Acute Pericarditis

1. Overview

Acute pericarditis is defined as inflammation of the pericardial sac, the double-layered fibroserous membrane that envelops the heart. It represents the most common pericardial disease encountered in clinical practice, accounting for approximately 5% of emergency department presentations with non-ischaemic chest pain and 0.1-0.2% of all hospital admissions. [1,2]

The condition presents with characteristic pleuritic chest pain, often relieved by sitting forward, and may be accompanied by a pathognomonic pericardial friction rub. The addition of colchicine to conventional anti-inflammatory therapy has revolutionised management, reducing recurrence rates by approximately 50% and establishing the current standard of care. [3,4]

While most cases are idiopathic or presumed viral in origin and follow a benign self-limiting course, acute pericarditis may herald serious underlying pathology including tuberculosis, malignancy, or autoimmune disease. Recognition of high-risk features mandating hospitalisation remains essential for optimal patient outcomes.

Clinical Summary Table

Red Flags Requiring Hospitalisation

⚠️ Red Flag: The following features indicate high-risk pericarditis requiring inpatient management:

Major Criteria (Admit):

• Temperature > 38°C (suggests purulent or tuberculous aetiology)
• Subacute onset over weeks (malignancy or TB)
• Large pericardial effusion > 20mm on echocardiography
• Cardiac tamponade (haemodynamic compromise)
• Failure to respond to NSAIDs within 7 days

Minor Criteria (Consider Admission):

• Elevated troponin (myopericarditis)
• Immunosuppression
• Oral anticoagulant therapy
• Recent trauma or cardiac procedure
• Pregnancy

---

2. Epidemiology

Incidence and Prevalence

Acute pericarditis has an estimated incidence of 27.7 cases per 100,000 population per year, though this likely underestimates true prevalence as mild cases may resolve spontaneously without medical attention. [2] Hospital admission rates range from 3.3 to 5.4 per 100,000 population annually.

Demographics

Acute pericarditis demonstrates a male predominance with a male-to-female ratio of approximately 2:1. The condition occurs across all age groups but peaks between 16 and 65 years. In contrast, recurrent pericarditis shows female predominance, possibly reflecting the higher incidence of autoimmune conditions in women. [5]

Risk Factors for Recurrence

The following factors have been identified as predictors of recurrent pericarditis:

1. Incomplete initial treatment - Stopping colchicine prematurely or inadequate NSAID dosing
2. Corticosteroid use - First-line steroid therapy increases recurrence 2-4 fold [6]
3. Female sex - Higher risk in recurrent disease
4. Autoimmune aetiology - Systemic lupus erythematosus, rheumatoid arthritis
5. Elevated CRP at diagnosis - Persistent inflammation predicts relapse
6. Previous episodes - Risk increases with each recurrence

Seasonal Variation

Viral pericarditis demonstrates seasonal clustering, with increased incidence following respiratory virus epidemics (influenza, adenovirus) and enterovirus outbreaks (Coxsackie B, Echovirus). This pattern supports the predominant viral/post-viral aetiology in idiopathic cases.

---

3. Aetiology and Pathophysiology

Anatomical Considerations

The pericardium consists of two layers with distinct clinical significance:

Visceral Pericardium (Epicardium):

• Single layer of mesothelial cells adherent to myocardium
• Produces pericardial fluid (~15-50mL, straw-coloured)
• Insensate - does not contribute to pain

Parietal Pericardium:

• Fibrous outer layer, 1-2mm thick
• Richly innervated by phrenic nerve (C3-C5) and intercostal nerves
• Source of pericarditic pain
• Pain referred to trapezius ridge (pathognomonic) via phrenic innervation

Pericardial Sinuses:

• Transverse sinus: Between aorta/pulmonary trunk anteriorly and atria posteriorly
• Oblique sinus: Cul-de-sac posterior to left atrium where effusions pool in supine position

Pathophysiology of Acute Pericarditis

Pericardial inflammation follows a characteristic sequence:

1. Inflammatory trigger - Viral infection, autoimmune activation, metabolic insult
2. Inflammatory cell infiltration - Neutrophils, lymphocytes, macrophages
3. Increased capillary permeability - Protein-rich exudate formation
4. Fibrin deposition - "Bread and butter" pericarditis appearance
5. Effusion accumulation - Variable volume depending on aetiology and chronicity
6. Resolution or progression - Healing vs constrictive pericarditis

Exam Detail: Molecular Mechanisms:

The inflammasome pathway, particularly NLRP3 (NOD-like receptor protein 3), plays a central role in pericardial inflammation. Activation of NLRP3 leads to:

• Caspase-1 activation
• IL-1-beta and IL-18 release
• Neutrophil chemotaxis and activation
• Perpetuation of inflammatory cascade

This mechanistic understanding explains the efficacy of colchicine (inhibits microtubule polymerisation, neutrophil migration, and NLRP3 activation) and IL-1 inhibitors (anakinra, rilonacept) in refractory cases. [7]

Aetiological Classification

The mnemonic "I-MINT-D" covers major causes:

Post-Myocardial Infarction Pericarditis

Two distinct syndromes occur following myocardial infarction:

Early Peri-Infarction Pericarditis (Epistenocardiac):

• Occurs within 1-4 days post-MI
• Direct extension of inflammation from necrotic myocardium
• Affects 5-10% of STEMI patients (less with early reperfusion)
• Indicates transmural infarction
• Management: Continue aspirin; avoid NSAIDs/colchicine if possible (may impair healing)

Dressler's Syndrome (Post-Cardiac Injury Syndrome):

• Occurs 2-10 weeks post-MI (classically 2-6 weeks)
• Autoimmune response to myocardial antigens
• Characterised by pericarditis, pleuritis, fever, elevated inflammatory markers
• Incidence reduced with early reperfusion (less than 1% in current era)
• Management: High-dose aspirin + colchicine
• Prevention: Colchicine peri-operatively reduces post-operative pericarditis [8]

Tuberculous Pericarditis

Clinical Pearl: TB Pericarditis - The Global Perspective:

Tuberculosis remains the leading cause of pericarditis in endemic regions (sub-Saharan Africa, South Asia) and in HIV-positive individuals. Key features:

• Presentation: Subacute onset (weeks), constitutional symptoms, large effusion
• Diagnosis: Pericardial fluid ADA > 40 U/L (sensitivity 87-89%), PCR (Xpert MTB/RIF), lymphocytic predominance
• Treatment: Standard 6-month anti-TB therapy (HRZE) + adjunctive corticosteroids
• Evidence: The IMPI trial demonstrated that corticosteroids reduced pericardial constriction but did not reduce mortality overall; benefit greatest in HIV-negative patients [9]
• Prognosis: 30-50% progress to constrictive pericarditis without early treatment

Uraemic Pericarditis

Occurs in two settings with distinct clinical features:

Malignant Pericarditis

Primary pericardial malignancy (mesothelioma, sarcoma) is rare. Secondary involvement occurs in:

• Lung cancer - Most common primary
• Breast cancer - Second most common
• Lymphoma/Leukaemia - May present with massive effusion
• Melanoma - High propensity for cardiac metastasis

Key features:

• Large, often rapidly accumulating effusion
• Haemorrhagic fluid (grossly bloody)
• Positive cytology in 60-80% of cases
• May require pericardial window for recurrent effusions
• Poor prognosis - median survival 3-6 months

---

4. Clinical Presentation

Symptoms

Cardinal Features:

1. Chest Pain (> 85% of cases)

   • Character: Sharp, stabbing, pleuritic
   • Location: Retrosternal or left precordial
   • Radiation: Trapezius ridge (pathognomonic for pericardial origin via phrenic nerve)
   • Aggravating factors: Inspiration, lying supine, coughing, swallowing
   • Relieving factors: Sitting forward ("tripod position")
   • Duration: Hours to days

2. Dyspnoea (30-50%)

   • Secondary to pain (splinting)
   • Large effusion causing compression
   • Associated pleural effusion

3. Prodromal Symptoms (common in viral aetiology)

   • Fever, malaise, myalgia
   • Upper respiratory tract infection
   • Gastrointestinal symptoms (Enterovirus)

Physical Examination Signs

Pericardial Friction Rub:

• Pathognomonic when present (sensitivity 85%, highly specific)
• Character: High-pitched, scratchy, "walking on fresh snow" or "creaking leather"
• Best heard: Left lower sternal border, patient leaning forward, end-expiration
• Classically triphasic: Atrial systole, ventricular systole, ventricular diastole
• May be monophasic or biphasic
• Evanescent - may come and go over hours; absence does not exclude diagnosis

Ewart's Sign (Large Effusion):

• Dullness to percussion at left scapular tip
• Bronchial breathing in same area
• Due to left lower lobe compression by pericardial effusion

Signs of Tamponade:

• Hypotension and tachycardia
• Elevated JVP with absent Y descent
• Muffled heart sounds
• Pulsus paradoxus > 10 mmHg

Clinical Vignettes

Clinical Case: Case 1: Classic Viral Pericarditis

Presentation: 28-year-old male gym instructor presents with 3 days of sharp retrosternal chest pain, worse when lying flat, relieved by leaning forward. Reports "man flu" symptoms one week ago.

Examination: Sitting forward on edge of bed. HR 95, BP 125/80. Pericardial friction rub audible at LLSB.

ECG: Widespread concave ST elevation in leads I, II, aVL, aVF, V2-V6. PR depression in limb leads. PR elevation in aVR.

Investigations: Troponin mildly elevated (45 ng/L). CRP 85 mg/L. Echo: Trivial pericardial effusion.

Diagnosis: Acute viral myopericarditis

Management: Ibuprofen 600mg TDS + Omeprazole 20mg OD + Colchicine 500mcg BD for 3 months. Activity restriction for 6 months due to troponin elevation. Cardiology follow-up in 4 weeks.

Clinical Case: Case 2: Uraemic Pericarditis

Presentation: 65-year-old female with ESKD (missed dialysis sessions) presents with progressive breathlessness over 5 days. Denies chest pain.

Examination: Elevated JVP, bilateral pitting oedema. Loud pericardial friction rub. Bibasal crackles.

Investigations: Urea 52 mmol/L, Creatinine 890 umol/L. Echo: Moderate pericardial effusion (15mm) without tamponade.

Diagnosis: Uraemic pericarditis

Management: Urgent dialysis. Avoid NSAIDs (renal). Consider prednisolone if no improvement with intensified dialysis. Daily echo surveillance.

Differential Diagnosis

---

5. Investigations

Diagnostic Criteria (ESC 2015 Guidelines)

Diagnosis requires at least 2 of the following 4 criteria: [1]

1. Pericarditic chest pain - Sharp, pleuritic, positional
2. Pericardial friction rub - Scratchy, triphasic
3. ECG changes - Widespread ST elevation and/or PR depression
4. Pericardial effusion - New or worsening on echocardiography

Supporting features (not diagnostic but supportive):

• Elevated inflammatory markers (CRP, ESR)
• Evidence of pericardial inflammation on CT or CMR

Electrocardiography

ECG changes evolve through four classical stages:

Exam Detail: ECG Differentiation: Pericarditis vs STEMI

Spodick's Sign: Downsloping TP segment best seen in lead II. Present in 80% of acute pericarditis cases. [10]

Laboratory Investigations

Inflammatory Markers:

• CRP: Elevated in > 75% of cases; useful for monitoring treatment response
• ESR: Elevated; less specific than CRP
• White cell count: May be elevated (leukocytosis)

Cardiac Biomarkers:

• Troponin: Elevated in 35-50% of cases, indicating myocardial involvement (myopericarditis) [11]
• If troponin elevated + normal LV function = myopericarditis (good prognosis)
• If troponin elevated + wall motion abnormality = consider myocarditis or infarction

Aetiological Workup (Selective):

• Renal function (uraemia)
• Thyroid function (hypothyroidism)
• Antinuclear antibody, dsDNA (SLE)
• Rheumatoid factor, anti-CCP (rheumatoid arthritis)
• HIV serology (if risk factors or TB)
• QuantiFERON/Mantoux (TB suspicion)
• Blood cultures (purulent pericarditis)

Imaging

Transthoracic Echocardiography (Essential):

All patients with suspected pericarditis require echocardiography to:

• Detect pericardial effusion (present in ~60% of acute cases)
• Assess effusion size and distribution
• Evaluate for tamponade physiology
• Assess ventricular function (exclude myocardial involvement)

Echocardiographic Features of Tamponade:

1. Right atrial collapse (systolic) - Early sign
2. Right ventricular diastolic collapse - More specific
3. Dilated IVC with less than 50% inspiratory collapse
4. Respiratory variation in mitral/tricuspid inflow (> 25% mitral, > 40% tricuspid)
5. "Swinging heart" in massive effusion

Chest Radiograph:

• Usually normal in uncomplicated pericarditis
• "Water bottle" silhouette only with large effusion (> 250mL)
• May show pleural effusion (pleuropericarditis)
• Calcification suggests chronic/constrictive pericarditis

Cardiac MRI:

• Gold standard for detecting pericardial inflammation (delayed gadolinium enhancement)
• Quantifies myocardial involvement
• Differentiates constrictive pericarditis from restrictive cardiomyopathy
• Indicated for: Recurrent pericarditis, diagnostic uncertainty, suspected myocardial involvement

CT Chest:

• Demonstrates pericardial thickening and calcification
• Alternative to MRI when contraindicated
• Useful for detecting associated pathology (malignancy, TB)

Pericardiocentesis and Fluid Analysis

Indications:

• Cardiac tamponade (therapeutic)
• Suspected purulent or tuberculous pericarditis (diagnostic and therapeutic)
• Large effusion of unknown aetiology
• Failure to respond to medical therapy

Fluid Analysis:

---

6. Classification and Staging

Temporal Classification

Risk Stratification (ESC 2015)

Exam Detail: High-Risk Features Requiring Hospitalisation:

Major Criteria (at least 1 = admit):

• Fever > 38°C
• Subacute onset
• Large pericardial effusion (> 20mm)
• Cardiac tamponade
• Failure to respond to NSAIDs after 1 week

Minor Criteria (at least 1 = consider admission):

• Myopericarditis (elevated troponin)
• Immunosuppression
• Trauma
• Oral anticoagulant therapy

Low-Risk Features (outpatient management appropriate):

• Absence of above features
• Typical viral prodrome
• Small/no effusion
• Normal troponin
• Rapid response to NSAIDs

---

7. Management

Treatment Goals

1. Symptom relief (pain control)
2. Resolution of inflammation
3. Prevention of recurrence
4. Management of complications

First-Line Therapy: NSAIDs + Colchicine

Evidence: The Colchicine Trials - Landmark Evidence:

COPE Trial (2005): First RCT demonstrating colchicine benefit. 120 patients randomised to aspirin ± colchicine. Recurrence at 18 months: 10.7% vs 32.3% (p=0.004). [3]

ICAP Trial (2013): 240 patients with first episode acute pericarditis. Colchicine + aspirin vs aspirin alone. Primary endpoint (recurrence/incessant disease): 16.7% vs 37.5% (NNT=4). [4]

CORP Trial (2011): 120 patients with first recurrence. Recurrence at 18 months: 24% vs 55% with colchicine. [12]

CORP-2 Trial (2014): 240 patients with multiple recurrences. Confirmed sustained benefit of colchicine in recurrent disease. [13]

Conclusion: Colchicine reduces recurrence by approximately 50% and is now mandated in all guidelines as first-line therapy alongside NSAIDs.

NSAID Selection:

NSAID Tapering Protocol:

• Reduce dose by 25-50% every 1-2 weeks
• Continue until CRP normalises
• Taper only if asymptomatic and CRP less than 3 mg/L

Colchicine:

• Dose: 500mcg twice daily (if > 70kg) or 500mcg once daily (if ≤70kg or intolerant)
• Duration: 3 months for first episode; 6-12 months for recurrent disease
• Mechanism: Inhibits microtubule polymerisation, neutrophil migration, and NLRP3 inflammasome activation
• Side effects: Diarrhoea (dose-limiting, ~10%), nausea
• Contraindications: Severe renal impairment (CrCl less than 30 mL/min), severe hepatic impairment, co-administration with strong CYP3A4 inhibitors or P-glycoprotein inhibitors

Drug Interactions:

Gastric Protection:

• All patients on NSAIDs should receive proton pump inhibitor cover (e.g., omeprazole 20mg OD)

Second-Line Therapy: Corticosteroids

Critical Principle: Corticosteroids are NOT first-line therapy and should be avoided if possible.

Clinical Pearl: Steroids Increase Recurrence:

ESC guidelines strongly advise AGAINST routine corticosteroid use. Evidence demonstrates:

• 2-4 fold increased risk of recurrence [6]
• Prolonged disease course
• Difficulty weaning (steroid-dependent pericarditis)

Use only when NSAIDs/colchicine are contraindicated or have failed.

Indications for Corticosteroids:

• True NSAID/colchicine contraindication (severe renal impairment, allergy)
• Failure of NSAID + colchicine combination
• Specific aetiologies: Autoimmune (SLE, RA), TB (adjunctive)

Dosing:

• Prednisolone 0.2-0.5 mg/kg/day (LOW dose)
• Maintain minimum effective dose for 2-4 weeks
• Taper SLOWLY (reduce by 2.5-5mg every 2-4 weeks)
• Continue colchicine throughout steroid treatment and taper
• Total taper duration: Several months

Third-Line Therapy: IL-1 Inhibitors

Anakinra (Kineret) and Rilonacept (Arcalyst):

Reserved for colchicine-resistant, steroid-dependent recurrent pericarditis.

Evidence: AIRTRIP Trial (2016): 21 patients with corticosteroid-dependent recurrent pericarditis received anakinra 100mg daily. During 2-month anakinra treatment, zero recurrences. After stopping, recurrence rate 30% in anakinra group vs 89% in placebo (pless than 0.001). [14]

RHAPSODY Trial (2021): Phase 3 trial of rilonacept (IL-1 trap) in recurrent pericarditis. 86 patients randomised after run-in period. Rilonacept group: 7% recurrence vs 74% placebo (HR 0.04; pless than 0.0001). [15]

Rilonacept received FDA approval for recurrent pericarditis in 2021.

Fourth-Line Therapy: Pericardiectomy

Indications:

• Refractory recurrent pericarditis failing all medical therapy
• Constrictive pericarditis

Considerations:

• High-risk surgery (5-10% perioperative mortality)
• Requires cardiothoracic referral
• Optimal timing controversial (earlier intervention may have better outcomes)

Specific Aetiologies

Tuberculous Pericarditis:

• Standard 6-month anti-TB therapy (2 months HRZE + 4 months HR)
• Adjunctive corticosteroids: Prednisolone 60mg/day tapered over 6-8 weeks
• Reduces constrictive pericarditis risk (NNT ~12) [9]
• Early pericardiectomy if constriction develops

Purulent Pericarditis:

• Surgical emergency
• Immediate pericardial drainage (pericardiocentesis or surgical)
• Broad-spectrum IV antibiotics (cover Staphylococcus, Streptococcus)
• Consider pericardiectomy for loculated effusion

Uraemic Pericarditis:

• Intensify dialysis (daily dialysis until resolution)
• NSAIDs contraindicated (renal toxicity)
• Consider low-dose corticosteroids if no response to dialysis
• Pericardiocentesis if haemodynamic compromise

Post-MI Pericarditis:

• Early peri-infarction: Continue aspirin; avoid other NSAIDs (may impair healing)
• Dressler's syndrome: High-dose aspirin (up to 650mg QID) + colchicine

Activity Restriction

Viva Point: Critical Exam Point - Exercise Restriction:

All patients with acute pericarditis should avoid competitive sports and strenuous exercise until:

1. Symptoms have resolved
2. CRP has normalised
3. ECG has normalised (or stabilised)
4. Echo shows no significant effusion

Duration:

• Non-athletes: Minimum 3 months
• Athletes: Minimum 3 months for uncomplicated pericarditis; 6 months for myopericarditis (troponin positive) [16]

Rationale: Exercise may exacerbate inflammation and, in myopericarditis, increases risk of arrhythmia and sudden cardiac death.

Special Populations

Pregnancy:

• NSAIDs: Safe in first and second trimester; CONTRAINDICATED after 20 weeks (premature ductus arteriosus closure, oligohydramnios)
• Colchicine: Limited data but emerging evidence suggests safety; use with caution
• Preferred approach in third trimester: Low-dose prednisolone (not extensively metabolised by placenta)
• Ibuprofen: Safe during breastfeeding

Renal Impairment:

• Avoid NSAIDs (AKI, fluid retention)
• Reduce colchicine dose (500mcg OD if CrCl 30-50; avoid if less than 30)
• Low-dose steroids may be necessary

Elderly:

• Avoid indomethacin (CNS effects)
• Monitor for NSAID complications (GI bleed, renal impairment, CV events)
• Reduce colchicine dose

Discharge Criteria and Follow-Up

Safe Discharge Checklist:

1. Pain controlled with oral analgesia
2. Haemodynamically stable
3. No evidence of tamponade on echo
4. Troponin stable or negative
5. Prescription: NSAID + PPI + colchicine (3 months)
6. Written safety-net advice (red flags for tamponade)
7. Follow-up arranged: Cardiology clinic 4-6 weeks, repeat echo

---

8. Complications

Cardiac Tamponade

The most immediately life-threatening complication, occurring when pericardial fluid accumulates faster than the pericardium can stretch, causing external cardiac compression.

Pathophysiology:

• Intrapericardial pressure exceeds right heart filling pressures
• Impaired diastolic filling → reduced stroke volume → shock
• Rate of accumulation more important than absolute volume
  • "Acute: 150-200mL may cause tamponade"
  • "Chronic: > 1000mL may be tolerated"

Beck's Triad:

1. Hypotension
2. Elevated jugular venous pressure
3. Muffled heart sounds

Pulsus Paradoxus:

• Exaggerated fall in systolic BP (> 10 mmHg) during inspiration
• Mechanism: Inspiration → increased RV filling → interventricular septum bows into LV → reduced LV filling → decreased stroke volume
• Assessed by: Sphygmomanometer (disappearance of Korotkoff sounds during inspiration)

Echocardiographic Features:

• RA systolic collapse (early, sensitive)
• RV diastolic collapse (more specific)
• Dilated IVC with less than 50% inspiratory collapse
• Exaggerated respiratory variation in mitral/tricuspid inflow velocities
• "Swinging heart" (massive effusion)

Management:

• Emergency pericardiocentesis (subxiphoid approach, ultrasound-guided)
• IV fluid bolus (increases preload, temporising measure)
• Avoid positive pressure ventilation if possible (further reduces venous return)
• Inotropes: Minimal effect; definitive drainage is key
• Surgical pericardial window for recurrent/loculated effusions

Pericardiocentesis Procedure

Procedure Detail: Technique (Subxiphoid Approach):

1. Position: Semi-recumbent (45°), continuous ECG monitoring
2. Site: Left paraxiphoid, between xiphisternum and left costal margin
3. Preparation: Local anaesthesia, ultrasound guidance (mandatory unless arrest imminent)
4. Insertion: 18G needle at 45° angle, directed towards left shoulder
5. Monitoring: Aspirate while advancing; connect needle to V lead of ECG (ST elevation = myocardial contact)
6. Aspiration: Straw-coloured, serosanguinous, or frankly bloody fluid
7. Seldinger technique: Guidewire → pigtail catheter for drainage
8. Samples: Send for biochemistry, cytology, microbiology (AFB, TB PCR)

Complications:

• Cardiac perforation (RV most common)
• Arrhythmias (VT/VF)
• Pneumothorax
• Hepatic injury
• Coronary artery laceration (rare)

Post-procedure:

• Leave drain in situ until output less than 25-30mL/24 hours
• Daily echocardiography
• Remove drain under sterile conditions

Recurrent Pericarditis

Affects 15-30% of patients after first episode; risk increases with each recurrence.

Definition: Recurrence after symptom-free interval of ≥4-6 weeks (distinguishes from incessant pericarditis)

Management Approach:

Constrictive Pericarditis

Late complication where scarred, fibrotic, ± calcified pericardium encases the heart, impairing diastolic filling.

Aetiology:

• Tuberculous pericarditis (highest risk: 30-50%)
• Post-cardiac surgery
• Post-radiation
• Recurrent idiopathic pericarditis (rare)

Clinical Features:

• Right heart failure predominates: JVP elevation, peripheral oedema, ascites, hepatomegaly
• Kussmaul's sign: Paradoxical rise in JVP with inspiration
• Pericardial knock: Early diastolic sound (earlier and higher-pitched than S3)
• May be confused with restrictive cardiomyopathy

Investigations:

• Echo: Septal bounce (ventricular interdependence), respiratory variation
• CT: Pericardial calcification, thickening
• MRI: Pericardial thickening, inflammation (if active)
• Cardiac catheterisation: Equalisation of diastolic pressures, "square root sign"

Differentiating Constriction from Restriction:

Management:

• Pericardiectomy (radical pericardial stripping)
• Operative mortality: 5-10%
• Better outcomes with earlier surgery (before end-stage disease)

Effusive-Constrictive Pericarditis

Hybrid presentation with features of both effusion and constriction. After pericardiocentesis, elevated filling pressures persist due to underlying visceral pericardial constriction.

---

9. Prognosis and Outcomes

Mortality:

• Viral/idiopathic: less than 1%
• TB: 17-40% (higher in HIV-positive)
• Purulent: 20-30% even with treatment
• Malignant: Related to underlying cancer prognosis

---

10. Key Guidelines

European Society of Cardiology (ESC) 2015 Guidelines [1]

Key recommendations:

• Diagnosis requires ≥2 of 4 criteria
• First-line: NSAIDs + colchicine
• Echo for all patients
• Avoid steroids unless contraindication to NSAIDs/colchicine
• Activity restriction until resolved

American Heart Association (AHA) Scientific Statement 2020 [17]

Recommendations align with ESC with additional emphasis on:

• Risk stratification to guide admission
• Role of cardiac MRI in diagnosis
• IL-1 inhibitors for refractory disease

---

11. Exam-Focused Section

Common Exam Questions

1. "What are the ECG features of acute pericarditis and how do you differentiate from STEMI?"
2. "Describe the management of acute pericarditis including evidence base"
3. "What are the indications for pericardiocentesis?"
4. "How do you differentiate constrictive pericarditis from restrictive cardiomyopathy?"
5. "What are the complications of pericarditis and how do you manage them?"

Viva Points

Viva Point: Opening Statement:

"Acute pericarditis is inflammation of the pericardial sac, presenting with pleuritic chest pain, pericardial friction rub, and characteristic ECG changes of widespread ST elevation with PR depression. It is most commonly idiopathic or viral in origin. First-line management consists of NSAIDs combined with colchicine, which reduces recurrence by approximately 50% as demonstrated in the COPE and ICAP trials."

Key Facts to Quote:

• Incidence: 27.7 per 100,000 per year
• Recurrence without colchicine: 15-30%
• Recurrence with colchicine: 10-15% (50% reduction)
• ICAP trial NNT = 4 to prevent one recurrence
• Troponin elevated in 35-50% (myopericarditis)

Common Mistakes

What gets you failed:

• Thrombolysing pericarditis (misdiagnosed as STEMI)
• Using steroids as first-line therapy
• Missing tamponade in hypotensive patient
• Forgetting colchicine in the treatment plan
• Not restricting activity in athletes
• Missing TB pericarditis in at-risk populations

Model Answer

Q: "A 30-year-old man presents with sharp chest pain worse on lying flat and relieved by sitting forward. His ECG shows widespread ST elevation. How would you approach this?"

A: "Based on the history of sharp, positional chest pain and ECG findings, I am concerned about acute pericarditis. I would:

First, differentiate from STEMI by examining the ECG - in pericarditis I would expect diffuse concave ST elevation across multiple vascular territories, PR depression, and absence of reciprocal changes, unlike the regional convex ST elevation with reciprocals seen in STEMI.

I would take a focused history asking about viral prodrome, autoimmune conditions, recent cardiac procedures, and risk factors for TB. On examination, I would listen specifically for a pericardial friction rub.

My investigations would include troponin (to assess for myopericarditis), inflammatory markers, renal function (to exclude uraemia), and an urgent echocardiogram to assess for pericardial effusion and exclude tamponade.

For management, assuming no contraindications and low-risk features, I would initiate high-dose ibuprofen 600mg TDS with PPI cover, plus colchicine 500mcg BD for 3 months. I would advise activity restriction until symptoms, CRP and ECG have normalised, typically at least 3 months.

I would arrange outpatient cardiology follow-up with repeat echo. Red flag symptoms warranting immediate return would include worsening breathlessness, syncope, or new fever."

---

12. Patient Information

Key Messages

1. Take your medications as prescribed - Colchicine for 3 months prevents recurrence
2. Rest is essential - Avoid strenuous exercise until cleared by your doctor
3. Know the warning signs - Seek immediate help for worsening breathlessness, fainting, or high fever

Frequently Asked Questions

"Is this a heart attack?" No, your heart arteries are fine. Pericarditis is inflammation of the protective sac around the heart, not a blockage.

"Why can't I exercise?" Exercise can worsen inflammation and delay healing. In some cases, it can trigger dangerous heart rhythms. Rest is part of your treatment.

"Will it come back?" About 1 in 4 people experience a recurrence, but taking colchicine reduces this risk by half.

"How long until I'm better?" Most people feel significantly better within 1-2 weeks. Complete recovery typically takes 2-3 months.

When to Seek Emergency Help

Contact emergency services (999/911) immediately if you experience:

• Severe breathlessness, especially lying flat
• Fainting or near-fainting
• Chest pain that changes character (becomes crushing/heavy)
• High fever (> 38°C)
• Feeling very unwell

Lifestyle Advice

• Return to work: Most can return within 1-2 weeks if pain controlled
• Driving: Safe when not taking sedating painkillers and pain doesn't distract
• Sexual activity: Safe to resume when pain controlled (counts as moderate exercise)
• Flying: Avoid long-haul flights during acute phase

---

13. References

1. Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J. 2015;36(42):2921-2964. doi:10.1093/eurheartj/ehv318 PMID: 26320112

2. Imazio M, Cecchi E, Demichelis B, et al. Indicators of poor prognosis of acute pericarditis. Circulation. 2007;115(21):2739-2744. doi:10.1161/CIRCULATIONAHA.106.662114 PMID: 17502574

3. Imazio M, Bobbio M, Cecchi E, et al. Colchicine in addition to conventional therapy for acute pericarditis: results of the COlchicine for acute PEricarditis (COPE) trial. Circulation. 2005;112(13):2012-2016. doi:10.1161/CIRCULATIONAHA.105.542738 PMID: 16186437

4. Imazio M, Brucato A, Cemin R, et al. A randomized trial of colchicine for acute pericarditis (ICAP). N Engl J Med. 2013;369(16):1522-1528. doi:10.1056/NEJMoa1208536 PMID: 23992601

5. Imazio M, Spodick DH, Brucato A, Trinchero R, Adler Y. Controversial issues in the management of pericardial diseases. Circulation. 2010;121(7):916-928. doi:10.1161/CIRCULATIONAHA.108.844753 PMID: 20177006

6. Imazio M, Brucato A, Cumetti D, et al. Corticosteroids for recurrent pericarditis: high versus low doses: a nonrandomized observation. Circulation. 2008;118(6):667-671. doi:10.1161/CIRCULATIONAHA.107.761064 PMID: 18645054

7. Lazaros G, Imazio M, Brucato A, et al. The role of the inflammasome in pericarditis: molecular insights and potential therapeutic implications. Eur Heart J. 2018;39(9):745-751. doi:10.1093/eurheartj/ehx760

8. Imazio M, Brucato A, Ferrazzi P, et al. Colchicine for prevention of postpericardiotomy syndrome and postoperative atrial fibrillation: the COPPS-2 randomized clinical trial. JAMA. 2014;312(10):1016-1023. doi:10.1001/jama.2014.11026 PMID: 25172965

9. Mayosi BM, Ntsekhe M, Bosch J, et al. Prednisolone and Mycobacterium indicus pranii in tuberculous pericarditis (IMPI). N Engl J Med. 2014;371(12):1121-1130. doi:10.1056/NEJMoa1407380 PMID: 25178809

10. Rossello X, Wiegerinck RF, Alguersuari J, et al. New electrocardiographic criteria to differentiate acute pericarditis and myocardial infarction. Am J Med. 2014;127(3):233-239. doi:10.1016/j.amjmed.2013.11.006 PMID: 24280354

11. Imazio M, Demichelis B, Parrini I, et al. Day-hospital treatment of acute pericarditis: a management program for outpatient therapy. J Am Coll Cardiol. 2004;43(6):1042-1046. doi:10.1016/j.jacc.2003.09.055 PMID: 15028364

12. Imazio M, Brucato A, Cemin R, et al. Colchicine for recurrent pericarditis (CORP): a randomized trial. Ann Intern Med. 2011;155(7):409-414. doi:10.7326/0003-4819-155-7-201110040-00359 PMID: 21969341

13. Imazio M, Belli R, Brucato A, et al. Efficacy and safety of colchicine for treatment of multiple recurrences of pericarditis (CORP-2): a multicentre, double-blind, placebo-controlled, randomised trial. Lancet. 2014;383(9936):2232-2237. doi:10.1016/S0140-6736(13)62709-9 PMID: 24694983

14. Brucato A, Imazio M, Gattorno M, et al. Effect of Anakinra on recurrent pericarditis among patients with colchicine resistance and corticosteroid dependence: the AIRTRIP randomized clinical trial. JAMA. 2016;316(18):1906-1912. doi:10.1001/jama.2016.15826 PMID: 27825009

15. Klein AL, Imazio M, Cremer P, et al. Phase 3 trial of interleukin-1 trap rilonacept in recurrent pericarditis (RHAPSODY). N Engl J Med. 2021;384(1):31-41. doi:10.1056/NEJMoa2027892 PMID: 33200890

16. Pelliccia A, Solberg EE, Papadakis M, et al. Recommendations for participation in competitive and leisure time sport in athletes with cardiomyopathies, myocarditis, and pericarditis: position statement of the Sport Cardiology Section of the European Association of Preventive Cardiology (EAPC). Eur Heart J. 2019;40(1):19-33. doi:10.1093/eurheartj/ehy730 PMID: 30561613

17. Chiabrando JG, Bonaventura A, Vecchie A, et al. Management of acute and recurrent pericarditis: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020;75(1):76-92. doi:10.1016/j.jacc.2019.11.021 PMID: 31918837

18. Troughton RW, Asher CR, Klein AL. Pericarditis. Lancet. 2004;363(9410):717-727. doi:10.1016/S0140-6736(04)15648-1 PMID: 15001332

19. Imazio M, Gaita F, LeWinter M. Evaluation and treatment of pericarditis: a systematic review. JAMA. 2015;314(14):1498-1506. doi:10.1001/jama.2015.12763 PMID: 26461998

20. Lazaros G, Antonopoulos AS, Lazarou E, et al. Age- and sex-based differences in patients with acute pericarditis. Eur J Clin Invest. 2021;51(3):e13392. doi:10.1111/eci.13392 PMID: 32936459

---

Copyright 2025 MedVellum. All rights reserved. This content is for educational purposes only and does not constitute medical advice.