Acute pericarditis is more common in adults (typically between 20 to 50 years old) and in men.[7] It is the most common disease of the pericardium encountered in clinical practice. The true incidence and prevalence of the disease are unknown and there are a large number of undiagnosed cases. However, it may account for up to 5% of presentations to emergency departments for chest pain and up to 0.1% of hospital admissions.[9]

Risk factors

Acute pericarditis is described more commonly in men, particularly in the viral form in which there is a 3:1 male-to-female ratio.[7]

The disorder is more commonly described in adults aged 20 to 50 years.[7]

Two forms of pericarditis following myocardial infarction (MI) exist: 'early' (pericarditis epistenocardica) and 'delayed' (Dressler's syndrome).[14][15] The early form is caused by local inflammation at the epicardial MI border with direct exudation. It occurs in 5% to 20% of transmural MIs, but is not often recognised clinically. The delayed form occurs from 1 week to several months post-infarction and does not require a transmural infarction. Its incidence is 0.5% to 5% (and <0.5% in patients treated with thrombolytics). The incidence of pericarditis following transmural MI has declined since the use of thrombolytics and myocardial re-vascularisation.

Post-pericardiotomy syndrome has been reported in up to 20% of cases 4 weeks after coronary artery bypass grafting. It develops days to months post-operatively. Compared with the post-infarction syndrome, there is a greater anti-heart antibody response (anti-sarcolemmal and anti-fibrillatory) with higher release of antigens.[1][5]

Pericarditis generally results from local tumour invasion, lymphatic spread, or haematogenous spread of a malignant neoplasm. Primary malignant pericardial disease is rare.[2][5]

The patient may present with a recent history of an upper respiratory tract infection or diarrhoeal illness.[8]

Viral pericarditis is the most common pericardial infection.[1][5] The inflammation is due to direct viral attack and/or an immune response (antiviral or anticardiac).

Bacterial pericarditis is a purulent pericarditis caused by bacterial pathogens and occurs in 5% of cases. Pericardial infection can occur by haematogenous spread or by direct extension from adjacent organs, notably the lungs and/or pleural space.

In developed countries, 4% of acute pericarditis cases are due to Mycobacterium tuberculosis.[16]

Two forms exist: uraemic pericarditis and dialysis-associated pericarditis. Uraemic pericarditis is reported in 6% to 10% of patients with acute or chronic renal failure prior to or shortly after institution of dialysis. The likelihood of pericarditis increases with the severity of azotaemia (blood urea nitrogen >21.4 mmol/L [>60 mg/dL]).[1]

Dialysis-associated pericarditis is reported in up to 13% of patients receiving chronic haemodialysis. It is occasionally seen in patients on peritoneal dialysis who have not been adequately dialysed. Most patients respond to intensive dialysis within 1 to 2 weeks.

Pericarditis is commonly associated with diseases such as rheumatoid arthritis and lupus but may not be clinically apparent.[1]

Occurs weeks to months post-event.

Radiotherapy-associated acute exudative pericarditis is rare. Delayed acute pericarditis is more common, and occurs weeks after radiotherapy. It is generally manifested as an asymptomatic pericardial effusion or symptomatic pericarditis. Delayed chronic pericarditis may appear weeks to years after radiotherapy and cause constrictive pericarditis.[17]

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