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Recurrent pericarditis, like chronic myocarditis, is often considered to be an autoimmune consequence of a prior viral infection.1 Both the pericardium and the heart develop from the mesoderm, but embryologically the two organs are quite distinct. The embryonic heart enters and invaginates the pericardial sac giving rise to the visceral pericardium or epicardium on the heart surface, and to the parietal peritoneum.2 They are separated by the pericardial cavity which normally contains 15–50 ml of straw-coloured fluid.
The diagnosis of acute pericarditis is usually based on severe chest pain, diminished heart sounds, sometimes with an audible pericardial friction rub, and typical electrocardiographic changes.3 4 A long list of aetiologies has been associated with pericarditis, including infectious and non-infectious causes. Infectious agents include viral, bacterial and mycotic agents. The viruses implicated in pericarditis include Coxsackievirus B, adenovirus, rhinovirus, echovirus, influenza, cytomegalovirus, herpesvirus and human immunodeficiency virus (HIV). Polymerase chain reaction (PCR) and in situ hybridisation, together with the presence of antibody, are used to identify the most common infectious agents.
Although the diagnosis of pericarditis is relatively straightforward, the aetiology and pathogenesis of the disease remain biological enigmas.5 Many of the problems linked to understanding of the pathogenesis of pericarditis are reflected in other inflammatory diseases that reputedly follow a viral infection. How much of the disease can be attributed to the infectious process itself and how much to a host generated immune response? The issue is not one of purely academic interest. It relates importantly to the approach to treatment. Often acute pericarditis seems to resolve spontaneously.2 Sometimes, however, one or more recurrences take place and the disease may progress to a constrictive pericarditis resulting …