2025 ACC专家共识声明：心包炎的诊断和管理

2025 Concise Clinical Guidance:An ACC Expert Consensus Statement on the Diagnosis and Management of Pericarditis

A Report of the American College of Cardiology Solution Set Oversight Committee

Writing Committee

Members

Tom Kai Ming Wang, MBCHB, MD, FACC, Chair Allan L.Klein,MD,CM,FACC,Vice Chair

Paul C. Cremer, MD, FACC Massimo Imazio, MD Sarah Kohnstamm, MD, FACC

Sushil Allen Luis,MBBS,FACC Vartan Mardigyan,MD Monica Mukherjee,MD,MPH,FACC Karen Ordovas, MD, MAS Sneha Vakamudi, MD, FACC

Solution Set Oversight

Committee

Gurusher S.Panjrath,MBBS,FACC,Chair Oncol Mbe M. Bhave, MD,FACC,Immediate Past Chair*

Niti R. Aggarwal, MD, FACC*

Katie Bates, ARNP, DNP

Eugene Chung, MD, MPH, FACC

David M. Dudzinski, MD, JD, FACC

John P. Erwin III, MD, FACC*

Martha Gulati, MD, MS, FACC

Robert Hendel, MD, MACC

Dharam J. Kumbhani, MD, SM, FACC*

Chayakrit Kritanawong, MD, FACC

Barbara Wiggins, PharmD, FACC

Megan Coylewright, MD, MPH, FACC-Ex Officio

*Former SSOC members who provided oversight during the development of this document.

TABLE OF CONTENTS

PREFACE$$\begin{array}{l}\bullet\\ \end{array}$$

1.INTRODUCTION $\ldots$ 3

2. ASSUMPTIONS AND DEFINITIONS $\ldots$ $\ldots$ $\ldots$ $\ldots$ $\ldots$ $\ldots$ $\ldots$ $\ldots$ $\ldots$ $\ldots$ $\ldots$ $\ldots$ $\ldots$ $\ldots$

2.1. General Clinical

Assumptions 3

This document was approved by the American College of Cardiology Clinical Policy Approval Committee in May 2025.

The American College of Cardiology requests that this document be cited as follows: Wang TKM, Klein AL, Cremer PC, Imazio M, Kohnstamm S,Luis SA, Mardigyan V, Mukherjee M, Ordovas K, Vakamudi S, Wohlford GF. 2025 concise clinical guidance: an ACC expert consensus statement on the diagnosis and management of pericarditis: a report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol 2025;XX:XXX-XXX.

Copies: This document is available on the website of the American College of Cardiology(www.acc.org). For copies of this document, please contact the Elsevier Inc.Reprint Department, via(212) 633-3820 or e-mail(reprints@elsevier.com).

Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American College of Cardiology. Requests may be completed online via the Elsevier site(https://www.elsevier.com/about/policies/copyright/permissions).

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2.2. Definitions 3

2.3. Abbreviations $\ldots$ 3

3.SUMMARY GRAPHIC\longdots4

Figure 1. Novel Clinical and Advanced Multimodality Imaging Evaluation Guiding Therapeutics for Pericarditis 4

4. DESCRIPTION, RATIONALE, AND IMPLICATIONS... 4

4.1. General Perspectives for Pericardial Diseases. 4

4.1.1. Anatomy and Physiology 4

Figure 2. Anatomy of the Pericardium 5

4.1.2. Epidemiology and Etiologies 6

4.1.3. The Role of Inflammation in Pericardial Disease 6

Figure 3. Pathophysiology of

Pericardial Inflammation 7

4.1.4. Multimodality Imaging and Pericardial Disease 7

4.1.5. Pericardial Diseases Center of Excellence... 8 Figure 4. Framework and Components of a Pericardial Diseases Center 9

4.2. Pericarditis

4.2.1. Novel Clinical Diagnostic Criteria and Perspectives 9

4.2.2. Evaluation and Multimodality Imaging $\ldots$ 11 Figure 6. Hallmarks of Pericarditis on Cardiac Magnetic Resonance $\ldots$ 12

Figure 7. Proposed Pericardial Late Gadolinium Enhancement Grading Criteria by Cardiac Magnetic Resonance $\ldots$ 13

4.2.3. Management $\ldots$ 13 Figure 8. Proposed Schematic Algorithm for Treatment of Recurrent Pericarditis $\ldots$ 15

4.3. Complications of Pericarditis 16

4.3.1. Pericardial Effusion 16 Figure 9. Pericardial Effusion Sizing Evaluation by Echocardiography 18

4.3.2. Cardiac Tamponade and Pericardiocentesis 16 Figure 10. Echocardiography Signs of Cardiac Tamponade 19

4.3.3.Constrictive Pericarditis Figure 11. Echocardiography Features of Constrictive Pericarditis 21

Figure 12. Echocardiography Parameters and Diagnostic Algorithm and Validation for Constrictive Pericarditis 22

Figure 13. Invasive Diagnosis of Constrictive Pathophysiology.23

Figure 14. Treatment Approach for Constrictive Pericarditis 25

<BeginOfPara>4.3.4. Pericarditis in Oncologic Patients 20

5.CONCLUSIONS 25

REFERENCES 26

APPENDIX 1

Author Relationships with Industry and Other Entities(Relevant)

APPENDIX 2

Peer Reviewer Relationships with Industry and Other Entities (Comprehensive)

PREFACE

The American College of Cardiology(ACC) has a long history of developing documents(eg, decision path-ways, appropriate use criteria) to provide clinicians with guidance on both clinical and nonclinical topics relevant to cardiovascular care. In most circumstances, these documents have been created to complement clinical practice guidelines and to inform clinicians about areas where evidence is new and evolving or where sufficient data is more limited. Despite this, numerous gaps persist, highlighting the need for more streamlined and efficient processes to implement best practices in pa-tient care.

Central to the ACC's strategic plan is the generation of actionable knowledge-a concept that places emphasis on making clinical information easier to consume, share,integrate, and update. To this end, the ACC has shifted from developing isolated documents to creating inte-grated“solution sets.” These are groups of closely related activities, policy, mobile applications, decision-support tools, and other resources necessary to transform care and/or improve heart health. Solution sets address key questions facing care teams and offer practical guidance to be applied at the point of care. They use both estab-lished and emerging methods to disseminate information for cardiovascular conditions and their related manage-ment. The success of solution sets rests firmly on their ability to have a measurable impact on the delivery of care. Because solution sets reflect current evidence and ongoing gaps in care, the associated tools will be refined over time to match changing evidence and member needs.

Concise Clinical Guidance (CCG) documents are a key component of solution sets. Highly focused and limited in scope, CCGs provide recommendations where none currently exist and/or outline actions required for evi-dence to be implemented in practice for specific patient populations. CCGs aim to illustrate clinical decision-making processes using tools (ie, figures, tables, and checklists) and are limited in scope focusing on patient populations that share certain characteristics, such as

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conditions, subtypes, or lines of therapy. In some cases,covered topics will be addressed in subsequent expert consensus decision pathways, appropriate use criteria,clinical practice guidelines, and other related ACC clinical policy as the evidence base evolves. In other cases, these will serve as stand-alone policy and represent best standards.

Gurusher Panjrath,MBBS,FACC Chair,ACC Solution Set Oversight Committee

1. INTRODUCTION

Pericardial diseases represent a heterogenous spectrum of disorders, including acute and chronic inflammation of the pericardium(pericarditis), pericardial effusion,constrictive pericardits, and pericardial masses with malignant infiltration(Figure 1).1 Clinical management of pericarditis may be challenging, and consensus guidelines focusing on diagnosis, risk stratification, and treatment are vital for standardizing care, reducing variability in clinical practice, and improving patient outcomes. This CCG addresses diagnostic and thera-peutic advances in acute and recurrent pericarditis and their complications, employing a multimodality imaging-guided therapeutic approach. This document is targeted at assisting cardiologists, emergency and in-ternal medicine physicians, primary care physicians, and rheumatologists, and other physicians and cardiovas-cular care team members who manage these complex patients in the real world.

In accordance with the ACC's Relationships With In-dustry policy, relevant disclosures for the writing com-mittee and comprehensive disclosures for external peer reviewers can be found in Appendixes 1 and 2.

To ensure complete transparency, a comprehensive Relationships With Industry table for the writing com-mittee, including relationships not pertinent to this document, has been created. It is available in the Supplemental Appendix.

2. ASSUMPTIONS AND DEFINITIONS

2.1. General Clinical Assumptions

1. This CCG presumes the physician will collaborate with appropriate specialists, such as a cardiologist, phar-macist, and/or other relevant specialists(eg, rheuma-tologist, cardiac surgeon, radiologist), and/or pericardial center of excellence program members,including advanced practice providers, to guide clinical management.

2. In all cases, clinical management should be guided by evidence-based clinical judgment, with shared deci-sion-making that incorporates patient preferences and values.

3. This CCG is based on the latest pericardial evidence and literature available. At any point in time, physicians should be aware that this CCG's recommendations may be superseded by new data.

The writing committee endorses the recommendations of the document“Pericardial Diseases: International Po-sition Statement on New Concepts and Advances in Mul-timodality Cardiac Imaging" recently published in JACC:Cardiovascular Imaging, endorsed by the ACC Imaging Council and Society of Cardiovascular Magnetic Reso-nance Imaging.

2.2. Definitions

Pericarditis: Inflammation of the pericardium leading to characteristic pleuritic chest pain, which can be accom-panied by pericardial rub on auscultation, typical elec-trocardiogram changes, new or worsening pericardial effusion, and elevated inflammatory markers on labora-tory tests. See document for novel diagnostic criteria.

Pericardial effusion: Fluid accumulation in the pericardial space visible on cardiac imaging such as echocardiography.

Cardiac tamponade: Compression of the heart by abnormal fluid accumulation in the pericardial space,leading to impaired cardiac output and hemodynamic compromise.

Constrictive pericarditis: Loss of elasticity and often abnormal thickening of the pericardium, impairing dia-stolic filling and leading to heart failure syndrome. This can be transient/subacute(predominantly inflammatory and reversible) or advanced/chronic(often calcified and irreversible) constrictive pericarditis.

Effusive constrictive pericarditis: Presence of persis-tent constrictive physiology even after drainage of peri-cardial effusion.

2.3. Abbreviations

ACC= American College of Cardiology CCG= Concise Clinical Guidance CCT= cardiac computed tomography CMR=cardiac magnetic resonance CRP= C-reactive protein IL-1= interleukin-1 LGE= late gadolinium enhancement NSAID= non-steroidal anti-inflammatory drug PDC= pericardial diseases center TTE= transthoracic echocardiography

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3. SUMMARY GRAPHIC

FIGURE 1 Novel Clinical and Advanced Multimodality Imaging Evaluation Guiding Therapeutics for Pericarditis

Clinical Evaluation

1. Echo: assess pericardial effusion and constrictive physiology

2.CMR(if indicated): assess and grade pericardial thickness, inflammation, effusion and constrictive physiology

3.CCT(if indicated): assess pericardial thickness, calcification,constrictive physiology, pre-operative planning

 1. Colchicine and NSAIDs(or aspirin): first line for acute and first recurrence. Exercise restriction. If not responding,then next step(s) are:

2.Anti-IL1 agents(rilonacept, anakinira): second line for inflammatory phenotype,may consider for non-inflammatory phenotype, may consider for non-inflammatory phenotype, low-to-medium dose and slow wean

3.Steroids: second line for non-inflammatory phenotype and systemic autoimmune diseases, may consider in inflammatory phenotype, low-to-medium dose and slow wean

4. Radical pericardietomy:medically refractory pericarditis or constrictive pericarditis, at expert surgical center

5.Treat underlying etiology

<BeginOfPara>6.Consider referral to PDC, especially for complicated cases

Figure panel illustrates a pericarditis case: left image-small pericardial effusion on echocardiography; middle image-pericardial late gadolinium enhancement that indicates inflammation on CMR; right image-pericardial calcifications consistent with constrictive pericarditis on CCT. CMR= cardiac magnetic resonance; CRP= C-reactive protein; CCT= cardiac computed tomography; ECG= electrocardiogram; echo= echocardiography; ESR=erythrocyte sedimentation rate; IL= interleukin; NSAID= nonsteroidal anti-inflammatory drug.

4. DESCRIPTION, RATIONALE,AND IMPLICATIONS

4.1. General Perspectives for Pericardial Diseases

4.1.1. Anatomy and Physiology

The pericardial anatomy, through the interplay of its fibrous parietal layer and elastic visceral layer, have pivotal roles in modulating cardiac pressure-volume dynamics, ensuring optimal chamber restraint and pre-venting overexpansion during cardiac cycles.1-3 The

parietal pericardium is an outer fibrous sac lined by a single layer of mesothelial cells, which envelops the proximal great arteries, pulmonary veins, and venae cavae to form pericardial sinuses and recesses. The visceral pericardium is a serous membrane that directly covers and protects the cardiac surface. Cardiac motion is enhanced by 20 to 50 mL of serum ultrafiltrate within the pericardium, which is drained by lymphatic vessels on the epicardial and parietal surfaces into mediastinal,peribronchial, and tracheobronchial lymph nodes(Figure 2).

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FIGURE 2 Anatomy of the Pericardium

 (A) Pericardium with mediastinal pleura and epipericardial adipose tissue. Arrowheads indicate the sternopericardial ligaments.(B) Fibrous pericardium after removal of adipose tissue.(C) The fibrous pericardium is continuous with the adventitia of the aorta(Ao) and pulmonary artery(PA) superiorly(red arrowheads) and is anchored to the central tendon of the diaphragm inferior(white arrowheads).(D) Anterior(1), superior(2), and inferior(3) aortic recesses of the transverse sinus. Adapted with permission from Klein et al. ${}^{1}$ IV $=$ innominate vein; SVC= superior vena cava

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|TABLE 1|Pericardial Functions| |---|---| |Category|Specific Functions| |Mechanical|Limits short-term cardiac distention Facilitates cardiac chamber coupling and interaction Maintains pressure-volume relations of cardiac chambers and their output| |Membranous/ serosal|■Lubricates, reduces friction Equalizes gravitational, hydrostatic, and inertial forces Mechanical barrier to infection| |Metabolic|■Immunologic Vasomotor Fibrinolytic Modulates sympathetic neurotransmission and contractility| |Ligamentous|■Limits displacement of the heart Neutralizes the effects of respiration and change of body position ■Contributes to apparent compliance of the pericardium|

Adapted with permission from Klein et al.

The pericardium performs a multifaceted role in car-diac function, encompassing mechanical, membranous,metabolic, and ligamentous features(Table 1).1 The peri-cardium mechanically limits short-term cardiac disten-tion to optimize pressure-volume relationships of cardiac chambers and their output, mitigates the effects of respiration and positional changes, and enhances overall pericardial compliance.4 The pressure-volume relation-ship of the pericardium is dynamic with small increases in cardiac volume, resulting in minimal changes to intra-cavitary pressure. As volume increases above the upper limit of normal cardiac filling, there is a sharp transition where further volume increases result in disproportionate increases in pressure. The abrupt change to the pressure-volume relationship highlights the limited reserve ca-pacity and decreased compliance of the pericardial sac,restraining further cardiac expansion and resulting in ventricular interdependence. Despite the understood function of the pericardium, absence of the pericardium does not alter cardiac function, as seen in patients post-pericardietomy or with congenital absence.

4.1.2. Epidemiology and Etiologies

Pericarditis accounts for 0.1% of hospital admissions and 5% of emergency department evaluations for chest pain.1,6 Approximately 0.2% of all cardiovascular ad-missions are attributable to acute pericarditis, occurring more commonly in men aged 16 to 65 years, and declining by an estimated 51% per 10-year increase in age, although recurrent pericarditis is more common in women.Pericarditis is classified based on etiology, clinical course,morphology, and associated impact of fluid characteris-tics, size, and hemodynamics.1,7 Idiopathic and viral etiologies are the most common cause of pericarditis in

TABLE 2 Etiologies of Pericardial Diseases

|Category|Examples| |---|---| |Idiopathic|Without identifiable etiology or trigger, presumed autoinflammatory, may be viral| |Infective|Viral: coxsackieviruses, echoviruses, adenovi-ruses, parvovirus B-19, herpesviruses, HIV, COVID-19 Bacterial: Mycobacterium species, including tuberculosis,Staphylococcus, Streptococcus, Pneumococcus, Mycoplasma, Hemophilus, Neis-isa, Mycoplasma, Chlamydia, Legionlla, Leptospira, Listeria, Coxiella, Borrelia burgor-feri, Cutibacterium acnes, Trypanosoma cruzi Fungal: Candida, histoplasmosis, coccioidomycosis Protozoal: toxoplasma| |Autoimmune|• Systemic conditions: systemic lupus erythe- matosus, rheumatoid arthritis, scleroderma, systemic sclerosis, dermatomyositis, polymoxy-sitis, mixed connective tissue disease, vascu-litis, inflammatory bowel disease, sarcoidosis, Behcset disease, Still disease, immunoglobulin G4-related diseases, Erdheim-Chester disease G4-related diseases, Erdheim-Chester disease Autoinflammatory conditions: familial Mediterranean fever, tumor necrosis factor re-ceptor 1-associated periodic syndrome Drug induced: procainamide, isoniazid, hydralazine, cyclosporine| |Neoplastic|• Primary: mesothelioma, fibrosarcoma, lipoma Secondary/metastic: lung cancer, breast cancer, lymphoma, Kaposi sarcoma| |Radiation|• Radiotherapy| |Hemopericardium/Post-cardiac injury|• Postcardiotomy/thoracotomy(any cardiac or thoracic surgery) ■ Percutaneous/transcatheter procedures: catheter ablation(including epicardial access), cardiac implantable electronic devices, percu-taneous coronary intervention, transcatheter valve or congenital heart interventions, endo- myocardial biopsy| ||Trauma ■ Myocardial infarction complicated by free wall rupture ■ Aortic dissection ■ Anticoagulation| |Primary cardiac|■ Myocardial infarction(Dressler syndrome) ■ Myocarditis (perimomyocarditis and myo-pericarditis) Stress cardiomyopathy| |Congenital|■ Pericardial cysts/divectiuli ■ Congenital absence of the pericardium| |Metabolic|■ Uremia, dialysis associated ■ Endocrine: hyperthyroidism, hypothyroidism, cholesterol, anorexia| |Other|■ Amyloidosis ■ Polycystic kidney disease ■ Chylopericardium ■ Pulmonary arterial hypertension ■ Pectus excavatum ■ Other drugs including chemotherapy|

Adapted with permission from Klein et al.

high-income countries, whereas tuberculosis, often HIV-associated, is the most common cause in low-income countries. Table 2 summarizes the various etiologies of pericardial diseases.

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4.1.3. The Role of Inflammation in Pericardial Disease

Pericarditis is characterized by a severe inflammatory response to injury of the mesothelial cells of the pericar-dium, triggered by factors such as viral infections, cardiac surgery or procedures, or immune derangements. ${}^{8-10}$ The initial immune reaction is typically a result of an unre-lated stimulus that activates the inflammasome, a macromolecular cellular structure, that then activates inflammatory cytokines, such as interleukin-1β. The un-derlying etiology, whether infectious, autoimmune, or related to mechanical injury, also contributes to inflam-mation through distinct mechanisms, including the tran-scription and translation of proinflammatory genes and inflammasome components, leading to the activation of

caspase-1 and maturation of interleukin-1β and other in-flammatory cytokines. Derangements in the innate and adaptive immune response contribute to disparate clin-ical phenotypes and account for significant patient-level variability. ${}^{11}$ Dysregulated immunity is often implicated in recurrent and chronic cases, and identification of these derangements can refine targeted immunosuppressive therapies(Figure 3).

4.1.4. Multimodality Imaging and Pericardial Disease

Novel advanced multimodality imaging techniques such as echocardiography, cardiac magnetic resonance(CMR),and cardiac computed tomography(CCT) play crucial roles in diagnosis, prognosis, and management, offering

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TABLE 3 Standard Multimodality Cardiac Imaging Techniques and Protocols for Evaluating Pericardial Diseases

TTE CCT CCT Technique a) 2-dimensional echocardiography A) Axial imaging, multiplanar recon- a) Cine white-blood imaging(steady- technique volume-rendered state free precession) b) Doppler echocardiography 2) M-mode echocardiography imaging+ contrast and delayed b) Black-blood imaging(T1W or T2W turbo spin echo, fat suppression may 2) Cine white-blood imaging(St-2W images are selected b) Cine imaging(retrospective ECG c) T2-STIR Chapter gating) d) LGE imaging(fat suppression recommended)Evaluation a) Pericardial thickness PFef:location, size, fluid characteristics PFef:location, size, fluid characteristics, performance, color, fluid characteristics, conical deformaceis approach b) Cine white-blood images, IVC plethora tethering, ventricle conical deformity, pericardial formation Perciald mass characterization c) Cine white-blood images are selected e) Pierd-20: STIR CFC: IVC plethora and respiophasic septal shift, wall Chapter scattering Chamber tethering, ventricle conical deformity, pericardial Sptal bounce

Adapted with permission from Klein et al.

CCT=cardic computed tomography;CMR=cardic magnetic resonance;CP=constrictive pericarditis;CTP=cardiac tamponade;ECG=electrocardiogram;IVC=inferior vena cava;LGE=late gadolinium enhancement;PEff=pericardial effusion;STIR=short-tau inversion recovery;T;W=TT1-weighted,T2W=T2-weighted,TTE=transthoracic echocardiography.

detailed assessment of pericardial inflammation, effu-sion, and constrictive physiology-while enhancing diag-nostic precision for assessing disease activity and monitoring progression and responses to therapy.1,3,12 Table 3 shows the standard imaging techniques and pro-tocols of multimodality imaging.

4.1.5. Pericardial Diseases Center of Excellence

A pericardial diseases center(PDC) offers a structured solution to managing the complexity of pericardial dis-orders, which can otherwise strain healthcare sys-tems. ${}^{13,14}$ These centers are particularly effective in improving care and outcomes for patients with recurrent or refractory pericarditis, as well as those requiring frequent follow-ups, while reducing emergency visits and hospitalizations. Indications for referral to a specialized pericardial center include recurrent, inces-sant or chronic pericarditis, suspected or confirmed constrictive pericarditis, large or complex pericardial effusion requiring pericardial drainage or window, or

when advanced therapies, such as biologics and peri-cardiectomy, are being considered. PDCs also play a vital role in screening patients for clinical trials and moni-toring responses and adverse events of emerging treat-ments. Figure 4 summarizes the framework and key components of a PDC.

The development of such a PDC begins with a needs assessment, considering local disease prevalence,healthcare gaps, and resource availability. A well-defined protocol is critical, outlining staff re-sponsibilities, referral processes, clinical workflows, and strategies for continuous quality improvement. These centers should provide access to specialized resources,including multimodality imaging(eg, echocardiography,CMR,CCT), rheumatology, infectious diseases, genetics,consultation with cardiothoracic surgery, and specialty pharmacies. Advanced practice providers play a major role in the workflow of a PDC.14 Clear communication pathways ensure timely referrals and follow-ups,particularly for high-priority cases. Key components of

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 a PDC include comprehensive evaluations, timely im-aging and laboratory investigations, and personalized treatment plans. Patients benefit from dedicated edu-cation on self-management strategies and access to rapid interventions, which help mitigate disease flares.Follow-up schedules are adjusted based on individual patient needs, ranging from frequent visits during active phases(such as every 3 months) to less frequent visits when stable(such as every 6-12 months). Pro-tocols for medication adjustments, escalation, or tapering are also integral, ensuring effective disease management in collaboration with multidisciplinary teams. As patient volumes increase, PDCs can evolve from being part of broader cardiovascular services to standalone units, optimizing specialized care delivery.By enhancing patient outcomes and streamlining healthcare utilization, PDCs represent a valuable model

for managing these conditions within tertiary care centers.

4.2. Pericarditis

4.2.1. Novel Clinical Diagnostic Criteria and Perspectives

Based on expert consensus, we propose the following novel diagnostic criteria for pericarditis(Figure 5):

1. Pleuritic chest pain for equivalent with suggestive clinical presentation(must be present)

2. Plus≥1 additional finding(0= unlikely, 1= possible,and 2+= definitive diagnosis).

a. Pericardial friction rub(<1/3)

b. Electrocardiogram changes consisting of diffuse ST-segment elevation and/or PR-segment depres-sion(up to 60%)

c.Inflammatory biomarkers elevation(such as C-reac-tive protein[CRP], sedimentation rate)

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FIGURE 5 Novel Diagnostic Criteria and Classification by Duration for Pericarditis

Diagnosis of Pericarditis

1. Pleuritic chest pain or equivalent suggestive clinical presentation(must be present)

2.Plus at least 1 more finding(0= unlikely,1=possible,2+=definite diagnosis)a) Pericardial friction rub

b) ECG changes: diffuse ST-elevation and/or PR-segment depression

c) Inflammatory biomarkers elevation(C-reactive protein, sedimentation rate)

d) Cardiac imaging evidence of new or worsening pericardial effusion(especially echocardiography, other imaging modalities as alternative)

e) Cardiac imaging evidence of pericardial inflammation(cardiac magnetic resonance pericardial late gadolinium enhancement and/or edema,computed tomography with contrast as alternative)

Duration of Pericarditis Classification

1. Acute: Event lasting<4-6 weeks

2. Incessant: Event lasting>4 to 6 weeks without remission

3. Recurrent: New episode with signs and symptoms of pericardial inflammation after a symptom-free interval of 4 to 6 weeks

4.Chronic: Event lasting>3 months

Duration of pericarditis classification is adapted with permission from Chiabrando et al.8 ECG= electrocardiogram.

d. Cardiac imaging(especially echocardiography evi-dence) of new or worsening pericardial effusion(up to 60%)

e. Cardiac imaging evidence of pericardial inflamma-tion(especially CMR pericardial late gadolinium enhancement/edema, computed tomography as alternative)

These criteria, in comparison with the prior 2015 Eu-ropean Society of Cardiology guidelines criteria, place more emphasis on the clinical presence of classic chest pain or equivalent(typically sharp, pleuritic, relieved by sitting up or leaning forward) being necessary for diag-nosis, incorporating equally elevated inflammatory bio-markers and multimodality cardiac imaging findings of pericardial effusion and inflammation into the criteria,and dividing into categories of definite, possible, and unlikely pericarditis diagnoses. The diagnostic criteria likely perform best in patients with acute pericarditis,though can be applicable to patients with recurrences/flares.

About 15% of patients will have concomitant myocar-ditis such as peri-myocarditis(myocarditis dominant) or myo-pericarditis(pericarditis dominant), manifested by elevated markers of myocardial injury(troponin) and left

ventricular global or regional systolic dysfunction. ${}^{7,15}$ Pericarditis encompasses several conditions including a noninflammatory phenotype(low or near normal CRP,often associated with autoimmune conditions) seen in 10% to 20% of cases, and an inflammatory phenotype seen in 80% to 90% of patients. These patients with an in-flammatory phenotype and elevated CRP can present with high fever, neutrophilic leukocytosis, and pericardial and/or pleural effusions. ${}^{16,17}$ If treated with appropriate anti-inflammatory therapies, most acute pericarditis cases will have a benign course and resolve without recurrence.Risk factors for a poor prognosis and/or need for hospi-talization include high fevers, subacute course, presence of large pericardial effusion with echocardiography fea-tures of tamponade physiology, failure to respond to nonsteroidal anti-inflammatory drugs(NSAIDs), as well as concomitant myocarditis. ${}^{1}$

Acute pericarditis refers to the diagnosis with full res-olution of symptoms within 4 weeks. Recurrent pericar-ditis is diagnosed when there is a relapse of symptoms following a symptom-free interval of≥4 to 6 weeks after the initial flare, with completion of medical therapy.Recurrence rates after an initial episode vary from 15% to 30% and further increase to 50% after a first recur-rence.7,15 Risk factors for recurrence include a lack of

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response to NSAIDs, early use of corticosteroids, high CRP, and severe pericardial LGE on CMR.18 Patients who do not achieve remission and have symptoms for>4 to 6 weeks but<3 months before resolution no longer have acute pericarditis, and are labeled as having incessant pericarditis, which can be more aggressive, whereas chronic pericarditis requires>3 months of symptoms. As with acute pericarditis, the presentation of recurrent or incessant/chronic pericarditis can be either inflammatory or noninflammatory, a distinction that significantly in-fluences therapeutic approaches.

4.2.2. Evaluation and Multimodality Imaging

Evaluation starts with a thorough history, physical ex-amination, electrocardiogram, and laboratory tests,especially elevation in sedimentation rate and CRP, along with troponin levels if myocarditis is suspected(Figure 5).In the presence of personal and family history or risk factors of infections, autoimmune diseases, or malig-nancies, associated investigations should be performed.1 Multimodality cardiac imaging has become a crucial pillar in the evaluation of pericarditis. Transthoracic echocardiography(TTE) remains the first-line imaging modality for assessing suspected pericarditis.1.3 Although often normal, pericarditis findings on TTE may include presence of pericardial effusion(without or with tampo-nade), pericardial thickening, features of constrictive physiology,and/or myocardial involvement in the setting of myo-pericarditis(such as left ventricular systolic impairment and/or regional wall motion abnormalities)(Table 4).1 TTE can be serially used to monitor for improvement or worsening of these abnormal findings when present(Table 5). TTE's main limitation is the inability of tissue characterization to identify and grade pericardial inflammation. TTE will also provide additional information regarding cardiac chamber size and function,valvular abnormalities, pulmonary hypertension, and aortic diseases. Transesophageal echocardiography and stress echocardiography are not generally required for diagnosing pericarditis.

CMR has become a valuable comprehensive second-line imaging modality in the diagnosis, risk stratifica-tion, and surveillance(including response to therapy) of pericarditis.19 CMR should be considered in patients with acute complicated, incessant, recurrent, or chronic peri-carditis, especially when diagnostic uncertainties exist;patients who do not respond to standard first-line thera-pies and/or in whom escalation of therapies is planned;and patients with suspected pericardial complications such as complex effusions and/or constrictive physiology(Table 5).1 The main CMR findings of pericarditis include pericardial late gadolinium enhancement on phase-sensitivity inversion recovery sequence(ideally fat-

TABLE 4 Characteristic Imaging Features in Pericarditis

|TTE|CCT|CMR| |---|---|---| |■ Normal findings in some patients. Peri--cardial thickening|■ Noncalcified peri-cardial thickening|■ Thickening of pericardium at T1-weighted BB images(>3 mm)| |■ Segmental wall mo- tion abnormalities or pathological myocardial strain values(in case of myocarditis)|■ Enhancement of the thickened visceral and parietal surface of the pericardial sac at late postcontrast CT scan|Enhancement of pericardium on LGE sequence (inflammation) and T2-STIR sequence (edema) consistent with active inflam- mation and neo- vascularization(of prognostic importance) LGE+/T2-STIR+: acute/subacute phase or recurrent flares ● LGE+/T2-STIR-: subacute or chronic phase ● LGE-/T2-STIR-: resolu- tion or end-stage/ calcific phase| |■ Feff with or without 40%-50% of cases)|■ PEff presence. CT attenuation values of the PEff may help distinguish between exudative and tran-sudative fluid(on noncontrast CT)|■ PEff presence. High signal intensity on T1-weighted BB images is suggestive of exudative PEffs| |■ Sign of CP(of often transient)||■ Loss of the normal sliding between pericardial layers during the cardiac cycle is one feature consistent with pericarditis| |Dapted with permission from Klein et al.1 BB= black-blood; CCT=cardiac computed tomography;CMR=cardiac magnetic resonance; CP= constrictive pericarditis; CT= computed tomography; LGE= late gadolinium enhancement; Peff= pericardial effusion; T2-STIR= T2-short tau inversion recovery; TTE=transthoracic echocardiography.|||

Adapted with permission from Klein et al.

BB=black-blood;CCT=cardiac computed tomography;CMR=cardiac magnetic resonance;CP=constrictive pericarditis;CT=computed tomography;LGE=late gadolinium enhancement; Peff= pericardial effusion; T2-STIR=T2-short tau inversion recovery;TTE=transthoracic echocardiography.

suppressed) indicating neovascularization/inflammation(Figure 6, and new grading criteria Figure 7), increased pericardial signal on T2-short tau inversion recovery sequence indicating edema, pericardial thickening(>3 mm) especially on black-blood spin echo sequence, and pericardial effusion, whilst features of constructive phys-iology may also be observed(Table 4).1,19 With adequate treatment leading to resolution of the acute pericarditis flare, pericardial edema disappears and pericardial effu-sion and constriction may improve, whereas pericardial late gadolinium enhancement lags behind clinical improvement and typically decreases but not entirely resolves into the chronic phase in those with recurrent,incessant, or chronic pericarditis, before disappearing either after a longer period of resolution or in patients with burned out calcific constrictive pericarditis.1,20

CCT is the preferred modality in the assessment of pericardial calcifications in constrictive pericarditis. Other

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Recommendations for Diagnostic Evaluation,TABLE 5 Multimodality Cardiac Imaging, and Management for Pericarditis|Recommendation|s of Pericarditis

Adapted with permission from Klein et al.

CCT= cardiac computed tomography; CMR= cardiac magnetic resonance; ECG=electrocardiogram; IL-1= interleukin-1; LGE= late gadolinium enhancement; NSAID=nonsteroidal anti-inflammatory drug; TTE= transthoracic echocardiography.

FIGURE 6 Hallmarks of Pericarditis on Cardiac Magnetic Resonance A 0 B B C

CCT findings in pericarditis may include the presence of pericardial effusion, thickening, and inflammation on delayed contrast sequence(although less accurate than CMR)(Table 4).1,3 While CCT is not primarily used for diagnosing pericarditis, it can be valuable for preopera-tive planning in cardiac surgeries, such as peri-cardiectomy. Additionally, CCT is more useful in assessing other differential diagnoses of chest pain, such as acute aortic syndromes, pulmonary embolism, and coronary artery disease, although disadvantages include radiation exposure and, when iodinated contrast is used,

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FIGURE 7 Proposed Pericardial Late Gadolinium Enhancement Grading Criteria by Cardiac Magnetic Resonance

A

Qualitative Assessment of LGE Severity

 None

 None No pericardial enhancement

Trivial

Enhancement present, but not reaching mild criteria

C

Mild

 ●≥50% circumferential extent,<3 slices,<3mm OR

●<50% circumferential extent,<3 slices,>3 mm

Moderate

 ●≥50% circumferential extent,3 slices OR>3mm(not both);

OR

●<50% circumferential extent,3 slices,AND>3mm OR

D

Severe

 Severe

●≥50% circumferential extent,3 slices AND>3mm

Pericardial LGE severity grading criteria on CMR PSIR-LGE sequence(fat-suppressed sequence suggested), based on pericardial enhancement thickness and circumferential extent on short-axis imaging at basal, mid, and apical slices. Adapted with permission from Klein et al.1 CMR= cardiac magnetic resonance;LGE=late gadolinium enhancement; PSIR-LGE= phase-sensitive inversion recovery late gadolinium enhancement.

risks of kidney disease and contrast allergy. Use of nuclear imaging such as fludeoxyglucose-positron emission to-mography for assessing pericarditis is currently limited to the research setting or in patients who cannot have CMR(ie,claustrophobia,dagolinium allergy,severe obesity).21

4.2.3. Management

Contemporary management of pericarditis aims to control symptoms and prevent complications(mainly recurrences) and hospitalizations.22 First-line pharmaco-logical treatment includes dual anti-inflammatory ther-apy with colchicine(3 months following first flare,≥6 months following first recurrence) and NSAIDs or aspirin(starting at high dose and tapering after symptoms resolve and inflammatory markers normalize)(Tables 5

and 6). Acid suppression therapies(eg, proton-pump in-hibitors) are often concomitantly prescribed with NSAIDs for gastric protection.1 Exercise restriction for≥1 month(maximal heart rate<100 beats/min with physical activ-ity) until clinical remission is important.3 Increased heart rate can trigger pericardial inflammation by enhancing the frequency of friction of pericardial layers. In patients with autoimmune pericarditis, the focus should be on treating the underlying autoimmune condition first, as the pericarditis often improves or resolves with that alone. Hospital admission may be necessary in compli-cated high-risk cases, such as large pericardial effusion and/or tamponade, severe pain refractory to first-line therapies, and symptomatic constrictive pericarditis. Of note, prompt diagnosis and therapy are recommended for

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TABLE 6 Common Therapeutic Options for Acute Pericarditis and Recurrent Pericarditis

|Therapy|Dosing|Duration*|Tapering|Monitoring|LOE| |---|---|---|---|---|---| |Aspirin|500-1,000 mg 3 times daily|wks(acute) to mo(recurrent)|Weekly|Needed|A| |Ibuprofen|600-800 mg 3 times daily|wks(acute) to mo(recurrent)|Weekly|Needed|A| |Indomethacin|25-50 mg 3 times daily|wks(acute) to mo(recurrent)|Weekly|Needed|B| |Colchicine,1|0.6 mg twice daily or 0.6 mg once daily (<70 kg, severe renal/hepatic impairment)|3 mo(acute), 6-12 mo(recurrent)|May be considered|Needed|A| |Prednisone#|0.2-0.5 mg/kg/d|wks to mo|Several mo|Needed|B| |Anti-IL-1 agents**|||||| |Anakinra|1-2 mg/kg/d up to 100 mg/d in adults|>12 mo|Needed|Needed|A| |Riloncept|320 mg once followed by 160 mg weekly|>12 mo|Stopping vs tapering under investigation|Needed|A| |Goflikice(Not yet available in United States)|80 mg every 2 wks|>12 mo(under investigation)|Unknown|Needed|B| |Azathioprine|Starting with 1 mg/kg per d then gradually increased to 2-3 mg/kg/d|Several mo|Several mo|Needed|C| |IVIG|400 to 500 mg/kg IV daily for 5 d|5 d|Not required|Needed|C| |Radical pericardiectomy|High-volume pericidal surgical centers|Not applicable|Not applicable|Needed|C|

Adapted with permission from Klein et al.

*Therapy duration at initial dosing; duration of therapy is until clinical remission(typically longer times for recurrent cases).Thmonitoring is mandatory for all medications and may include assessment of blood count, renal function, creatine kinase, liver enzymes, lipid pro

tMonitoring is mandatory for all medications and may include assessment of blood count, renal function, creatine kinase, liver enzymes, lipid profile, and echocardiography, along with C-reactive protein and sedimentation rate to monitor pericarditis response to therapy or diagnose recurrence.

$A=A\text{. Data derived from multiple randomized clinical trials or meta-analyses. B= Data derived from a single randomized clinical trial or large nonrandomized studies(in this review, a}$$study with≥100 patients is considered"large").C=Consensus of opinion of experts and/or small studies, retrospective studies, and registries.

$5 lbupenprosin and aspirin are common first-level treatments for the first episode of pericaditis(acute pericaditis) associated with colchicine for 3 months(usually longer times for recurrent cases). Aspirin often considered when patients are already on or have another indication to be on aspirin. Aspirin can be given as 325-650 mg 3 times daily.

||In patients with a relative contraindication to NSAIDs(S such as heart failure, chronic kidney disease, peptic ulcer disease, bleeding diathesis or cancer-related hypercoagulability, or when coprescribing with diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, calcineurin inhibitors or anticoagulants), NSAIDs should be prescribed at the lowest effective dose and for the shortest duration possible, and alternatives should be considered(such as high-dose aspirin in those without elevated bleeding risk).

Dose reductions(0.3-0.6 mg daily) should be considered when coprescribing colchicine with potent inhibitors of P-glycrotein(P-gp) and/or cytochrome P450 3A4(CYP3A4) to improve tolerability and reduce the risk of toxicity. Of note, dose reduction for drug-drug interactions was not evaluated in colchicine pericarditis clinical trials. Adjusting concomitant medications(via therapeutic substitutions that avoid P-gp or CYP3A4 interactions) can also be considered to maximize the tolerated dose of colchicine prescribed."Increased risk of recurrence if used in first episode pericarditis.

**Before starting anti-IL-1 agents, patients should be screened to be negative for hepatitis, human immunodeficiency virus, and tuberculosis.

IL-1=interleukin-1;IV=intravenous;IVIG=intravenous immunoglobulin;LOE=Level of Evidence;NSAID=nonsteroidal anti-inflammatory drug.

pericarditis following cardiac procedures, as they are often underdiagnosed or misdiagnosed. Anti-inflammatory prophylaxis, such as colchicine, can be considered to prevent post-cardiac injury pericarditis,although data supporting this approach are limited.

Traditionally, for patients deemed to be nonresponders to first-line dual therapy(experiencing recurrence or intolerance to treatment with first-line agents), cortico-steroids were added to the treatment regimen. Low to moderate doses of corticosteroids(eg, prednisone 0.2-0.5 mg/kg/day) are initiated and maintained until clinical remission, followed by a slow tapering over months(Table 5).22 Corticosteroids are prescribed with caution because of the plethora of known side effects, such as weight gain, hypertension, hyperglycemia, osteoporosis,

increased risk of infections, gastrointestinal ulcers, and risk of adrenal suppression. Pharmacological prophylaxis for pneumostasis pneumoniae and osteoporosis should be considered for patients requiring glucocorticoid doses equivalent to>20 mg of prednisone for 1 month or longer.

Anti-interleuk-in(anti-IL-1) agents have been demon-strated in several recent phase 3 randomized clinical trials to have strong efficacy in pericarditis patients with elevated CRP(>1 mg/dL or>10 mg/L) to achieving clinical remission, improve symptoms, reduce recurrences, and normalize inflammatory markers while maintaining good safety profile. ${}^{1,24-26}$ As a result, there has been a recent paradigm shift in managing patients with the inflammatory phenotype(fever and/or elevation of CRP and/or CMR im-aging evidence of pericardial inflammation) who meet the

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 aforementioned indications for corticosteroids or have become steroid-dependent, for the initiation of novel therapies targeted at the autoinflammatory process. These agents should be considered the preferred option over corticosteroids in this setting(Figure 8). Typically, other anti-inflammatories may be sequentially weaned off once established on anti-IL-1 agents(such as prednisone, then NSAID, then colchicine), although colchicine may some-times be continued, with some limited evidence for addi-tive or synergistic benefits, further reducing recurrence compared with using an anti-IL-1 agent alone, particularly with anakinra. 27,28 The optimal treatment duration with anti-IL-1 therapies remains uncertain, as recurrence rates are very low while on treatment, and many patients(~50%-75%) have recurrence upon discontinuation. A recently published long-term extension of the RHAPSODY(Rilonace in Acute Pericarditis Study) trial25 supports prolonged therapy beyond 18 months to achieve a better and prolonged control of the disease, ${}^{29}$ and further research is necessary to determine the optimal treatment duration and stopping or weaning method for each anti-IL-1 agent. In contrast, low-dose corticosteroids are typically

utilized for patients lacking evidence of the inflammatory phenotype, as autoimmune mechanisms are presumed to play a more significant role in these patients(Table 5 and Figure 8).

Azathioprine and intravenous immunoglobulins may also be considered for patients who fail corticosteroids and anti-IL-1 agents.30 Radical pericardiectomy on car-diopulmonary bypass can be considered as a last resort or alternative option at high-volume experienced pericardial surgical centers, especially when patients fail to respond to the aforementioned pharmacotheries, have contra-indications to conventional therapy, or desire pregnancy.In this setting, anti-inflammatory medications, including corticosteroids and/or anti-IL-1 agents, may be continued until surgery to dampen inflammation as much as possible, and may be continued for 3 to 6 months as indicated for ongoing symptoms of pericardial inflam-mation or active inflammation noted on the pericardial pathology. Novel risk scores including machine learning models have been developed to help with risk prognos-tication of recurrent pericarditis flares to guide management.31

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4.3. Complications of Pericarditis

4.3.1. Pericardial Effusion

Pericardial effusion is defined by the accumulation of>50 mL of fluid in the pericardial space and can be a result of numerous pathologies.3,7 Approximately one-half of pericardial effusions are idiopathic, and in North America and Western Europe, postviral infection is the most common identifiable cause, whereas tuberculosis is the most common cause in places where it is endemic(Table 2).30,32 Malignancies are also an important cause of pericardial effusion and can present as an inflammatory effusion with negative cytology for cancer.33,34

The objectives of imaging pericardial effusions are to support diagnosis, evaluate the size and location of the effusion, assess its hemodynamic impact, and inform decisions regarding drainage, if indicated(Tables 7 and 8).1 TTE is the first-line imaging investigation because it is readily available and accurately achieves these objectives). The size of a pericardial effusion is determined by measuring the greatest diameter perpen-dicular to the epicardium and parietal pericardium at end-diastole or-systole adjacent to ventricles and atria, respectively, with the following categories: trivial

(<1.0 cm and not visualized throughout cardiac cycle),small(<1.0 cm), moderate(1.0-1.9 cm), large(2.0-2.5 cm),and very large(>2.5 cm)(Figure 9).3 Common mimickers of a pericardial effusion echocardiography are a left pleural effusion, which is posterior to the descending thoracic aorta on a parasternal long-axis view, and an epicardial fat pad, which has a heterogenous echodensity,moves with the myocardium, and is often located anterior to the right ventricle.

CCT is a second-line investigation, and potential ad-vantages include further delineation of the size and extent of a pericardial effusion, characterizing pericardial fluid based on Hounsfield units, informing secondary causes such as malignancy, and guiding drainage(Tables 7 to 9).1,35 CMR imaging is also a second-line investigation that has the additional advantage of assessing for peri-cardial inflammation and constriction(Tables 7 to 9).19

4.3.2. Cardiac Tamponade and Pericardiocentesis

The hemodynamic consequences of a pericardial effusion are more closely related to the rapidity of fluid accumu-lation within the pericardium, not the absolute fluid vol-ume because pericardial compliance can increase when

TABLE 7 Multimodality Imaging Protocols for Pericardial Effusions

|Echocardiography|Echocardiography|CCT|CCT|CMR| |---|---|---|---|---| |2D with respirometer||Noncontrast ECG-gated(single phase)||Cine white-blood imaging±tagging| |Size and characterize PEFF in multiple projection ±-aff-axis views||Distinguish mimickers||Detect and size PEFF| |Right ventricle diastolic chamber collapse with CTP||Detect pericardial calcification or hemorrhage||Distinguish mimickers| |Respirophasic septal shift and IVC dilatation with CTP,||||Evaluate for ECP and TCP(free-| |CP,E and TCP||||breathing sequence)| |Identify pocket with clear path of vital structures for||||Assess pericardial thickness and| |pericofrontesis||||identify adhesions(tagging)| |M-mode with respirometer||Arterial ECG-gated(single or multiphase)||T1W BB(±T1 mapping)| |Higher sensitivity for diastolic chamber collapse with CTP||Detect, size, and characterize content of Peff||Detect and characterize PEff| |Higher sensitivity for respiprohasic septal shift with CTP,||Identify secondary causes and mimickers||Identify secondary causes and mimickers| |ECP, and TCP||Evaluate pericardial thickness||| |Doppler with respirometer|± delayed ECG-gated(single phase)||T2-STIR|| |Respirophasic changes in atrioventricular and hepatic vein|Detect pericardial inflammation||Detect and characterize PEff|| |velocities with CTP,ECP, and TCP||Evaluate for acute bleeding with contrast||Evaluate for pericardial edema| |±3D echocardiography||extravasation into pericardium||Evaluate for myocardial edema| |±incremental value in PEFi|zing and spatial relationship||LGE|| |with surrounding structures||||and inflammation| |±improved visualization of pericardial adhesions/strands in||||Evaluate for pericardial malignancies| |complex PEff|||||

Adapted with permission from Klein et al. ${}^{1}$

2D=2-dimensional;3D=3-dimensional;BB=black-blood;CC=cardiac computed tomography;CMR=cardiac magnetic resonance;CTP=cardiac tamponade;ECG=elec trocardiogram;ECP=efusive constrictive pericarditis;IVC=inferior vena cava;LGE=late gadolinium enhancement;PEFF=pericardial effusion;STIR=short tau inversion recovery;$$T_{1},W=T_{1}\text{-weighted;}T_{2}W=T_{2}\text{-weighted;}TCP=\text{transient constrictive pericarditis.}$$

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TABLE 8 Multimodality Cardiac Imaging Indications, Characterization, and Added Value for Evaluating Pericardial Effusions

|Imaging Modality|Echocardiography|CCT|CMR| |---|---|---|---| |Indications|■ First-line imaging|■ Second-line if echocardiography inconclusive, or suspects second- ary causes|Second-line if echocardiography inconclusive, or suspects pericarditis, pericardial malig- nancy, and/or CP| |PEff characterization|■ Transudate: anechoic, homogenous, free flowing ■ Exudate/complex: echogenic, heterogenous ± loculations, stranding or adhesions|Transudate: 0-20 HU Exudate: 0-20 HU Hemorrhagic:>50-60 H U If very high HU: pericardial leakage of contrast (eg, ruptured aortic dissection) ■ Chylous:-60 to -80 HU|Transdate(homogenous): Low Si on T1W or T2W BB High Si on TW2/cine white-blood T, time >3,015 ms (1.5-T) Jet-black on LGE PSIR Exudate/complex(nonhomogenous): Intermediate/mixed Si on T1W or T2W BB T1 time<3,015 ms (1.5-T) Acute hemorrhagic: High Si in T1W or T2W BB Subsume hemorrhagic: Intermediate Si in T1W or T2W BB Chronic hemorrhagic: Low Si in T1W or T2W BB| |Added value|Evaluate for coexisting CTP or ECP Guide pericardiocentesis Guide pericardiocentesis TEE useful in detecting focal CTP (eg, post-cardiac surgery)|■ Identify secondary causes and mimickers minickers UFF focal TCP stability patients) May identify pericardial inflamma- tion with late iodine enhancement CT-guided pericardiocentesis in challenging cases|Evaluate for coexisting pericarditis Evaluat for constriction if echocardiography equivocal Use useful when suspecting pericardial malignancy Assess for loculated PEff/focal CTP (stable patients) (stable patients)|

Adapted with permission from Klein et al.1

BB=black-blood;CCT=cardic computed tomography;CMR=cardiac magnetic resonance;CP=strictive pericarditis;CT=cardiac tamopade;ECP=effusive constrictive pericarditis; HU= Hounsfield units; LGE= late gadolinium enhancement; Peff= pericardial effusion; PSIR= phase-sensitive inversion-recovery; S1= signal intensity; $T_{1} W=T_{1}$ -weighted; $T_{2} W=T_{2}$ -weighted; $T_{1} C=$ transient constrictive pericarditis; TEE= transesophageal echocardiography.

effusions slowly develop.32 When pericardial reserve volume is exhausted, additional pericardial fluid results in a marked increase in pericardial pressure with increased and equalized end-diastolic intracardiac pres-sures.36 Cardiac output may be maintained initially by a compensatory sinus tachycardia prior to hemodynamic deterioration, and other clinical features include pulsus paradoxus, and hypotension in most but not all cases.Echocardiography is essential in suspected cardiac tam-ponade, and clinical correlation with symptoms, heart rate, and blood pressure are vital. A dilated inferior vena cava(>2.1 cm) with minimal or no respiratory variation is a useful tool to screen for tamponate(high sensitivity)but does not confirm it, whereas diastolic right ventricular collapse is the most specific finding. Right atrial inversion beyond one-third of the cardiac cycle and marked respi-ratory variation in ventricular inflow(trans-mitral>30%and trans-tricuspid>60%) are also features of cardiac tamponade(Figure 10).3

Pericardiocentesis is therapeutically performed in cases of impending or established cardiac tamopale,especially in urgent or emergency settings with echocar-diography guidance, and diagnostically when there is concern for specific causes, such as bacterial, tubercu-lous, or malignant etiologies.7 In patients with an inflammatory pericardial effusion and no concern for

tamponade, anti-inflammatory therapy should be pur-sued prior to pericardiocentesis. Anatomical approaches to pericardiocentesis include subxiphoid, apical, and parasternal. In an emergency, a subxiphoid or apical approach is preferred. Otherwise, the approach should be determined by where pericardial fluid is most accessible with the least likelihood of damaging intervening vital structures. Echocardiography, fluoroscopy, and/or computed tomography may be utilized to guide the peri-cardiocentesis procedure. Surgical creation of a pericar-dial window is considered in select patients with recurrent large pericardial effusions and/or cardiac tam-ponade despite prior pericardiocentesis. In certain rare cases, radical pericardiectomy surgery may be indicated for recurrent pericardial effusions, even following the creation of a pericardial window, especially when there is concomitant medically refractory constructive pericarditis or pericarditis.

4.3.3. Constrictive Pericarditis

Constrictive pathophysiology arises from a loss of peri-cardial elasticity, which impairs diastolic ventricular filling and presents as a heart failure syndrome, typically with normal ejection fraction.1,37 This condition can be caused by irreversible pericardial thickening and fibrosis,termed chronic constrictive pericarditis, or from

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FIGURE 9 Pericardial Effusion Sizing Evaluation by Echocardiography

 Representative(A) small,(B) moderate,and(C) large Peffs(*).Representative(D) simple Peff with fibrin strands,(E) exudative Peff, and(F) malignant Peff(*) caused by pericardial mesothelioma. Adapted with permission from Klein et al.1 Peff= pericardial effusion; TTE= transthoracic echocardiography.

significant pericardial inflammation, termed transient constrictive pericarditis. This distinction is crucial, as the former usually requires surgical radical pericardiotomy,whereas the latter may resolve spontaneously or with anti-inflammatory therapy given for 3 to 6 months. ${}^{38}$ In areas where tuberculosis is endemic, it is the most com-mon cause of constrictive pericarditis. ${}^{39}$ Outside of this setting, the most common cause is idiopathic, followed by post-cardiac surgery and prior mediastinal radiation. ${}^{1}$

Effusive constrictive pericarditis is a distinct entity defined as persistent constrictive pathophysiology after drainage of a pericardial effusion. Classically, this phe-nomenon was diagnosed invasively by a failure of the right atrial pressure(or pericardial pressure) to decrease following pericardiocentesis and is attributed to marked

inflammation of the visceral pericardium.40 Currently,this condition is often diagnosed based on features of constrictive pathophysiology with echocardiography that appear after pericardial effusion drainage.41

The primary objectives of imaging here are to identify constrictive pathophysiology and to assess the presence and severity of pericardial inflammation. Echocardiogra-phy and CMR imaging play complementary roles, with echocardiography serving as the primary and initial mo-dality, whereas CMR offers the most comprehensive assessment of pericardial inflammation.42 The predomi-nant hemodynamic features of constrictive pathophysi-ology are dissociation of intrathoracic and intracardiac pressures during respiration with resultant accentuated interventricular dependence and elevated diastolic filling

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|Recommendations for Multimodality Cardiac|| |---|---| |TABLE 9|Imaging Evaluation and Management for Pericardial Effusions and Cardiac Tamponade| |Recommendation|Recommendation| |TTE to identify pericardial effusion and assess for cardiac tamponade|Recommended| |CCT/CMR or transesophageal echocardiogram to confirm Recommended of pericardial effusion when clinically indicated if TTE inconclusive|| |CCT/CMR to assess for secondary causes of pericardial effusion When clinically indicated when clinically indicated|| |CCT/CMR for routine assessment of cardiac tamponade|| |Transesophageal echocardiogram/CCT to confirm clinical diagnosis of focal cardiac tamponade in cases of high suspicion with unrevealing/equivocal TTE|| |TTE for surveillance of pericardial effusion(at least moderate in size)|| |Pericardiocentesis for cardiac tamponade|Recommended| |Pericardiocentesis for pericardial effusion without tamponade|Not recommended| |Pericardial window after prior pericardiocentesis for recurrent large pericardial effusion and cardiac tamponade|Reasonable|

Adapted with permission from Klein et al.

$$\text{CCT}=\text{ cardiac computed tomography; CMR}=\text{ cardiac magnetic resonance;}$$TTE= transthoracic echocardiography.

pressures in right- and left-side cardiac chambers. On echocardiography, this hemodynamic abnormality results in shift of the interventricular septum to the left with inspiration, an E-wave predominant mitral inflow pattern,an elevated medial e' tissue Doppler velocity, a plethoric inferior vena cava, and late-diastolic flow expiratory reversal in the hepatic veins(Tables 10 and 11, Figures 11 and 12). 43,44

With CMR imaging, early inspiratory septal shift during a free-breathing nine-ce-blood acquisition is indicative of constrictive pathophysiology. Pericardial thickness is also readily assessed. Inflammation is characterized based on whether there is increased pericardial signal on T2-short tau inversion recovery imaging indicative of edema and late gadolinium enhancement compatible with neovascularization and inflammation. CCT evaluates pericardial calcifications and defines thoracic anatomy before pericardiac picture, particularly the relationship be-tween cardiovascular structures and the sternum(Tables 10 and 11).1 If clinical and imaging data are incongruent, a detailed invasive hemodynamic evalua-tion should be performed with right and left heart cath-eterization, including an assessment for respiratory

FIGURE 10 Echocardiography Signs of Cardiac Tamponade

 (A) TTE in parasternal long-axis view featuring moderate-to-large PEff(*).(B) Parasternal long-axis and short-axis views demonstrate end-diastolic right ventricular free wall collapse. Significant respirophasic tricuspid (C) and mitral (D) inflow velocity variation is noted, and there is a plethoric IVC (E). Adapted with permission from Klein et al. ${}^{1}$ Exp = expiration; Insp =inspiration; IVC =inferior vena cava; PEff = pericardial effusion; TTE = transthoracic echocardiography.

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TABLE 10 Multimodality Imaging Features of Constrictive Pericarditis TTE CCT CMR Respirathic ventric- ■Increased pericardial ular dependence/septal pericardial thickness ■Respirophasic ventric-■E-wave predominant Pericardial LV filling with respir- calcification free breathing cine or phasic variation Dilatedinao inferior vena]■Wall tethering and cava with<50%collapse</td> <td></td> <td></td> <td></td> </tr> <tr> <td></td> <td></td> <td></td> <td></td> </tr> <tr> <td></td> <td></td> <td></td> <td></td> </tr> <tr> <td></td> <td></td> <td></td> <td></td> </tr> <tr> <td></td> <td></td> <td></td> <td></td> </tr> <tr> <td></td> <td></td> <td></td> <td></td> </tr> <tr> <td></td> <td></td> <td></td> <td></td> </tr> <tr> <td></td> <td></td> <td></td> <td></td> </tr> <tr> <td></td> <td></td> <td></td> <td></td> </tr> <tr> <td></td> <td></td> <td></td> <td></td> </tr> <tr> <td></td> <td></td> <td></td> <td></td> </tr> <tr> <td></td> <td></td> <td></td> <td></td> </tr> </table>

No single isolated imaging finding is diagnostic of CP; a constellation of findings in conjunction with clinical features of CP is required to make the diagnosis. Adapted with permission from Klein et al.'

CCT= cardiac computed tomography;CMR= cardiac magnetic resonance;CP=constrictive pericarditis; LGE= late gadolinium enhancement; LV= left ventricular;STIR= short tau inversion recovery; TCP= transient constrictive pericarditis; TTE=transthoracic echocardiography.

discordance in left and right ventricular systolic pressures using systolic area index(Figure 13). ${}^{45,46}$ Table 12 com-pares the characteristics of constrictive pericarditis with cardiac tamponade and restrictive cardiomyopathy.

For patients with underlying pericardial inflammation as in transient constriction, anti-inflammatory therapy should be initiated before considering pericardietomy(Figure 14). ${}^{48}$ This approach may resolve the constrictive pathophysiology, or if pericardietomy remains indicated,facilitates a more successful surgery on a less-inflamed pericardium. ${}^{38}$ In tuberculous constrictive pericarditis,antituberculous therapy may resolve constrictive patho-physiology, and corticosteroids may enhance clinical improvement. ${}^{49}$ In patients with chronic constrictive pericarditis and heart failure, diuretic therapy can treat volume overload but does not alter the natural history,Goal-directed heart failure therapy may be implemented,

Table 11 Recommendations for Multimodality Cardiac Imaging Evaluation and Management for Constrictive Pericarditis

|Recommendation|Class| |---|---| |Noninvasive hemodynamic assessment by TTE for the diagnosis of constrictive pericarditis and effusive constructive pericarditis|Recommended| |CMR to provide supportive evidence of constrictive pericarditis, especially when TTE inconclusive|Reasonable| |CMR to identify pericardial inflammation as an etiology of for constrictive pericarditis|Recommended| |CCT to identify pericardial calcifications as supplementary evidence for constriction, and for preoperative pericardectomy surgery|Reasonable| |Invasive cardiac catheterization for the diagnosis of constrictive pericarditis, where noninvasive methods are nondiagnostic or equivocal|Recommended| |First-line treatment of inflammatory constrictive pericarditis with anti-inflammatory therapy|Recommended| |Duires for symptomatic treatment of constrictive pericarditis|Reasonable| |Radical surgical pericardectomy for noninflammatory constrictive pericarditis and inflammatory constrictive pericarditis anti-inflammatory therapy|Recommended| |Partial anterior and/or diaphragmatic pericardiectomy for constrictive pericarditis|Not recommended| |Partial anterior and/diaphragmatic pericardiectomy for constrictive pericarditis|Not recommended|

Adapted with permission from Klein et al.

$$\text{ CMR}=\text{ cardiac magnetic resonance; CCT}=\text{ cardiac computed tomography; TTE}=$$transthoracic echocardiography.

although evidence is limited. Surgical radical peri-paridctomy is preferred, with resection of the entire pericardium-including anterior, diaphragmatic and pos-terior segments-on cardiopulmonary bypass, and should be performed at experienced tertiary surgical centers for optimal clinical outcomes. ${}^{38}$

4.3.4. Pericarditis in Oncologic Patients

Pericardial involvement in the setting of known malig-nancy can occur with direct spread or hematologic or lymphatic dissemination.50 Most pericardial metastases are identified as part of a staging chest computed to-mography or positron emission tomography-computed tomography study. Frequently, the presence of new pericardial effusion or nodularity in staging imaging studies is the first clue for pericardial malignant involvement. The presence of hemorrhagic or complex pericardial effusion increases the likelihood of pericardial metastasis in that setting. Symptoms of pericardial metastasis, if present, are related to associated pericardial

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21

FIGURE 11 Echocardiography Features of Constrictive Pericarditis

 (A) M-mode subcostal view showing dilated IVC measuring 2.7 cm with<50% collapse.(B) Tissue Doppler of mitral annulus lateral e' lower than medial e',indicating annulus reversus.(C) Parasternal ventricular short-axis view with respiratory interventicular septal shift(arrow).(D) Apical 4-chamber view with pericardial calcifications and tethering at the lateral to mitral and tricuspid annulus(white arrows); and left ventricle cylindrical(yellow arrow) and right ventricle conical(red arrow) deformities.(E) Mitral valve inflow pulsed-wave Doppler indicating significant>25% resiprophasic variation.(F) Hepatic vein pulsed-wave Doppler indicating expiratory end-diastolic reversal flow velocity/forward flow velocity≥0.8. Adapted with permission from Klein et al.| Exp= expiration; Insp= inspiration IVC= inferior vena cava.

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Diagnosis and Management of Pericarditis

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FIGURE 12 Echocardiography Parameters and Diagnostic Algorithm and Validation for Constrictive Pericarditis

 ||Sensitivity|Specificity|PPV|NPV| |---|---|---|---|---| |①|94%|73%|93%|77%| |②|81%|91%|97%|58%| |③|71%|79%|93%|45%| |④|73%|66%|86%|42%| |① and|80%|96%|99%|58%| |① with both|2 and 4|67%|99%|100%|

Adapted with permission from Klein et al.1 NPV= negative predictive value; PPV= positive predictive value.

effusion or pericarditis. When pericardial involvement is suspected, the main role of imaging is to confirm the presence of metastases and to identify associated com-plications, including pericarditis, hemorrhage, CP, and

hemodynamic consequence of pericardial tumor infiltra-tion. Table 13 lists imaging findings of pericardial manifestations associated with malignancy by echocar-diography, computed tomography, and CMR. Cardiac

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FIGURE 13 Invasive Diagnosis of Constrictive Pathophysiology

 imaging, especially CMR, also plays a critical role in differentiating pericardial masses, including cysts,diverticulum, and complex effusions; benign tumors such as lipomas, fibromas, hemangiomas, and teratomas; and malignant tumors, such as mesothelioma, sarcoma, lym-phoma, or metastases.

Pericarditis may be another first manifestation of malignancy involving the pericardium; however, peri-carditis is more frequently related to the oncologic treat-ment in these patients.50 Infectious pericarditis may be seen in immunosuppressed patients, and the etiology in this setting is different than in noncologic patients.

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Clinical Features,Test Results, and Management of Cardiac Tamponade, Constrictive Pericarditis, and Restrictive Cardiomyopathy

|Features|Cardiac Tamponade|Constrictive Pericarditis|Restrictive Cardiomyopathy| |---|---|---|---| |Physical examination|Tachycardia ■|↑ JVP with prominent x and y descents ■|↑ JVP with prominent y and attenuated x descents ■ Kussmaul's sign ■ Kussmaul's sign| ||Pulsus paradoxus ↑ JVP with prominent x and absent y descent ■ Muffled heart sounds|Pericardial knock ■ Ascites ■ Peripheral edema|■ Kussmaul's sign ■ Third heart sound (S3) Peripheral edema| |ECG|Tachycardia ■ Low voltage amplitude ■ Electrical alternans|No pathognomonic features ■ Low voltage amplitude Atrial fibrillation|No pathognomonic features Atrial fibrillation| |Chest x-ray|↑ Cardiac silhouette|Pericardial calcification seen in one-third of patients|No pericardial calcification| |Echocardiography|■ Pericardial effusion ■ Cardiac chamber compression or collapse ■ Respirophasic ventricular interdependence by 2D and M-mode ■Respiprophasic ventricular interdependence by 2D and M-mode ■Respiprophasic variation in interdependence by 2D and M-mode ■Respiprophasic variation in mitral and tricuspid inflow Doppler ■Amitral annular e'velocities annular e'velocities ■Adlinulus reversal ■ Dilated inferior vena cava ■ Dilated inferior vena cava Dilated inferior vena cava Dilated inferior vena cava Dilated|||

*While mild pericardial late gadolinium enhancement may be present in constrictive pericarditis due to pericardial fibrosis, the presence of significant pericardial late gadolinium enhancement and/or pericardial edema on T2 short tau inversion recovery imaging suggests the presence of transient constructive pericarditis secondary to pericardial inflammation.tln patients with pericardial inflammation by inflammatory markers or cardiac magnetic resonance imaging, consider a trial of anti-inflammatory therapy as first-line therapy and proceed to surgical pericardectomy if this fails to resolve constrictive physiology.

JVP=jugular venous pressure; RA=right atrial.

Fungal and bacterial etiologies have a higher prevalence in this population compared with that of nonconologic patients. Inflammatory pericarditis and concomitant myocarditis are commonly associated with chemotherapy and immunotherapy and may be subclinical or cause significant symptoms. In patients undergoing radiation

treatment, pericarditis and CP are notable complications when radiation field includes or is near the pericardium.

Pericarditis treatment in oncologic patients is tailored to the underlying etiology and is aimed at providing symptomatic relief and achieving hemodynamic stability.Although treatment of pericarditis is this setting should

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 follow general recommendations, it should be adapted to the goals of care of each patient. Improvement of the underlying disease is generally associated with improve-ment of the pericardial inflammation. When pericarditis is related to the oncologic treatment, discontinuation or alternative drug regimen may be necessary to alleviate symptoms. Treatment of large pericardial effusions to alleviate symptoms with pericardiocentis, and some-times with pericardial window given recurrences, are options in advanced stages of disease. ${}^{51}$

5. CONCLUSIONS

Pericarditis remains a challenging and heterogenous condition not infrequently encountered in clinical

practice. A novel diagnostic criteria for pericarditis has been devised, consisting of pericarditic chest pain with 5 additional criteria( $0=$ unlikely pericarditis, 1=possible pericarditis, 2+= definite diagnosis). These criteria include clinical findings of pericardial rub, ECG changes, new or worsening pericardial effusions, sero-logic findings of elevated inflammatory markers, and imaging findings of pericardial inflammation on CMR or CT.

Multimodality cardiac imaging-including echocardi-ography,CCT,and CMR-play a critical and complimen-tary role in the diagnosis, risk stratification, treatment guidance, and surveillance of pericarditis. Recent ad-vances in targeted biologic therapies have led to a para-digm shift, positioning these agents as second-line

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TABLE 13 Pericarditis in Oncologic Patients

|TTE|TTE|CCT|CMR| |---|---|---|---| |May identify nodular pericardial thickening or|Nodular pericardial thickening and enhancement|Pericardial nodular thickening with intermediate to high Sl on|| |pericardial masses when malignant involvement||on contrast-enhanced CCT is highly indicative of pericardial metastasis|TTW with contrast enhancement after gadolinium If large mass, used to characterize the size, tissue characteristics, and relationship with adjacent structures| |If large mass, used to characterize hemodynamic impairment|If large mass, used to characterize the size and relationship with adjacent structures|and relationship with adjacent structures|Best method to identify cardiac involvement characterized by abnormal Si of the myocardium adjacent to pericardial lesion, and lack of normal sliding on cine white-blood images| |Best modality for evaluating calcified structures|||| |Segmental wall motion abnormalities or|Enhancement of the thickened visceral and parietal surfaces of the pericardium, best seen on|Pericardial inflammation diagnosed by enhancement of|| |pathological myocardial strain values(in case of associated myocarditis)|surfaces of the pericardium, best seen on|pericardium on LGE sequence(inflammation) or T2-STIR sequence(edema)|| |PEff presence and volume||PEff presence and volume|PEff presence and volume High S1 on T1-weighted BB images and intermediate intensity on| |Abnormal echogenicity suggestive of||may help distinguish between exudative,|cine white-blood is suggestive of exudative PEffs| |Best method to identify signs of tamponade||hemorrhagic, and transudative fluid|Hemorrhagic effusion can be characterized and imaging| |Evaluate features of CP physiology||May be useful to guide intervention or surgery|appearance depends on acuity of bleeding: ■ Acute: high SI in T1W or T2W BB| |||when indicated|■ Evaluate: intermediate SI in T1W or T2W BB|

BB=black-blood; CMR= cardiac magnetic resonance; CCT= cardiac computed tomography; CP= constrictive pericardis; CT= computed tomography; LGE= late gadolinium enhancement; PEff= pericardial effusion; Sl= signal intensity; T1,W= T-weighted; T2-STIR= T2-short tau inversion recovery; T2W= T2-weighted; TTE= transthoracic echocardiography.

treatments after traditional first-line anti-inflammatory therapies, as reflected in new treatment algorithms. PDC are excellent multi-disciplinary destinations for referrals,management of complex cases, education, and research.

This CGG aims to guide clinicians to optimize evalua-tion and management of patients with pericarditis, with the goal of improving clinical outcomes.

PRESIDENT AND STAFF

American College of Cardiology

Christopher M. Kramer, MD, FACC

Cathen C. Gates, Chief Executive Officer

Richard J. Kovacs, MMD, MACC, Chief Medical Officer Brendan Mullen, Senior Executive Vice President

Amy Dearborn, Team Leader, Decision Science

Ashleigh M. Congress, MA, Team Leader, Decision Sci-ence Delivery

Alan Shinkar, MPH, Project Manager, Decision Science Delivery

Grace D. Ronan, Senior Production and Operations Manager, Clinical Policy Publications

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$$\text{JACC VOL.}\blacksquare\text{NO.}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}\blacksquare\text{2025}

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incidence, associated findings, and natural history.JACC Cardiovasc Imaging. 2018;11:534-541.

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43. Qamruddin S, Alkharabsheh SK, Sato K, et al.Differentiating constriction from restriction(from the Mayo Clinic echocardiographic criteria). Am J Cardiol.2019;124:932-938.

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KEY WORDS ACC Concise Clinical Guidance,anti-inflammatory agents, computed tomography, constrictive pericarditis,echocardiography,magnetic resonance imaging,pericardial effusion, pericarditis, pericardium

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APPENDIX 1. AUTHOR RELATIONSHIPS WITH INDUSTRY AND OTHER ENTITIES(RELEVANT)-2025 CONCISE CLINICAL GUIDANCE: AN ACC EXPERT CONSENSUS STATEMENT ON THE DIAGNOSIS AND MANAGEMENT OF PERICARDITIS

|Committee Member|Committee Member|Employment|Consultant|Speakers Bureau|Ownership/ Principal|Personal Research|Institutional, Organizational, or Other Financial Benefit|Expert Witness| |---|---|---|---|---|---|---|---|---| |Tom Kai Ming Wang(Chair)|Cleveland Clinic Center for the Diagnosis and Treatment of Pericardial Diseases, Section of Cardiovascular Imaging, Department of Cardiovascular Medicine, Heart, Vascular and Thoracic Institute-Assistant Professor of Medicine|None|None|None|None|None|None|None| |Tom Kai Ming Wang(Chair)||None|None|None|None|None|None|None| |Allan L. Klein (Vice Chair)|Cleveland Clinic Center for the Diagnosis and Treatment of Pericardial Diseases, Section of Cardiovascular Imaging, Department of Cardiovascular Medicine, Heart, Vascular and Thoracic Institute-Based Professor of Medicine|■ Cardiol Therapeutics ● Kiniksa* PfzerVenty|None|None|■ Kiniksa↑ Ventyxt|■ Pericarditis Alliance|None|| |Paul C. Cremer|Northwestern University Feinberg School of Medicine, Department of Medicine, Division of Cardiology, Bluhm Cardiovascular Institute- Associate Professor of Medicine|■ Cardiol Therapeutics of Kiniksa ■ Monte Rosa Therapeutics ■$ Pzer|None|None|None|None|None|None| |Massimo Imazio|University of Udine, Cardiothoracic Department, University Hospital Santa Maria della Misericordia, ASUFC, and Department of Medicine- Chief of Cardiology and Professor of Medicine|None|None|None|None|$$\blacksquare$$|Monte Rosa Therapeutics|None| |Sarah|University of Michigan, Division of Cardiovascular|Cardiol|None|None|None||None|None| |Kohnstamm|Diseases, Department of Internal Medicine- Clinical Assistant Professor of Medicine|||||||| |Sushil Allen Luis|Mayo Clinic, Division of Structural Heart Disease, Department of Cardiovascular Medicine, Associate Professor of Medicine|■ Cardiol|None|None|None|■|Pericarditis Alliance|None| |Sushil Allen Luis||||||||| |Vartan Mardigyan|McGill University Health Centre, Assistant Professor of Medicine|None|None|None|None|None|None|None| |Monica Mukherjee|Johns Hopkins University School of Medicine- Associate Professor of Medicine|None|None|None|None|None|None|None| |Karen Ordovas|University of Washington-Professor of Medicine|None|None|None|None|None|None|None| |Sneha Vakamudi|University of Texas at Austin Dell Medical School- Ascension Texas Cardiovascular-Assistant Professor of Medicine|■ Abbott ■ Bristol Myers Squibb|None|None|None|None|None|None| |George F. Wohlford|UVA Health, Department of Pharmacy Services- Cardiovascular Pharmacsturist|None|None|None|None|None|None|None|

This table represents the relationships of committee members with industry and other entities that were determined to be relevant to this document. These relationships were reviewed and updated in conjunction with all meetings and/or conference calls of the writing committee during the document development process. The table does not necessarily reflect relationships with industry at the time of publication. A person is deemed to have a significant interest in a business if the interest represents ownership of≥5% of the voting stock or share of the business entity or ownership of≥5,000 of the fair market value of the business entity; or if funds received by the person from the business entity exceed 5% of the person's gross income for the previous year. Relationships that exist with no financial benefit are also included for the purpose of transparency. Relationships in this table are modest unless otherwise noted. According to the ACC, a person has a relevant relationship IF: a) the relationship or interest relates to the same or similar subject matter, intellectual property or asset, topic, or issue addressed in the document; b) the company/entity(with whom the relationship exists) makes a drug, drug class, or device addressed in the document or makes a competing drug or device addressed in the document; or c) the person or a member of the person's household, has a reasonable potential for financial, professional, or other personal gain or loss as a result of the issues/content addressed in the document.

*Significant relationship.

tNo financial benefit.

ACC=American College of Cardiology; ASUFC= Azienda Sanaria Universitaria Friuli centrale; SOBI=Swedish Open Bulivitrum AB; UVA, University of Virginia.

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Wang et al Diagnosis and Management of Pericarditis

APPENDIX 2. PEER REVIEWER RELATIONSHIPS WITH INDUSTRY AND OTHER ENTITIES(COMPREHENSIVE)-2025 CONCISE CLINICAL GUIDANCE: AN ACC EXPERT CONSENSUS STATEMENT ON THE DIAGNOSIS AND MANAGEMENT OF PERICARDITIS

|Reviewer Representation Employment Consultant Speaker/ Ownership/ Personal/ International, Expert|||||||| |---|---|---|---|---|---|---|---| |Antonio Abbate|Content Reviewer-ACC Expert|University of Virginia-Professor of Medicine|Cardiol Kiniksa' Monte Rosa Therapeutics Novo Nordisk|None|None|Personal Research|Non| |Syed W. Haider|Content Reviewer-ACC Expert|Medstar Health-Attending Cardiologist|None|None|None|None|None| |David Lin|Content Reviewer-ACC Expert|Allina Health-Cardologist|None|None|None|None|$$\blacksquare$$| |Gurusher S. Panjath|Content Reviewer-ACC Expert|Goldward-Director,Heart Failure and Mechanical Support Program|Bridge Bio $^{*}$ CVR*|Alnylam Pfizer*|Allnyam Pfizer|None|None| |Britty Weber|Content Reviewer-ACC Expert|Brigham and Women's Hospital- Director,Cardio-Rheumatology Clinic,Associate Physician in Prevention Cardiology|Kiniksa' Nordisk|None|None|AHA ASNC"|None|

This table includes all relationships with industry and other entities that were reported by reviewers at the time this document was under review, including those not considered relevant to the document.The table does not necessarily reflect relationships with industry at the time of publication.A person is deemed to have a significant interest in a business if the interest represents ownership of≥5% of the voting stock or share of the business entity, or ownership of≥5,000 of the fair market value of the business entity; or if funds received by the person from the business entity exceed 5% of the person's gross income for the previous year. Relationships that exist with no financial benefit are also included for the purpose of transparency. Relationships in this table are modest unless otherwise noted. Please refer to https://www.acc.org/Guidelines/About-Guidelines-and-Clinical-Documents/Relationships-with-Industry-Policy for definitions of disclosure categories or additional information about the ACC Disclosure Policy for Writing Committees.

*Significant relationship.

+Relationship with this company is limited to enrolling patients in clinical trials. This disclosure was entered under the Clinical Trial Enroller category in the ACC's disclosure system.To appear in this category, the author acknowledges that there is no direct or institutional relationship with the trial sponsor as defined in the ACC Disclosure Policy for Writing Committees.

ACC=American College of Cardiology; AHA=American Heart Association; ASC=American Society of Nuclear Cardiology; NIH=National Institutes of Health.