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

George F. Wohlford, PHARMD

Solution Set

Oversight

Committee

Gurusher S. Panjrath, MBBS, FACC, Chair

Nicole 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 Krittanawong, 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 ............................................ 2

1. INTRODUCTION .................................... 3

2. ASSUMPTIONS AND DEFINITIONS .................... 3

2.1. General Clinical

Assumptions ................................... 3

ISSN 0735-1097/$36.00 https://doi.org/10.1016/j.jacc.2025.05.023

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.

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JACC VOL. -, NO. -, 2025

ª 2025 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION

PUBLISHED BY ELSEVIER

2.2. Definitions .................................. 3

2.3. Abbreviations ............................... 3

3. SUMMARY GRAPHIC ............................ 4

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 ................................ 9

4.2.1. Novel Clinical Diagnostic Criteria

and Perspectives ....................... 9

Figure 5. Novel Diagnostic Criteria and

Classification by Duration for Pericarditis ..... 10

4.2.2. Evaluation and Multimodality Imaging .... 11

Figure 6. Hallmarks of Pericarditis on

Cardiac Magnetic Resonance .............. 12

Figure 7. Proposed Pericardial Late Gadolinium

Enhancement Grading Criteria by Cardiac

Magnetic Resonance ..................... 13

4.2.3. Management .......................... 13

Figure 8. Proposed Schematic Algorithm for

Treatment of Recurrent Pericarditis ......... 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 ................ 17

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

4.3.4. Pericarditis in Oncologic Patients ......... 20

5. CONCLUSIONS ................................ 25

REFERENCES ................................... 26

APPENDIX 1

Author Relationships with Industry and Other Entities

(Relevant) ..................................... 28

APPENDIX 2

Peer Reviewer Relationships with Industry and

Other Entities (Comprehensive) ................... 29

PREFACE

The American College of Cardiology (ACC) has a long

history of developing documents (eg, decision pathways, 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 patient 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 integrated “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 established and emerging methods to disseminate information

for cardiovascular conditions and their related management. 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 evidence to be implemented in practice for specific patient

populations. CCGs aim to illustrate clinical decisionmaking 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 pericarditis, 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 therapeutic 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 internal medicine physicians, primary care physicians,

rheumatologists, and other physicians and cardiovascular care team members who manage these complex

patients in the real world.

In accordance with the ACC’s Relationships With Industry policy, relevant disclosures for the writing committee 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 committee, 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, pharmacist, and/or other relevant specialists (eg, rheumatologist, 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 decision-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 Position Statement on New Concepts and Advances in Multimodality Cardiac Imaging” recently published in JACC:

Cardiovascular Imaging, endorsed by the ACC Imaging

Council and Society of Cardiovascular Magnetic Resonance Imaging.1

2.2. Definitions

Pericarditis: Inflammation of the pericardium leading to

characteristic pleuritic chest pain, which can be accompanied by pericardial rub on auscultation, typical electrocardiogram changes, new or worsening pericardial

effusion, and elevated inflammatory markers on laboratory 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 diastolic 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 persistent constrictive physiology even after drainage of pericardial effusion.

2.3. Abbreviations

ACC ¼ American College of Cardiology

CCG ¼ Concise Clinical Guidance

CCT ¼ cardiac computed tomography

CMR ¼ cardiac magnetic resonance

CRP ¼ C-reactive protein

IL-1 ¼ interleukin-1

LGE ¼ late gadolinium enhancement

NSAID ¼ non-steroidal anti-inflammatory drug

PDC ¼ pericardial diseases center

TTE ¼ transthoracic echocardiography

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3. SUMMARY GRAPHIC

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 preventing 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).

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

1. Pleuritic chest pain or equivalent suggestive presentation

2. Plus ≥1 additional finding (0 = unlikely, 1 = possible, and

 2+ = definite diagnosis)

 a) Pericardial friction rub

 b) ECG changes (diffuse ST-elevation, PR-depression)

 c) Inflammatory biomarkers elevation (CRP, ESR)

 d) Cardiac imaging evidence of new or worsening

 pericardial effusion (echo preferred, CMR, CCT)

 e) Cardiac imaging evidence of pericardial

 inflammation (CMR preferred, CCT)

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, anakinra): second line for

 inflammatory phenotype, may consider for non-inflammatory

 phenotype

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 pericardiectomy: medically refractory pericarditis

 or constrictive pericarditis, at expert surgical center

5. Treat underlying etiology

6. Consider referral to PDC, especially for complicated cases

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

Clinical Evaluation Multi-Modality Imaging Management

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 ¼ cardiac

magnetic resonance; CRP ¼ C-reactive protein; CCT ¼ cardiac computed tomography; ECG ¼ electrocardiogram; echo ¼ echocardiography; ESR ¼

erythrocyte sedimentation rate; IL ¼ interleukin; NSAID ¼ nonsteroidal anti-inflammatory drug.

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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 inferiorly (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 ¼ innominate vein; SVC ¼ superior vena cava.

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The pericardium performs a multifaceted role in cardiac function, encompassing mechanical, membranous,

metabolic, and ligamentous features (Table 1).1 The pericardium mechanically limits short-term cardiac distention 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 relationship of the pericardium is dynamic with small increases in

cardiac volume, resulting in minimal changes to intracavitary 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 capacity 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 postpericardiectomy 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.1,5,6 Approximately 0.2% of all cardiovascular admissions 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 characteristics, size, and hemodynamics.1,7 Idiopathic and viral

etiologies are the most common cause of pericarditis in

high-income countries, whereas tuberculosis, often HIVassociated, is the most common cause in low-income

countries. Table 2 summarizes the various etiologies of

pericardial diseases.

TABLE 2 Etiologies of Pericardial Diseases

Category Examples

Idiopathic n Without identifiable etiology or trigger,

presumed autoinflammatory, may be viral

Infective n Viral: coxsackieviruses, echoviruses, adenoviruses, parvovirus B-19, herpesviruses, HIV,

COVID-19

n Bacterial: Mycobacterium species, including

tuberculosis, Staphylococcus, Streptococcus,

Pneumococcus, Mycoplasma, Hemophilus, Neisseria, Mycoplasma, Chlamydia, Legionella,

Leptospira, Listeria, Coxiella, Borrelia burgdorferi, Cutibacterium acnes, Trypanosoma cruzi

n Fungal: Candida, histoplasmosis,

coccidioidomycosis

n Protozoal: toxoplasma

Autoimmune n Systemic conditions: systemic lupus erythematosus, rheumatoid arthritis, scleroderma,

systemic sclerosis, dermatomyositis, polymyositis, mixed connective tissue disease, vasculitis, inflammatory bowel disease, sarcoidosis,

Behçet disease, Still disease, immunoglobulin

G4–related diseases, Erdheim-Chester disease

n Autoinflammatory conditions: familial

Mediterranean fever, tumor necrosis factor receptor 1–associated periodic syndrome

n Drug induced: procainamide, isoniazid,

hydralazine, cyclosporine

Neoplastic n Primary: mesothelioma, fibrosarcoma, lipoma

n Secondary/metastatic: lung cancer, breast

cancer, lymphoma, Kaposi sarcoma

Radiation n Radiotherapy

Hemopericardium/Postcardiac injury

n Postcardiotomy/thoracotomy (any cardiac or

thoracic surgery)

n Percutaneous/transcatheter procedures:

catheter ablation (including epicardial access),

cardiac implantable electronic devices, percutaneous coronary intervention, transcatheter

valve or congenital heart interventions, endomyocardial biopsy

n Trauma

n Myocardial infarction complicated by free wall

rupture

n Aortic dissection

n Anticoagulation

Primary cardiac n Myocardial infarction (Dressler syndrome)

n Myocarditis (perimyocarditis and

myo-pericarditis)

n Stress cardiomyopathy

Congenital n Pericardial cysts/diverticuli

n Congenital absence of the pericardium

Metabolic n Uremia, dialysis associated

n Endocrine: hyperthyroidism, hypothyroidism,

cholesterol, anorexia

Other n Amyloidosis

n Polycystic kidney disease

n Chylopericardium

n Pulmonary arterial hypertension

n Pectus excavatum

n Other drugs including chemotherapy

Adapted with permission from Klein et al.1

TABLE 1 Pericardial Functions

Category Specific Functions

Mechanical n Limits short-term cardiac distention

n Facilitates cardiac chamber coupling and interaction

n Maintains pressure–volume relations of

cardiac chambers and their output

Membranous/

serosal

n Lubricates, reduces friction

n Equalizes gravitational, hydrostatic, and inertial forces

n Mechanical barrier to infection

Metabolic n Immunologic

n Vasomotor

n Fibrinolytic

n Modulates sympathetic neurotransmission and

contractility

Ligamentous n Limits displacement of the heart

n Neutralizes the effects of respiration and change of

body position

n Contributes to apparent compliance of the

pericardium

Adapted with permission from Klein et al.1

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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 pericardium, 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 unrelated stimulus that activates the inflammasome, a

macromolecular cellular structure, that then activates

inflammatory cytokines, such as interleukin-1b. The underlying etiology, whether infectious, autoimmune, or

related to mechanical injury, also contributes to inflammation through distinct mechanisms, including the transcription and translation of proinflammatory genes and

inflammasome components, leading to the activation of

caspase-1 and maturation of interleukin-1b and other inflammatory cytokines. Derangements in the innate and

adaptive immune response contribute to disparate clinical 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

FIGURE 3 Pathophysiology of Pericardial Inflammation

Mesothelial Cell

ANAKINRA

RILONACEPT

IL-1 IL-1

IL-1

IL-1

PAMPs CORTICOSTEROIDS

DAMPs

DAMPs

TLRs

IL-1R

Pro-IL-1 +

+ NOD2

Aggregation

ASC NLRP3 Pro-Caspase-1 COX-2

ASA

NSAIDs

Inflammasome components

PLA2 Expression COLCHICINE

Endocardium

Myocardium

Pericardium

Pericardial Space

CORTICOSTEROIDS

Arachidonic Acid

Prostaglandins

Thromboxanes

ACUTE INFLAMMATION

(pain, edema, effusion)

Transcription of:

NLRP3 inflammasome

components (NLRP3, ASC,

Pro-caspase 1, Pro-IL-1)

and >1,000 inflammatory

mediators

(i.e.COX2, PLA2, TLRs)

NF-B

Injury to the pericardium leads to the release of DAMPs and PAMPs and induces NF-kB synthesis, which increases the transcription of precursors of inflammatory

molecules and associated cytokines (NLRP3, ASC, pro–caspase-1) required for the polymerization of the NLRP3 inflammasome, ultimately releasing IL-1b and IL-18.

NF-kB stimulates the synthesis of phospholipase-A2 required for promoting the arachidonic acid pathway and the subsequent synthesis of prostaglandins and

thromboxanes. The IL-1 receptor (IL-1R) occupies a central role, as IL-1a functions as an alarmin or DAMP being released during tissue injury, and IL-1b is

processed and released by the inflammasome, leading to amplification of the process. Adapted with permission from Chiabrando et al.8 ASA ¼ acetylsalicylic

acid; ASC ¼ apoptosis-associated Speck-like protein containing a carboxyterminal caspase-recruiting domain; DAMP ¼ damage-associated molecular pattern;

IL ¼ interleukin; NF-kB ¼ nuclear factor kappa-light-chain enhancer of activated B cells; NLRP3 ¼ NACHT, leucine-rich repeat, and pyrin domain-containing

protein 3; NOD ¼ nucleotide-binding oligomerization domain; NSAID ¼ nonsteroidal anti-inflammatory drug; PAMP ¼ pathogen-associated molecular pattern;

PLA2 ¼ phospholipase A2; TLR ¼ toll-like receptor.

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