-pain presentations in the emergency room. In recent years, new scenarios (immune checkpoint inhibitor myocarditis, autoinflammatory syndromes, post-COVID sequelae) have added layers of complexity.
Against this background, the 2025 ESC Guidelines for the management of myocarditis and pericarditis mark an important milestone. For the first time, ESC places both conditions under a single umbrella document, explicitly framing them as a spectrum of Inflammatory Myopericardial Syndrome (IMPS).
This unification is also what differentiates the European approach from that of American societies. The American Heart Association (AHA) and American College of Cardiology (ACC) have historically published separate documents: a 2015 scientific statement on pericardial diseases, and more recent expert consensus pathways on myocarditis, including ICI-related cases. While the philosophies overlap (emphasis on CMR, selective biopsy, risk-stratified care) the U.S. texts maintain distinct entities, whereas the ESC has opted for a truly integrated framework. For cardiologists, this matters: many patients do not fit neatly into one box, and IMPS allows faster decisions without semantic delays.
The introduction of IMPS is more than semantics. It tells clinicians: do not waste time arguing whether this is primarily myocardial or pericardial: treat it as inflammatory heart disease until proven otherwise. This is particularly helpful in mixed forms such as myopericarditis, which often left doctors uncertain about how aggressively to treat or monitor.
By grouping these under IMPS, the guideline encourages clinicians to:
The expectation is that IMPS will harmonize practice across Europe, reduce variability, and facilitate data collection for future studies.
One of the most appreciated innovations is the presentation-driven approach. Instead of a linear work-up, the guideline proposes flowcharts that stratify patients based on presentation: acute chest pain, arrhythmia, new-onset heart failure, or tamponade.
In nearly every branch of these pathways, cardiac magnetic resonance (CMR) is the non-invasive cornerstone. Using the updated Lake Louise criteria - at least one T2-based oedema marker plus ideally one T1-based fibrosis marker (LGE, native T1, ECV) - CMR provides both sensitivity and specificity. For pericarditis, the demonstration of oedema and enhancement adds diagnostic certainty beyond clinical signs and CRP.
CMR also helps risk-stratify: extensive late gadolinium enhancement in myocarditis portends worse prognosis, while normal findings in pericarditis reassure both clinician and patient. Thus, CMR is not only diagnostic but prognostic, guiding intensity of follow-up.
Other tools retain their role but in a supporting hierarchy. Troponin is sensitive but nonspecific, as mild elevation may occur in pericarditis or systemic illness. ECG remains essential for detecting diffuse ST changes or arrhythmias but lacks specificity. Echocardiography is useful to detect pericardial effusion, LV dysfunction or wall motion abnormalities, and is often the first-line tool in emergency rooms. Nuclear imaging and PET may be helpful in selected contexts such as sarcoidosis.
The message for daily practice is simple: use ECG, troponins and echo as the frontline triage, but proceed quickly to CMR whenever available, since it provides the most decisive information.
For years, EMB was surrounded by ambiguity: some centres performed it liberally, others avoided it altogether. The 2025 guideline cuts through the uncertainty: do it when it will change management. That includes suspected giant-cell myocarditis, cardiac sarcoidosis, ICI-myocarditis, or fulminant myocarditis with rapid deterioration. In these settings, histology and immunohistochemistry can guide immunosuppression or escalation to transplant consideration.
In practical terms, consider a young patient with new heart failure, conduction block and arrhythmias, here, EMB could reveal giant-cell myocarditis, prompting immediate immunosuppression. By contrast, in a patient with mild chest pain, normal function and clear CMR findings of acute myocarditis, biopsy adds little.
This selective approach reduces unnecessary risk, aligns with resource use, and clarifies for clinicians when they should insist on referral to centres capable of EMB.
For pericarditis, the backbone remains NSAIDs plus colchicine. The guideline specifies dosing by body weight, treatment duration, and tapering strategy. Importantly, colchicine is no longer “optional” but integral.
For recurrent or incessant pericarditis, IL-1 inhibitors (anakinra or rilonacept) are recommended in refractory cases. Their formal recognition is a landmark: cardiologists can now prescribe biologics with guideline backing rather than as experimental therapy. This will likely accelerate adoption, particularly in patients debilitated by multiple relapses.
For myocarditis, urgency is paramount in fulminant cases. Rapid ICU admission, initiation of mechanical circulatory support (MCS) such as VA-ECMO or Impella, and guideline-directed medical therapy for heart failure are emphasized. Immunosuppression is reserved for biopsy-proven or highly suspected immune etiologies. This prevents indiscriminate steroid use, which in viral myocarditis may worsen outcomes.
The arrhythmic dimension receives strong attention: ventricular arrhythmias may require temporary protection with a wearable defibrillator, while ICD implantation is considered in persistent LV dysfunction beyond the acute phase. The guideline highlights careful balance: not every patient with reduced EF post-myocarditis requires an ICD; timing and recovery trends matter.
For patients, perhaps the most tangible change is the new return-to-activity framework. Gone are the blanket six-month exercise bans. Instead, return is based on clinical stability, ventricular function, normalization of biomarkers and, when available, CMR recovery.
For cardiologists, this means a more nuanced conversation: we will monitor you closely and guide you back when safe, not automatically exclude you for half a year.
Practical scenarios illustrate the change. A 25-year-old amateur footballer with uncomplicated viral pericarditis, resolved pain, normalized CRP and a clean CMR may return to training after weeks rather than months. By contrast, a professional athlete with myocarditis, extensive LGE and reduced EF will need longer restriction and staged testing before clearance.
The guideline also highlights the mental health dimension: prolonged inactivity and uncertainty can fuel anxiety and depression. Integrating psychological support into follow-up is explicitly recommended, a detail often overlooked in cardiology but welcomed by patients.
Another practical advance is the emphasis on structured follow-up. Rather than leaving patients to fragmented outpatient visits, the guideline suggests clear timelines: clinical review at 1-3 months, repeat imaging (often echo, sometimes CMR) to confirm recovery, and troponin/CRP checks if relapse is suspected.
Patients with recurrent pericarditis should have a long-term care plan, including education on early recognition of flares and clear instructions on when to seek help. Myocarditis survivors with persistent LGE require longer surveillance for arrhythmic risk, even when EF normalizes.
This systematic approach reduces missed relapses and provides patients with reassurance, improving adherence and outcomes.
The document provides practical tables for scenarios that often perplex clinicians: tuberculous pericarditis, neoplastic involvement, pregnancy, sarcoidosis and overlap with inherited cardiomyopathies. It also clarifies when to employ CT, nuclear imaging or electro-anatomical mapping.
Yet, much of the evidence remains low-grade. The guideline is transparent: many recommendations are level C, based on expert consensus. Clinicians must therefore apply judgment, balancing guidelines with patient-specific factors. Commentators stress that the value lies in standardizing a language and structure even in areas of uncertainty.
For the practicing cardiologist, these three shifts stand out. These are not abstract principles but daily decisions: who to admit, what test to order, when to biopsy, which drug to prescribe, when to allow return to play. The guideline provides clarity and consistency where previously there was heterogeneity.
The 2025 ESC guidelines for myocarditis and pericarditis deliver more than incremental updates: they provide a practical playbook. By unifying the conditions under IMPS, centring diagnosis on CMR, clarifying biopsy indications, endorsing biologics for refractory pericarditis and individualizing return-to-activity, the document speaks directly to the dilemmas cardiologists face in clinics and wards.
Compared with the American approach, where myocarditis and pericarditis remain addressed separately, the ESC text offers a unique integrated framework, one that resonates with the real world of overlapping presentations. Implementation challenges remain, especially regarding access to imaging and biologics, but the path is clearer. For clinicians, the guidelines mark a turning point; for patients, they promise more timely, individualized and hopeful care.