Acute pericarditis
Description
- Inflammation of the pericardium, with or without effusion
Diagnostic criteria - >=2 of 4
1. Pleuritic chest pain - sharp, worse lying flat and on inspiration, relieved by sitting forward
2. Pericardial friction rub - scratchy, triphasic, best at the left sternal edge leaning forward, evanescent
3. Widespread concave ("saddle-shaped") ST elevation, or PR depression
4. New or worsening pericardial effusion
- Supporting: raised CRP/ESR, pericardial inflammation on CT or CMR
Nomenclature
| Term | Definition |
|---|---|
| Acute | First episode |
| Incessant | Symptoms continuing >4-6 weeks but <3 months without remission |
| Recurrent | New episode after a symptom-free interval of >=4-6 weeks |
| Chronic | >3 months |
Myopericarditis vs perimyocarditis
- Myopericarditis - pericarditis predominant + raised troponin, preserved LV function
- Perimyocarditis - myocardial predominant + new LV dysfunction or wall motion abnormality
- Troponin elevation occurs in ~15-30%, does not worsen prognosis in myopericarditis, but does change management: exercise restriction and avoidance of high-dose NSAIDs
Epidemiology
- ~0.1% of hospital admissions; ~5% of ED chest pain presentations without MI
- Incidence ~27 per 100,000/yr
- M>F, peak 20-50 yrs
- ~80-90% idiopathic (presumed viral) in developed countries
- Tuberculous pericarditis dominates in high-TB-prevalence settings and in HIV - the commonest cause worldwide
Aetiopathogenesis
Causes
- Idiopathic/viral ~80-90% - enterovirus, echovirus, adenovirus, EBV, CMV, influenza, parvovirus B19, HIV, SARS-CoV-2
- Bacterial - tuberculosis (dominant globally), purulent (staphylococcal, pneumococcal - rare, fulminant, high mortality)
- Autoimmune/inflammatory - SLE, rheumatoid arthritis, systemic sclerosis, Sjogren, vasculitis, sarcoid, familial Mediterranean fever, TRAPS, IBD
- Post-cardiac injury syndromes
- Dressler syndrome - weeks after MI, immune-mediated
- Post-pericardiotomy syndrome - after cardiac surgery
- After PCI, ablation or device implantation (consider perforation)
- Neoplastic - lung, breast, lymphoma, melanoma, mesothelioma; usually with effusion
- Metabolic - uraemia (classically with a rub and no ECG changes), dialysis-associated, myxoedema
- Radiation - previous mediastinal radiotherapy; drives late constriction
- Drugs - hydralazine, procainamide, isoniazid, phenytoin (drug-induced lupus); immune checkpoint inhibitors; minoxidil; mRNA COVID-19 vaccines (young males, self-limiting)
- Trauma, aortic dissection extending into the pericardium
Mechanism
- Inflammation -> fibrinous exudate -> rub; +/- exudative effusion
- Recurrence is driven by autoinflammation, principally the IL-1 pathway (NLRP3 inflammasome -> IL-1beta)
- This is why colchicine works, and why IL-1 blockade works when nothing else does
- Corticosteroids impair viral clearance and promote a steroid-dependent relapsing course
Diagnosis
ECG - four classical stages (only a minority show all)
| Stage | Finding |
|---|---|
| I | Widespread concave ST elevation + PR depression; *PR elevation and ST depression in aVR* |
| II | ST normalises, T waves flatten |
| III | Widespread T wave inversion |
| IV | Normalisation (weeks-months) |
Pericarditis vs STEMI - the discrimination that matters
| Pericarditis | STEMI | |
|---|---|---|
| ST morphology | Concave (saddle) | Convex (tombstone) |
| Distribution | Widespread, crosses territories | Territorial |
| Reciprocal change | None (except aVR and V1) | Present |
| PR segment | Depressed (elevated in aVR) | Normal |
| Q waves | Absent | May develop |
| Evolution | Days-weeks | Hours |
- Spodick's sign - downsloping TP segment - supports pericarditis
Investigations
- Troponin - identifies myocardial involvement
- CRP/ESR - elevated in ~75%; used to guide duration of therapy and confirm resolution before tapering
- FBE, UEC (uraemia), TFT, blood cultures if febrile
- CXR - usually normal; enlarged cardiac silhouette only if effusion >300 mL
- Echocardiography in everyone - effusion, tamponade physiology, LV function, wall motion
- CMR - pericardial late gadolinium enhancement (active inflammation), oedema, myocardial involvement; useful in recurrent disease to decide whether to escalate or taper
- Targeted: autoimmune serology, TB testing (quantiferon, sputum, pericardial fluid ADA), HIV
- Routine extensive aetiological screening in a first, uncomplicated episode is low-yield and not recommended
Admit if any high-risk feature
Major
- Fever >38 degrees C
- Subacute onset
- Large pericardial effusion (echo-free space >20 mm) or tamponade
- Failure to respond to NSAIDs + colchicine after 7 days
Minor
- Myopericarditis (raised troponin)
- Immunosuppression
- Trauma
- Oral anticoagulant therapy
- Any one major or minor criterion, or an identified non-idiopathic cause, warrants admission
Management
A. First episode - NSAID + colchicine together
Not sequential. Colchicine is added from the outset, not after NSAID failure - it roughly halves recurrence.
- NSAID at full anti-inflammatory dose until symptoms resolve and CRP normalises, then taper
- Ibuprofen 600 mg TDS, or aspirin 750-1000 mg TDS (aspirin preferred post-MI), or indometacin
- Typically 1-2 weeks, then taper over 2-4 weeks
- Add a PPI
- Colchicine for 3 months
- 0.5 mg BD (0.5 mg daily if weight <70 kg, elderly, or renal impairment)
- Reduces recurrence from ~30% to ~15%
- Diarrhoea is the dose-limiting effect; check interactions - statins, clarithromycin, ciclosporin, and avoid in significant renal or hepatic impairment
- Exercise restriction until symptom resolution and normal CRP (athletes: >=3 months, and longer with myocardial involvement)
- Taper only once CRP has normalised - tapering on symptoms alone drives relapse
B. Corticosteroids - the trap
- *Steroids increase the risk of recurrence and create steroid dependence - they are not first-line*
- Reserve for:
- NSAID + colchicine failure
- Specific indications: autoimmune/connective tissue disease, uraemic pericarditis, pregnancy (after 20 weeks NSAIDs are contraindicated), NSAID contraindication
- If used: low-to-moderate dose (prednisolone 0.2-0.5 mg/kg/day), not 1 mg/kg, with a very slow taper, and always with colchicine continued
C. Recurrent pericarditis
- Colchicine for at least 6 months + NSAID, tapering the NSAID with CRP guidance
- IL-1 blockade - anakinra, rilonacept (goflikicept in trials)
- Now positioned before or instead of escalating steroids: second-line after NSAID + colchicine where steroids are contraindicated or there are high-risk features, and third-line for steroid-dependent or colchicine-resistant disease
- Rapid symptom relief and marked reduction in recurrence (RHAPSODY, AIRTRIP)
- Injection site reactions are near-universal with anakinra; infection risk; availability in Australia is limited - discuss with rheumatology/cardiology
- Relapse commonly follows withdrawal -> taper slowly, guided by CRP and CMR
- Azathioprine, IVIg - alternative steroid-sparing options
- Pericardiectomy - last resort for refractory, frequently relapsing disease in expert centres
D. Cause-specific
- Purulent - urgent pericardiocentesis/surgical drainage + IV antibiotics; mortality is high without drainage
- Tuberculous - standard anti-tuberculous therapy; adjunctive corticosteroids reduce constriction in HIV-negative patients
- Uraemic - intensify dialysis (the specific treatment); steroids if refractory
- Neoplastic - drainage +/- pericardial window, treat the malignancy, consider intrapericardial sclerosant
- Post-cardiac injury (Dressler, post-pericardiotomy) - aspirin + colchicine; avoid other NSAIDs early post-MI (impaired healing)
- Checkpoint inhibitor - withhold the drug, corticosteroid, oncology discussion
Avoid
- Anticoagulation where avoidable (haemorrhagic effusion) - but do not stop it in a mechanical valve; weigh individually
- Steroids in a first uncomplicated episode
- Stopping colchicine early because the patient feels well
Associations
- Recent viral illness or upper respiratory infection
- Myocardial infarction - early epistenocardiac pericarditis, or late Dressler syndrome
- Cardiac surgery, PCI, ablation, device implantation
- Autoimmune disease - SLE, rheumatoid arthritis, systemic sclerosis, vasculitis, sarcoidosis
- Autoinflammatory syndromes - familial Mediterranean fever, TRAPS (consider in unexplained recurrent pericarditis, especially with a relevant ancestry)
- Chronic kidney disease and dialysis
- Malignancy - lung, breast, lymphoma, mesothelioma
- Tuberculosis and HIV
- Previous mediastinal radiotherapy
- Hypothyroidism
- Drugs: hydralazine, procainamide, isoniazid, phenytoin, checkpoint inhibitors; mRNA COVID-19 vaccines
Natural history & complications
- Idiopathic acute pericarditis is self-limiting in most - symptoms settle within days to weeks on appropriate therapy
- Recurrence in ~15-30% after a first episode (~15% with colchicine, ~30% without)
- After a first recurrence, the risk of further recurrence rises to ~25-50%
- Predictors of recurrence: corticosteroid use, failure to use colchicine, incomplete CRP normalisation before taper, subacute onset
Complications
- Recurrent and incessant pericarditis - the commonest and most disabling outcome; major impact on work, exercise and mood
- Pericardial effusion and cardiac tamponade (~3% of idiopathic; higher in neoplastic, purulent and tuberculous)
- Constrictive pericarditis
- <1% after idiopathic pericarditis
- ~2-5% after autoimmune or neoplastic
- ~20-30% after purulent or tuberculous pericarditis
- Aetiology, not the number of recurrences, predicts constriction - a patient with many idiopathic recurrences is unlikely to constrict
- Transient constriction - resolves with anti-inflammatory therapy; do not rush to pericardiectomy
- Myocardial involvement - arrhythmia, LV dysfunction (usually recovers)
- Treatment complications: NSAID gastrointestinal and renal toxicity, colchicine diarrhoea and myotoxicity, steroid dependence with weight gain, diabetes, osteoporosis
- Prognosis in idiopathic pericarditis is excellent; the morbidity is from recurrence and from the steroids given to treat it
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