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Despite a long history, our understanding of the aetiology and pathophysiology of pericardial diseases is still evolving. Pericardial diseases were first described in the 17th century with the description of a disease characterised by dyspnoea and intermittent pulse.1 Pericardial syndromes include pericarditis, pericardial effusion, effusive–constrictive pericarditis, pericardial tamponade and constrictive pericarditis (CP).2 In high-income countries, the most common causes of CP are idiopathic or viral, followed by postcardiac surgery; however, in low-income countries, tuberculous pericarditis is still the most common aetiology of CP.2 Only relatively recently, in 1987, transient constrictive pericarditis (TCP) was first described by Sagristà-Sauleda et al in patients with effusive acute idiopathic pericarditis.3 Subsequently, TCP was described in chemotherapy, collagen vascular disease and bacterial endocarditis, and the natural history of TCP was well elucidated in 2004 by Haley et al, who described a transient form of CP which resolves over time.4 Resolution of TCP without surgery offers a therapeutic opportunity but raises the question—which patients with CP are most likely to benefit from intensive medical treatment, which comes with its own set of potential complications? Recent studies have examined treatment response using laboratory and/or imaging indicators of inflammation.5 6 However, available evidence is insufficient to adopt specific parameters in order to predict the response to anti-inflammatory therapy, especially in patients with minimal or no symptoms (New York Heart Association class I or II).
CP is a diagnosis made on clinical and invasive haemodynamic criteria. However, non-invasive multimodality imaging is the first step in the investigation of pericardial diseases in general and CP in particular.2 Whether imaging is useful for guidance of treatment is a separate question. Using echocardiography …
Contributors MM wrote the first draft. All authors revised the manuscript critically for important intellectual content, and gave approval for the final version.
Funding Dr Moharram was funded by a New Zealand Health Research Council Clinical Research Training Fellowship, reference 19/012.
Competing interests None declared.
Patient and public involvement Patients and/or the public were not involved in the design, conduct, reporting or dissemination plans of this research.
Provenance and peer review Commissioned; internally peer reviewed.
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