Background Information
Definition
Acute pericarditis:
- Inflammation of the pericardium
- Pericarditis can co-exist with myocarditis (inflammation of the myocardium), termed myopericarditis
Aetiology
Causes include: [ref]
- Idiopathic / Viral origin (e.g. Coxsackievirus)
- Most frequent cause in developed countries
- Bacterial, fungal and parasitic infection
- TB pericarditis is common in developing countries and endemic areas
- Autoimmune disorders (e.g. SLE, RA, sarcoidosis)
- Metabolic causes (e.g. uraemia, myxoedema)
- Radiotherapy
- Malignancy
- Trauma (chest)
- Post-cardiac injury syndrome
- Post-myocardial infarction
- Early pericarditis: 1-3 days after transmural MI, due to adjacent myocardial necrosis
- Late pericarditis (Dressler syndrome): 2-10 weeks post-MI, immune-mediated
- Post-cardiac procedures (~10% post AF ablation)
- Post-myocardial infarction
Complications
Acute complications: [ref]
- Pericardial effusion
- Cardiac tamponade
- Myopericarditis (poor prognosis – higher risk of heart failure)
- Atrial arrhythmia (e.g. AF or atrial flutter)
Chronic complications: [ref]
- Recurrence
- Constrictive pericarditis
Diagnosis
Diagnostic criteria: at least 2 out of 4 of the following are present:
- Characteristic chest pain
- Pericardial friction rub
- Suggestive ECG changes
- New or worsening pericardial effusion (on echocardiogram)
Clinical Features
Symptoms
Typical symptoms: [ref]
- Sudden onset of chest pain
- Pleuritic pain in nature
- Relieved by sitting up and leaning forward, but worse lying flat (supine)
- Retrosternal (but can be anywhere else)
- Radiation to the trapezius ridge is highly specific for pericarditis
- Non-productive cough
It is important and common for exam questions to test one’s ability to differentiate between acute pericarditis and ACS. The following favours a diagnosis of acute pericarditis:
- Young age
- Absence of risk factors for coronary artery disease
- Preceding viral infection
- Chest pain nature (i.e. pleuritic, relieved by sitting up and learning forward, worse lying flat)
Signs
Possible examination findings include: [ref]
- Low-grade fever
- Pericardial friction rub on auscultation (<30% patients, but highly specific)
- Best heard on expiration at the lower left sternal edge while learning forward
- Audible when patient holds their breath (distinguishes from pleural rub)
- Muffled heart-sounds (esp. if associated with moderate-large pericardial effusions and/or tamponade)
- Features of the underlying cause
Investigations and Diagnosis
Initial Work Up
- Bloods
- ↑ WCC
- ↑ CRP
- Troponin
- normal or mildly elevated in isolated pericarditis
- ECG
- Imaging
- 1st line (for all suspected cases): transthoracic echocardiography [Ref]
- Potential Findings
- Most common: pericardial effusion
- Other: pericardial thickening / ↑ pericardial brightness (hyperechoic)
- Normal in many cases
- Potential Findings
- Chest X-ray – mainly to exclude alternative causes of chest pain
- Normal in majority of pericarditis cases
- Very large pericardial effusions (>300ml): enlarged cardiac silhouette
- 1st line (for all suspected cases): transthoracic echocardiography [Ref]
Transoesophageal echocardiography (TEE) is NOT part of the routine diagnostic pathway for acute pericarditis. The 2025 ACC expert consensus states TEE (and stress echo) are not generally required for diagnosing pericarditis; it is reserved for specific situations where TTE is inadequate.[Ref]
ECG Findings
Characteristic ECG findings:
- Diffuse concave ST elevation
- Global PR depression
- Reciprocal changes in aVR and V1 (ST depression and PR elevation)
- Spodick’s sign (downsloping TP segment)
An important real-life and exam mimic of acute pericarditis is STEMI, as they both cause ST elevation on ECG.
Main distinguishing features are based on clinical presentation (see above) and ECG changes:
| ECG change | In STEMI | In acute pericarditis |
|---|---|---|
| ST elevation distribution | Localised to coronary artery territory (e.g. inferior leads, anterior leads) | Diffuse ‘global’ ST elevation across most leads, that does not follow the coronary artery territory |
| ST elevation morphology | Convex | Concave |
| Reciprocal ST depression | Seen in opposite coronary artery territory | Only seen in lead aVR |
| PR segment changes | No changes (unless there is concurrent heart block) | Diffuse PR depression (with reciprocal PR elevation in aVR) |
Management
Risk Stratification
If ANY of the following high-risk features are present → admit for inpatient management
- Fever (>38°C)
- Subacute course
- Large pericardial effusion (>20mm)
- Cardiac tamponade
- Failure to respond to aspirin / NSAIDs
- ↑ Troponin
- Immunosuppression
- Oral anticoagulant therapy
- Trauma
Management
Management depends on the cause of acute pericarditis.
Idiopathic / Viral Pericarditis
1st line: offer both of the following:
- Activity restriction
- Avoid strenuous physical activity until asymptomatic and biomarkers have normalised
- Advise athletes not to compete in competitive sports for at least 3 months post-resolution
- High-dose NSAIDs (usually ibuprofen or indomethacin) + colchicine
- Stop NSAIDs after symptom resolution
- Continue colchicine for another 3 months after symptom resolution
Consider low-dose steroids in those who did not respond to NSAIDs + colchicine
- For those with steroid dependence or multiple recurrences: IL-1 inhibitor (e.g. anakinra) is the steroid-sparing agent of choice
Dressler Syndrome
1st line: high-dose aspirin (until symptom resolves) + colchicine (until 3 months after symptom resolution)
Non-aspirin NSAIDs and steroids should be avoided due to increased risk of myocardial rupture and impaired healing after infarction.
TB Pericarditis
Treat with anti-tubercular therapy (usually rifampicin + isoniazid + vitamin B6 + pyrazinamide + ethambutol) +/- corticosteroids
Any Other Causes
Treat underlying cause + supportive care.
References