Pericardial Disease — Clinical Framework
Pericardial diseases represent a spectrum from acute inflammation to chronic constriction. Echocardiography is the first-line modality; CMR and CT provide complementary characterization of inflammation, thickness, and calcification. This card synthesizes the 2025 ACC Concise Clinical Guidance (Wang et al.), the 2024 International Position Statement (Klein et al., JACC Cardiovasc Imaging), and the 2023 JASE multimodality CP vs. RCM review (Lloyd et al.).
🫀 Spectrum of Pericardial Disease
Acute pericarditis — inflammation with chest pain, ECG changes, ± effusion
Recurrent/incessant pericarditis — ≥2 flares after symptom-free interval; IL-1 driven
Pericardial effusion — fluid accumulation; hemodynamic impact determines urgency
Cardiac tamponade — compressive physiology → impaired output → hemodynamic collapse
Constrictive pericarditis — loss of elasticity → diastolic restraint → HF syndrome
Effusive-constrictive — persistent constrictive physiology after effusion drainage
📊 Epidemiology & Etiology
Pericarditis accounts for ~0.1% of hospital admissions; ~5% of ED chest pain evaluations
More common in men aged 16–65; recurrent form more common in women
High-income countries: Idiopathic/viral most common (presumed autoinflammatory)
Low-income countries: Tuberculosis (often HIV-associated) predominates
Other etiologies: post-cardiac injury, autoimmune, neoplastic, uremic, radiation-induced
COVID-19 and post-procedural (ablation, TAVI, pacemaker) are emerging causes
🏥 Multimodality Imaging — Role of Each Modality
| Modality | First-Line Use | Key Strengths | Limitations |
|---|---|---|---|
| Echocardiography | |||
| TTE | All pericardial disease; first-line for effusion, tamponade, CP | Bedside accessible; Doppler respiratory variation; septal bounce; annulus reversus (e' medial > lateral) | Limited for pericardial thickness; acoustic windows |
| TEE | Suboptimal TTE; post-op focal hematoma | Superior spatial resolution for pericardial thickening | Invasive; not first-line in acute setting |
| Advanced Imaging | |||
| CMR | Suspected myocardial involvement; high-risk AP; recurrent pericarditis; inflammatory assessment in CP | Tissue characterization: T1 (thickening ≥3 mm), T2-STIR (edema/active inflammation), LGE (pericardial enhancement). Predicts anti-inflammatory therapy response. Quantitative LGE grading. | Availability; cost; time; no role in acute tamponade management |
| Cardiac CT | Pericardial calcification; pre-pericardiectomy planning; pericardial thickness | Highest sensitivity for calcification; multiplanar localization of complex effusions | Radiation; no hemodynamic data; limited soft tissue characterization |
ℹ️
Per the 2025 ACC CCG: Echo first → CMR if myocardial involvement suspected or inflammatory phenotyping needed → CT for calcification assessment and pre-op planning. CMR and CT are complementary at 6–12 month intervals to monitor treatment response in recurrent/chronic pericarditis.
Acute & Recurrent Pericarditis
The 2025 ACC CCG modernizes diagnostic criteria, elevating biomarkers and CMR from supportive to central diagnostic elements. A phenotype-driven approach guides therapy selection.
🩺 2025 ACC Diagnostic Criteria (Novel — Wang et al. JACC 2025)
📋
Required: Pleuritic chest pain or equivalent suggestive presentation, PLUS ≥1 additional finding:
(a) Pericardial friction rub on auscultation
(b) Typical ECG changes — diffuse ST-elevation, PR-depression
(c) Inflammatory biomarker elevation (CRP, ESR)
(d) Cardiac imaging evidence of new or worsening pericardial effusion (echo preferred; CMR or CT acceptable)
(e) Cardiac imaging evidence of pericardial inflammation (CMR preferred; CT acceptable)
✅ 2+ criteria = Definite
⚠️ 1 criterion = Possible
❌ 0 criteria = Unlikely
⚡
Key update vs. 2015 ESC "2 of 4" rule: The ACC 2025 criteria require pleuritic chest pain as a prerequisite and add CMR/CT pericardial inflammation as a formal diagnostic criterion. Biomarkers and CMR are now central, not merely supportive.
📅 Classification by Duration
Acute pericarditis: Symptoms duration <4–6 weeks
Incessant pericarditis: >4–6 weeks to 3 months without remission
Recurrent pericarditis (RP): New flare after symptom-free interval ≥4–6 weeks. Occurs in 20–30% after initial episode.
Chronic pericarditis: >3 months duration
🔬 Inflammatory vs. Non-Inflammatory Phenotype
Inflammatory phenotype: High fever, raised CRP, pleural involvement, neutrophilic leukocytosis, high neutrophil/lymphocyte ratio, CMR with active LGE and T2-STIR edema
Non-inflammatory phenotype: Absence of above features; normal CRP; CMR showing pericardial thickening without active enhancement; more common in autoimmune/post-radiation
ℹ️
Phenotype distinction drives second-line therapy: anti-IL-1 agents (rilonacept, anakinra) for inflammatory; corticosteroids for non-inflammatory/autoimmune
💊 Management Algorithm (2025 ACC CCG)
Step-Wise Treatment
1st
Colchicine + NSAIDs (or aspirin) — first-line for acute pericarditis and first recurrence. Add exercise restriction (HR <100 bpm max, ≥1 month minimum).
2nd
Anti-IL-1 agents (rilonacept, anakinra) — second-line for inflammatory phenotype; may consider for non-inflammatory phenotype if refractory.
Alt
Corticosteroids — second-line for non-inflammatory phenotype and systemic autoimmune diseases; low-to-medium dose with slow wean. Avoid high-dose steroids as first recurrence therapy.
Surg
Radical pericardiectomy — medically refractory pericarditis or constrictive pericarditis; requires expert surgical center. Partial pericardiectomy is inadequate (inferior long-term survival).
+
Treat underlying etiology. Consider referral to a Pericardial Diseases Center (PDC) for complex cases.
⚠️
CMR monitoring: CT and CMR can be used at baseline and at 6–12 month intervals to guide therapy and assess treatment response. In burned-out calcific pericarditis, CT is essential for pre-surgical planning.
🔬 CMR in Pericarditis — Hallmarks & LGE Grading
| CMR Sequence | Finding | Clinical Significance |
|---|---|---|
| T1-weighted (black-blood) | Pericardial thickening ≥3 mm | Structural pericardial involvement; present even in non-inflammatory phases |
| T2-STIR | Increased T2 signal (edema) | Active pericardial inflammation; grades severity of current inflammatory activity |
| Late Gadolinium Enhancement (LGE) | Pericardial gadolinium uptake | Neovascularization/active inflammation; predicts recurrence risk; guides anti-inflammatory therapy; resolves with disease remission |
| Chronic/Burned-out | No LGE; pericardial thickening ± calcification | Anti-inflammatory therapy NOT indicated; calcification detected better on CT; surgical planning |
✅
Key principle: CMR LGE predicts response to anti-inflammatory therapies. Anti-inflammatory therapy is NOT indicated in CP without evidence of active inflammation on CMR. Absence of LGE with pericardial thickening/calcification favors chronic irreversible disease.
Pericardial Effusion & Cardiac Tamponade
Tamponade is a dynamic process dependent on rate of fluid accumulation, not absolute volume. The 2025 ACC CCG reframes tamponade assessment around integrated clinical-hemodynamic-imaging evaluation rather than simple size thresholds.
📏 Pericardial Effusion Sizing (Echocardiography)
| Category | Size (Echo, Diastolic) | Approximate Volume | Notes |
|---|---|---|---|
| Trivial | Seen only in systole | <50 mL | Often physiologic; can be pericardial fat |
| Mild | <10 mm | ~50–200 mL | Typically well-tolerated; monitor for progression |
| Moderate | 10–20 mm | ~200–500 mL | Assess for hemodynamic compromise; Doppler evaluation mandatory |
| Large | >20 mm | >500 mL | High risk for tamponade; urgent Doppler + clinical assessment |
| Very Large | >25 mm | >500 mL | Often unevenly distributed; high suspicion for neoplasia, TB, or hypothyroidism |
⚠️
Critical principle (2025 ACC CCG / ASE 2013): Effusion volume does not reliably predict tamponade risk. A rapidly accumulating small effusion (e.g., post-procedural hemopericardium causing tamponade at ~250 mL) can be far more dangerous than a large chronic effusion. Small and very large effusions are most likely to be unevenly distributed.
🔬 Effusion Characterization — CT Attenuation Values (ASE 2013, Klein et al.)
| Effusion Type | CT Attenuation | Echo Appearance | Typical Etiology |
|---|---|---|---|
| Transudative | <10 Hounsfield units (near water) | Echolucent; motionless | Heart failure, hypothyroidism, idiopathic |
| Exudative | 20–60 Hounsfield units | May show stranding, loculations | Purulent, malignant, inflammatory, myxedematous |
| Chylous | −60 to −80 Hounsfield units (fat density) | Variable | Lymphatic obstruction, trauma, post-surgical |
| Hemorrhagic | >60 Hounsfield units | Echogenic, slow-swirling spontaneous contrast | Trauma, aortic dissection, post-procedural, malignancy, anticoagulation |
ℹ️
On CMR: transudative effusions appear dark on T1-weighted SE images and bright on cine (SSFP) sequences. Exudative and hemorrhagic effusions show higher T1W signal intensity due to elevated protein content. Fat suppression sequences help distinguish chylous effusion from fat.
⚡ Echocardiographic Signs of Cardiac Tamponade (ASE 2013 · Klein et al.)
Structural / 2D Signs
Right atrial systolic collapse: Duration >1/3 of cardiac cycle → ~100% sensitive and specific for clinical tamponade. Timing: near the R wave on ECG (atrial relaxation phase).
RV diastolic collapse: Early diastolic indentation of RV free wall after end of T wave. Initially only with inspiration; as tamponade worsens, persists throughout cycle. Occurs when cardiac output ↓ ~20% but BP not yet fallen.
Absence of all chamber collapse: >90% negative predictive value for clinical tamponade. Collapse may be absent in RVH, severe PAH, or elevated LV filling pressures.
Left atrial/LV collapse: Less common; suggests posterior loculated effusion or severe PAH. Often post-surgical.
Swinging heart: Pendular cardiac motion within large effusion; associated with electrical alternans on ECG.
Doppler / Respiratory Signs — ASE Consensus Formula
Formula: % variation = (expiration − inspiration) / expiration × 100%
Mitral E variation ≥30% (research threshold; >25% clinically significant): Lowest on first beat of inspiration, highest on first beat of expiration.
Tricuspid E variation ≥60%: Highest on first beat of inspiration; lowest on first beat of expiration (opposite to mitral). Calculated % will be a negative value.
IVC plethora: Dilated IVC (>2.1 cm) with <50% inspiratory collapse. Present in 92% of effusions requiring drainage. High sensitivity, low specificity.
Hepatic vein: Diastolic flow reversal on first beat of expiration (same time tricuspid E is lowest). Forward flow decreasing; in severe tamponade diastolic forward flow disappears entirely between inspiratory beats.
Do NOT use Doppler variation alone — requires concurrent: PEff + ↓ stroke volume/CO + elevated CVP + chamber collapse. COPD produces similar Doppler changes but largest beat occurs on 2nd inspiration beat (not 1st).
🚨
Special scenarios: Low-pressure (occult) tamponade in hypovolemic patients may lack classic RA/RV collapse; regional post-surgical tamponade from hematoma requires TEE. Positive-pressure ventilation reverses the Doppler respiratory variation pattern — standard criteria do not apply.
🗂️ Structured Echocardiographic Protocol for Effusion
Systematic 5-Step Assessment
1
Quantity & distribution: Measure effusion in multiple views (PLAX, PSAX, apical 4-chamber, subcostal); global vs. loculated; anterior vs. posterior
2
Quality of fluid: Echogenicity — fibrinous strands/loculations suggest exudative or hemorrhagic etiology; density suggests hemopericardium
3
Chamber collapse: Look for RA systolic collapse, RV diastolic collapse in all views; assess duration relative to cardiac cycle
4
Respiratory ventricular variation: M-mode PLAX/PSAX for septal shift; assess with patient breathing normally (not Valsalva)
5
IVC and hepatic vein flow: IVC diameter + collapsibility; hepatic vein Doppler for systolic/diastolic reversal pattern
🩺 Pericardiocentesis — When and How
Indications
Hemodynamic compromise (tamponade physiology)
Large effusion with concern for bacterial/neoplastic etiology
Moderate effusion not responding to anti-inflammatory therapy after 2–3 weeks
Diagnostic sampling when etiology uncertain
Imaging Guidance
TTE guidance preferred — real-time needle visualization; subcostal or apical approach
CT aids planning for small, multiloculated, or post-surgical effusions
Surgical window — when percutaneous not safe/feasible; malignant or recurrent loculated effusions; effusive-constrictive physiology
CMR indicated if coexisting pericarditis or pericardial malignancy suspected
Constrictive Pericarditis — Diagnosis & Management
CP results from loss of pericardial elasticity causing exaggerated interventricular dependence and dissociation between intracardiac and intrathoracic pressures. Echocardiography has high positive predictive value; CMR defines inflammation to guide therapy.
🔬 Pathophysiology of Constrictive Physiology
Key Hemodynamic Principles
Pericardial constraint: Fixed pericardial volume limits total cardiac filling — ventricular filling is volume-fixed
Ventricular interdependence: RV filling increase → septal shift → LV filling decrease (and vice versa). Exaggerated in CP.
Dissociation of intracardiac/intrathoracic pressures: Inspiratory fall in intrathoracic pressure is NOT transmitted to intracardiac chambers (pericardium blocks transmission)
Result: LV filling does not augment on inspiration (unlike normal); RV filling augments more than normal → septal bounce toward LV in early diastole
CP vs. Normal Physiology
Normal: Inspiration ↓ intrathoracic pressure → transmitted to cardiac chambers → pulmonary venous return unchanged → LV fills normally
CP: Inspiration ↓ intrathoracic pressure → NOT transmitted (rigid pericardium) → pulmonary venous return ↓ → LV filling ↓ → E wave ↓ ≥25%
Key contrast with RCM: In RCM, intracardiac pressures DO change with respiration (pericardium normal) → NO significant respiratory variation in mitral inflow
📋 Echocardiographic Criteria for CP — ASE 2013 Guideline Thresholds
| Finding | Threshold | Mechanism | Notes |
|---|---|---|---|
| Primary Criteria — High Specificity (ASE 2013 · Welch Circ CV Imaging 2014) | |||
| Interventricular septal bounce | Present on 2D/M-mode | Exaggerated ventricular interdependence; abrupt posterior septal motion in early diastole with inspiration; "septal shudder" | M-mode at PLAX/PSAX with respirometer confirms timing. Also: diastolic flattening of LV posterior wall. |
| Mitral E respiratory variation | ≥25% (clinical); ≥30% (research) | Dissociation of intrathoracic/intracardiac pressures. Formula: (exp − insp) / exp × 100%. | Lowest on first beat of inspiration. May be absent with markedly elevated LAP — unmask with upright/preload reduction. Respirometry mandatory. |
| Tricuspid E respiratory variation | ≥40% (first beat after inspiration) | Same mechanism; opposite direction to mitral. Formula: (exp − insp) / exp gives negative value. | Maximal drop is on first beat of expiration (same as hepatic vein diastolic reversal timing). |
| Annulus reversus | Medial e' > lateral e' | Lateral mitral annulus tethered to thickened pericardium; medial annular motion relatively preserved. | Normal pattern is lateral > medial. Inversely related to pericardial thickness at LV AV groove on CT. Normalizes after pericardiectomy. |
| Hepatic vein expiratory diastolic reversal | Diastolic reversal on expiration | Ventricular interaction and dissociation of pressures. Limited RV filling during expiration → retrograde flow to IVC/hepatic veins. | Inspiratory HV diastolic reversals suggest RCM (opposite). SVC flow shows less respiratory variation than HV in CP. |
| Supporting Criteria | |||
| Medial mitral annulus e' (tissue Doppler) | ≥9 cm/s (often higher; typically >7 cm/s) | Preserved longitudinal motion (myocardium normal; pericardial tethering relaxed longitudinally). | Annulus paradoxus: E/e' ratio inversely proportional to PCWP in CP (opposite to cardiomyopathy). |
| Color M-mode flow propagation Vp | ≥100 cm/sec | Rapid early diastolic filling (early filling phase is accelerated before pericardial restraint kicks in at mid-diastole). | Nyquist limit should be baseline-shifted to 30–40 cm/sec. Normal or increased in CP; reduced in RCM. |
| Pericardial thickening | >4 mm (CT/CMR); TEE correlates with CT | Structural marker of constriction. | Important caveat: 18–28% of surgically confirmed CP has normal pericardial thickness on CT/histology. Absence of thickening does NOT rule out CP. |
| IVC plethora | Dilated IVC (>2.1 cm); <50% collapse | Elevated RA pressure; venous congestion. | Non-specific; also present in RCM and right-sided failure from other causes. |
★ Respirometry technique (ASE 2013): Simultaneous respirometer recording is mandatory. Sweep speed 25–50 mm/sec. PW sample volume 1–2 mm for mitral/tricuspid inflow; 3–4 mm for hepatic vein. If respiratory variation absent at rest, repeat in upright position (preload reduction). M-mode of IVS is essential for subtle septal bounce.
⚠️ CMR accuracy: CMR has 93% accuracy for differentiating CP from RCM using pericardial thickening >4 mm as cutoff (ASE 2013 / Thavendiranathan et al.). CMR tagging sequences demonstrate pericardial-myocardial adherence — fibrotic adhesions are present when tag deformation is absent.
🔄 Transient vs. Chronic Constrictive Pericarditis
Transient/Subacute CP (Inflammatory)
Active pericardial inflammation driving reversible constriction
CMR: Active LGE and T2-STIR edema present
Anti-inflammatory therapy (colchicine ± NSAIDs ± steroids) for ≥8–12 weeks before re-evaluation
Resolution of constriction in ~50% with appropriate therapy — pericardiectomy can be avoided
Chronic/Advanced CP (Fibrocalcific)
Calcified, fibrotic pericardium; irreversible
CMR: No LGE; pericardial thickening ± calcification; CT best for calcification extent
Anti-inflammatory therapy NOT indicated
Radical pericardiectomy at expert center — comprehensive (not partial) resection required
🔑
CMR is the pivotal gatekeeper: The presence or absence of active pericardial LGE determines whether anti-inflammatory therapy is appropriate before pericardiectomy. Do not proceed to surgery without CMR assessment of inflammation where feasible.
💧 Effusive-Constrictive Pericarditis — A Distinct Entity (ASE 2013)
🔑
Definition: Persistent constrictive physiology (elevated RA pressure, dip-and-plateau RV/LV waveforms, ventricular interdependence) that persists even after pericardiocentesis. Prevalence: ~1.3% of all pericarditis; ~6.9% of those presenting with tamponade (Sagrista-Sauleda et al., NEJM 2004).
Pathophysiology
Involves both visceral and parietal pericardium with inflammation, fibrotic thickening, and myocardial adherence ("epicarditis")
Hallmark: a tense PEff accumulates between thickened, edematous or fibrotic parietal and visceral pericardium
Etiologies: idiopathic (most common), malignancy, radiation; post-surgical less common than in pure CP
Echo & Imaging Features
Echo: Echogenic/organized material in PEff; bandlike fibrinous strands traversing pericardial cavity; visceral pericardial thickening. Features of tamponade early → features of CP after drainage.
CT: PEff + pericardial thickening >3 mm; enhancing pericardial layers; nodular thickening; calcification; loculations
CMR: Pericardial LGE ± T2-STIR edema; ventricular interdependence on real-time cine; flattening/inversion of IVS
Clinical presentation: Three scenarios: (1) active pericarditis + echogenic effusion; (2) chronic PEff + right HF; (3) tamponade not improving after pericardiocentesis
✅
Management: Surgical pericardial window or pericardiectomy. Anti-inflammatory therapy if CMR shows active LGE. Idiopathic cases undergoing pericardiectomy have favorable outcomes. In the past, diagnosis required hemodynamic demonstration post-pericardiocentesis; now often detected earlier with imaging.
🏥 Invasive Hemodynamics — When and What to Expect
Indications: Equivocal non-invasive imaging; differentiation from RCM remains uncertain after echo + CMR/CT
Simultaneous RHC + LHC: Required to demonstrate ventricular interdependence directly
Classic Hemodynamic Findings in CP
Discordant RV/LV systolic pressures: On inspiration, RVSP increases while LVSP falls (opposite to normal concordant decline). Area index >1.1 (Nishimura criterion)
Dip-and-plateau ("square root sign"): Rapid early diastolic filling followed by abrupt cessation; seen in both RV and LV diastolic pressure tracings
Equalization of diastolic pressures: RVEDP ≈ LVEDP (within 5 mmHg); RA mean ≈ RV diastolic ≈ PCWP
Jain et al. (JAMA Cardiol 2022): Simplified criteria — concordant RV-LV systolic area index >1.1 on inspiration alone has high diagnostic accuracy for CP at catheterization
Constrictive Pericarditis vs. Restrictive Cardiomyopathy
CP and RCM share clinical presentation and many imaging features, but management differs fundamentally. An algorithmic multimodality approach is required. Based on Lloyd, Anavekar, Oh, Miranda (JASE 2023) and Geske et al. (JACC 2016).
🔀 Differentiating Algorithm — CP vs. RCM
📊 Systematic Comparison: CP vs. RCM
| Feature | Constrictive Pericarditis | Restrictive Cardiomyopathy |
|---|---|---|
| History & Exam | ||
| Typical etiology | Prior pericarditis, cardiac surgery, radiation, TB | Amyloidosis, Fabry, hemochromatosis, sarcoidosis, radiation (myocardial), idiopathic |
| Pericardial knock | Present (high-pitched early S3-like sound) | Absent |
| ECG | Non-specific; low voltage if extensive calcification | Low voltage (amyloid); LVH (early infiltration); conduction disease |
| Echocardiography — 2D | ||
| LV wall thickness | Normal | Increased (amyloid); can be normal (idiopathic) |
| LV size/EF | Normal; EF preserved | Normal/small; EF preserved until late; late systolic dysfunction |
| Septal motion | Septal bounce (exaggerated ventricular interdependence) | Normal |
| Pericardium | Thickened ± bright/calcified on echo; best on CT/CMR | Normal |
| Doppler | ||
| Mitral E respiratory variation | ≥25% decrease on inspiration | <10% (no significant variation) |
| Tricuspid E respiratory variation | ≥40% increase on inspiration | Minimal |
| Hepatic vein Doppler | Expiratory diastolic reversal | Inspiratory diastolic reversal (HV systolic blunting in both) |
| Tissue Doppler & Strain | ||
| Medial mitral annulus e' | ≥9 cm/s (relatively preserved) | <7 cm/s (reduced — myocardial disease) |
| Lateral vs. medial e' | Annulus reversus: Medial > lateral | Normal: Lateral > medial |
| GLS (global longitudinal strain) | Relatively preserved; may show basal-dominant reduction if pericardial tethering | Reduced globally; amyloid: apical sparing pattern (classic) |
| Advanced Imaging | ||
| Pericardial thickness | >3–4 mm (CT gold standard); calcification common in chronic disease | Normal (<2 mm) |
| CMR LGE | Pericardial LGE in inflammatory/transient CP; absent in fibrocalcific CP | Diffuse subendocardial (amyloid); focal (sarcoid); null-point shift (amyloid) |
| CMR T1/ECV | Normal myocardial T1 and ECV | Elevated T1 and ECV (amyloid); reduced T1 (Fabry/Anderson-Fabry) |
| Hemodynamics | ||
| Ventricular interdependence | Discordant RV/LV systolic pressures (Area index >1.1) | Concordant (both decline on inspiration) |
| Diastolic pressure equalization | RVEDP ≈ LVEDP ± 5 mmHg | May have gradient (LVEDP > RVEDP) |
🤖
Emerging data: Deep learning using apical 4-chamber TTE video clips achieved AUC 0.84 (external validation) for distinguishing CP from restrictive cardiomyopathy/cardiac amyloidosis in a 381-patient Mayo Clinic dataset (Chao et al. JACC Cardiovasc Imaging 2024;17:349–60). Clinical implementation pending prospective validation.
📐
Strain imaging — CP vs. RCM (ASE 2013, Sengupta et al.): In CP, circumferential strain and early diastolic untwisting are reduced while GLS is relatively preserved. In RCM, GLS is more profoundly reduced. The ratio of LV lateral wall strain to septal strain is more robust than regional annular velocity for differentiating the two. After pericardiectomy, longitudinal strain in RV/LV free walls and circumferential strain improve.
Multimodality Imaging Integration
Each modality contributes unique information. Integrated cMMI is pivotal for diagnosis, risk stratification, and monitoring. Based on Klein et al. JACC Cardiovasc Imaging 2024 International Position Statement and 2025 ACC CCG.
🗺️ Imaging-Guided Therapy — Pericarditis Continuum
| Stage | Echo Role | CMR Role | CT Role | Therapy Implication |
|---|---|---|---|---|
| Acute pericarditis | First-line: effusion size/location, tamponade, wall motion (myo-pericarditis) | If myocardial involvement suspected; high-risk features; T2-STIR + LGE for active inflammation | Seldom needed; pericardial thickening, excludes alternative thoracic pathology | NSAIDs + colchicine × 4–6 weeks (acute); exercise restriction |
| Recurrent pericarditis | Serial monitoring of effusion; tamponade signs | Diagnosis, prognostication, monitor response; LGE predicts recurrence risk | Pericardial thickening; calcification if chronic evolution | Colchicine + NSAIDs for first recurrence; anti-IL-1 (rilonacept/anakinra) if inflammatory phenotype |
| Transient CP | CP criteria present (septal bounce, respiratory variation); assess resolution | Active LGE/T2-STIR = inflammatory → anti-inflam trial for ≥8–12 wk before surgery | Thickening without heavy calcification | Anti-inflammatory therapy; re-evaluate with CMR at 8–12 weeks |
| Chronic/Calcific CP | CP criteria; may be minimal echo pericardial visualization | No LGE; pericardial thickening; anti-inflammatory NOT indicated | Defines extent + distribution of calcification; pre-op planning | Radical pericardiectomy at expert center |
| Effusive-constrictive | Persistent CP physiology after pericardiocentesis on echo/Doppler | Pericardial inflammation assessment; effusion characterization | Pericardial thickening; calcification | Surgical pericardial window or pericardiectomy; anti-inflammatory if LGE+ |
🔴 High-Risk Features Requiring Advanced Imaging
Fever >38°C at presentation
Subacute onset (no acute pleuritic pain)
Large pericardial effusion (>20 mm) or tamponade
Failure to respond to NSAID/colchicine after 7 days
Myopericarditis (troponin elevation, wall motion abnormality)
Immunocompromised state
Oral anticoagulation use
Trauma; post-cardiac surgery; suspected bacterial/neoplastic etiology
🏥
High-risk features: hospitalize; CMR ± CT; consider referral to Pericardial Diseases Center (PDC)
🟢 Low-Risk Features (Outpatient Management)
Young, otherwise healthy individual
Acute pleuritic chest pain improved by sitting forward
Typical ECG changes (diffuse ST elevation, PR depression)
Small or absent effusion
Normal troponin (no myocardial involvement)
Responds to NSAIDs within 7 days
✅
Low-risk: Outpatient management with NSAIDs + colchicine; close follow-up; exercise restriction
🏛️ Pericardial Diseases Center (PDC) — Referral Considerations
ℹ️
The 2025 ACC CCG introduces the concept of a multidisciplinary Pericardial Diseases Center integrating cardiology, cardiac surgery, rheumatology, and advanced cardiac imaging expertise for complex cases.
Recurrent pericarditis not responding to first-line therapy
Suspected effusive-constrictive physiology
Consideration for anti-IL-1 therapy (rilonacept, anakinra)
Constrictive pericarditis being evaluated for pericardiectomy
Pericardial disease in the setting of systemic autoimmune conditions
Pericardial malignancy or complex post-surgical pericardial syndromes
References & Sources
All clinical content on this card is derived from peer-reviewed guidelines and original research. This is an educational reference only and does not replace clinical judgment or individualized patient assessment.
📄 Primary Guidelines
| # | Citation | Scope on This Card |
|---|---|---|
| 1 | Wang TKM, Klein AL, Cremer PC, Imazio M, et al. 2025 Concise Clinical Guidance: An ACC Expert Consensus Statement on the Diagnosis and Management of Pericarditis. J Am Coll Cardiol. 2025;86(25):2691–2719. DOI 10.1016/j.jacc.2025.05.023 | Diagnostic criteria, phenotyping, treatment algorithm, tamponade reframing, CP management, PDC concept |
| 2 | Klein AL, Abbara S, Agler DA, Appleton CP, Asher CR, Hoit B, et al. ASE Clinical Recommendations for Multimodality Cardiovascular Imaging of Patients with Pericardial Disease. J Am Soc Echocardiogr. 2013;26:965–1012. Endorsed by SCMR and SCCT. DOI 10.1016/j.echo.2013.06.023 | All echo technique and thresholds: effusion sizing, tamponade Doppler formula and specific criteria, CP Doppler key points, color M-mode, annulus paradoxus/reversus, CT attenuation values, effusive-constrictive, strain differentiation, respirometry protocol |
| 3 | Klein AL, Wang TKM, Cremer PC, et al. Pericardial Diseases: International Position Statement on New Concepts and Advances in Multimodality Cardiac Imaging. JACC Cardiovasc Imaging. 2024;17:937–988. DOI 10.1016/j.jcmg.2024.02.013 | Multimodality imaging framework, IL-1 biology, imaging-guided therapy continuum, tamponade algorithm, CP multimodal approach |
| 4 | Lloyd JW, Anavekar NS, Oh JK, Miranda WR. Multimodality Imaging in Differentiating Constrictive Pericarditis From Restrictive Cardiomyopathy: A Comprehensive Overview for Clinicians and Imagers. J Am Soc Echocardiogr. 2023;36(12):1254–1265. DOI 10.1016/j.echo.2023.08.016 | CP vs. RCM differentiation algorithm, multimodality imaging approach, ambiguous cases pathway |
📄 Supporting References
| # | Citation | Scope on This Card |
|---|---|---|
| 5 | Welch TD, Ling LH, Espinosa RE, Anavekar NS, Wiste HJ, Lahr BD, Schaff HV, Oh JK. Echocardiographic diagnosis of constrictive pericarditis: Mayo Clinic criteria. Circ Cardiovasc Imaging. 2014;7:526–534. DOI 10.1161/CIRCIMAGING.113.001613 | Mayo Clinic echocardiographic criteria for CP diagnosis and validation |
| 6 | Jain CC, Miranda WR, Sabbagh AE, Nishimura RA. A Simplified Method for the Diagnosis of Constrictive Pericarditis in the Cardiac Catheterization Laboratory. JAMA Cardiol. 2022;7(1):100–104. DOI 10.1001/jamacardio.2021.3478 | Invasive hemodynamics for CP: discordant area index >1.1 |
| 7 | Geske JB, Anavekar NS, Nishimura RA, Oh JK, Gersh BJ. Differentiation of Constriction and Restriction: Complex Cardiovascular Hemodynamics. J Am Coll Cardiol. 2016;68(21):2329–2347. DOI 10.1016/j.jacc.2016.08.050 | Hemodynamic differentiation of CP vs. RCM |
| 8 | Chao CJ, Jeong J, Arsanjani R, et al. Echocardiography-based deep learning model to differentiate constrictive pericarditis and restrictive cardiomyopathy. JACC Cardiovasc Imaging. 2024;17(4):349–360. DOI 10.1016/j.jcmg.2023.09.011 | AI/deep learning differentiation of CP vs. RCM (AUC 0.84) |
| 9 | Sagrista-Sauleda J, Angel J, Sanchez A, Permanyer-Miralda G, Soler-Soler J. Effusive-constrictive pericarditis. N Engl J Med. 2004;350:469–475. | Effusive-constrictive pericarditis prevalence and clinical features |
| 10 | Sengupta PP, Krishnamoorthy VK, Abhayaratna WP, et al. Disparate patterns of left ventricular mechanics differentiate constrictive pericarditis from restrictive cardiomyopathy. JACC Cardiovasc Imaging. 2008;1:29–38. | Strain imaging patterns: circumferential (CP) vs. longitudinal (RCM) reduction |
| 11 | Klein AL, Wang TKM, Cremer PC, et al. (ACC.org Expert Analysis). Multimodality Imaging in Pericardial Diseases and the Role of Imaging-Guided Therapies. ACC.org. January 2025. ACC.org link | Contemporary multimodality imaging review; IL-1 biology; imaging-guided therapies framework |
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Educational use only. This card is a clinical reference tool for educational purposes. It does not replace individualized clinical judgment, formal guideline documents, or physician-patient consultation. Guidelines evolve — always verify against the current primary source.