Acute pericarditis is an acute inflammatory syndrome of the pericardium accounting for approximately 5% of all emergency department presentations for non-ischaemic acute chest pain 1,2. Diagnosis is established clinically using the European Society of Cardiology (ESC) criteria, and first-line management combines colchicine with aspirin or a non-steroidal anti-inflammatory drug (NSAID) to prevent recurrence 1,3.
Epidemiology
Acute pericarditis occurs across all age groups but exhibits a peak incidence in men aged 16–65 years 1,2. Up to 15–30% of patients treated without colchicine experience recurrent pericarditis within 18 months 3.
Aetiology
In developed countries, 80–90% of cases are idiopathic or presumed viral in origin 1,2:
infectious: viral (coxsackievirus, echovirus, adenovirus, SARS-CoV-2, HIV), bacterial (Mycobacterium tuberculosis — the leading cause in endemic regions), fungal
autoimmune and post-cardiac injury: systemic lupus erythematosus (SLE), rheumatoid arthritis, Dressler syndrome (post-myocardial infarction pericarditis), post-pericardiotomy syndrome 1
metabolic: uraemic pericarditis in advanced chronic kidney disease, myxoedema
neoplastic: metastatic lung or breast carcinoma, lymphoma
Clinical presentation
According to the European Society of Cardiology (ESC) guidelines, a clinical diagnosis of acute pericarditis requires at least 2 of the following 4 criteria 1:
pericarditic chest pain (>85–90% of cases): sharp, pleuritic retrosternal pain that radiates to the trapezius ridge (via phrenic nerve innervation) and improves upon sitting upright and leaning forward
pericardial friction rub (<33% of cases): high-pitched, scratchy, triphasic auscultatory sound best heard at the left lower sternal border with the patient leaning forward at end-expiration
characteristic ECG changes (up to 60% of cases): new widespread ST-segment elevation and/or PR-segment depression
pericardial effusion (up to 60% of cases): new or worsening effusion on transthoracic echocardiography
Investigations
ECG
The 12-lead ECG classically evolves through four sequential stages 1,2:
stage 1 (hours to days): widespread concave ("saddle-shaped") ST-segment elevation and PR-segment depression across limb and precordial leads, with reciprocal ST depression and PR elevation in lead aVR (and V1); presence of Spodick sign (downsloping TP segment)
stage 2 (1–2 weeks): normalisation of ST and PR segments with T-wave flattening
stage 3 (2–3 weeks): diffuse T-wave inversion (occurring only after ST segments have returned to baseline, unlike ST-elevation myocardial infarction)
stage 4 (weeks to months): return to normal baseline ECG
Laboratory
inflammatory markers: elevated C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and leucocytosis support the diagnosis and guide treatment duration 1
cardiac troponin: mildly elevated in 20–30% of patients indicating concomitant epicardial myocardial inflammation (myopericarditis) 1,2
Imaging
transthoracic echocardiography (TTE): recommended in all patients to quantify pericardial effusion and exclude cardiac tamponade (diastolic right ventricular collapse, right atrial systolic collapse, plethoric IVC) 1
cardiac MRI (CMR): demonstrates circumferential pericardial thickening (>3 mm), T2-STIR pericardial oedema, and late gadolinium enhancement (LGE) of the pericardium
Management
first-line medical therapy: high-dose aspirin (750–1000 mg every 8 hours) or ibuprofen (600 mg every 8 hours) with gastroprotection for 1–2 weeks, combined with low-dose colchicine (0.5 mg once daily if <70 kg or 0.5 mg twice daily if ≥70 kg) for 3 months, which halves the recurrence rate 1,3
exercise restriction: avoidance of strenuous physical activity until symptom resolution and normalisation of CRP, ECG, and echocardiogram (minimum 3 months for competitive athletes) 1
corticosteroids: reserved strictly for patients with contraindications to NSAIDs/colchicine or specific autoimmune indications, as early steroid use increases recurrence risk 1,3
Differential diagnosis
ST-elevation myocardial infarction (STEMI): convex ("tombstone") ST elevation localised to a coronary arterial territory, reciprocal ST depression in leads other than aVR/V1, and absence of PR depression 1,2
benign early repolarisation: ST elevation greatest in precordial leads (V2–V5) with J-point notching ("fish-hook" appearance), ST/T ratio <0.25 in lead V6, and no evolutionary changes
pulmonary embolism: pleuritic chest pain with tachycardia, hypoxia, and normal or right-heart strain ECG