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Jordi Soler-Soler, Jaume Sagristà-Sauleda, Gaietà Permanyer-Miralda, Aetiologic diagnosis of pericardial disease: worthy efforts may not be applied in the appropriate direction, European Heart Journal, Volume 27, Issue 16, August 2006, Pages 1898–1899, https://doi.org/10.1093/eurheartj/ehl156
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The aetiologic diagnosis of pericardial disease has something of a paradox. On the one hand, the precise aetiology of many, perhaps most, instances of pericarditis remains an enigma in individual patients. Fortunately, for management purposes, such precise diagnosis is virtually irrelevant in most cases, as spontaneous cure is the rule in such patients; however, in a few patients, it may prove crucial. On the other hand, because of the poor specificity of many clinical findings, patients needing aetiologically guided intervention may remain unnoticed until too late.
Not rarely, when concomitant disease does not point at a likely aetiological association, the only means of assessing if pericardial disease is due to specific mechanisms requiring individual therapy is to examine the pericardial fluid or tissue. If often poorly acknowledged as such, the challenge has always been to know in which patients the study of pericardial fluid or tissue is likely to be rewarding in terms of discovering specific, treatable disease. The key issue in acute pericardial disease is whether or when investigation of pericardial fluid or tissue in search of the aetiologic diagnosis is warranted for clinical purposes. To do too many invasive investigations would amount to a number of irrelevant or inconclusive findings in patients who will otherwise spontaneously recover (i.e. those with viral infection or with the classically called acute idiopathic pericarditis, no matter what its aetiologic or pathogenetic mechanisms are), whereas failing to investigate pericardial fluid or tissue in patients with purulent, tuberculous, or neoplastic pericardial disease would represent missing the opportunity to cure or alleviate serious disease. Algorithms have been proposed for guidance in that decision.1–5 As a rule, septic status or concomitant bacterial infection, haemodynamic compromise in the form of overt tamponade, or prolonged (more than 3 weeks) clinical course are the usual clues that help identifying patients with greater likelihood of specific, treatable disease in whom invasive pericardial studies are warranted. In the absence of these clinical features, the vast majority of patients with pericarditis has a full recovery only with symptomatic therapeutic measures. These algorithms are based on the epidemiological notions of what are the most common pericardial disorders in specific areas and could vary in specific regional or hospital settings where a given disease is more prevalent. In contrast, other current recommendations seem to be based on pursuing any likely abnormalities that can be detected by invasive pericardial studies, irrespective of their clinical significance or therapeutic relevance or the epidemiological background.6–8
