ArticleHeliyon2023
Transient constrictive pericarditis following coxsackievirus A4 infection as a rare cause of acute mediastinitis: A case report.
Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 3 citations in OpenAlex.
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2 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Background: Transient constrictive pericarditis (TCP) is a distinct constrictive pericarditis (CP) subtype characterized by acute pericardial inflammation and transient constrictive physiology. If left untreated, it may progress to irreversible CP requiring pericardiectomy. However, making an early diagnosis of TCP remains difficult. Case presentation: A 51-year-old man presented with fever, chest pain, and dyspnea following preceding flu symptoms. An initial investigation suggested right-sided heart failure. Laboratory results revealed elevated inflammatory markers and hepatic enzyme levels. Echocardiography revealed pericardial effusion with a normal ejection fraction and diastolic ventricular septal bounce suggestive of pericardial constriction. Computed tomography suggested acute descending mediastinitis with pericarditis and pleuritis; however, detailed examinations ruled out this possibility. The constellation of increased serological inflammation, pericardial thickness/effusion, and constrictive physiology suggested TCP, confirmed by cardiac magnetic resonance (CMR) and hemodynamic studies. CMR also revealed coexistent myocarditis. After a thorough assessment for the cause of TCP, a viral etiology was suspected. Paired serology for virus antibody titers revealed a significant increase only in coxsackievirus A4 (CVA4) titers. With prompt anti-inflammatory treatment, the patient's pericardial structure and function and concomitant inflammation of the surrounding tissues were nearly completely recovered, leading to a final diagnosis of TCP caused by CVA4. The subsequent clinical course was uneventful without recurrence at the 1-year follow-up. Conclusions: Here we described the first case of TCP caused by CVA4 concurrent with mediastinitis, myocarditis, and pleuritis, all of which were successfully resolved with anti-inflammatory treatment. Acute mediastinitis secondary to TCP is rare. This case highlights the clinical importance of assessing pericardial diseases as a source of acute mediastinitis and considering CVA4 as an etiology of TCP. An evaluation including multimodal cardiac imaging and serology for virus antibody titers may be useful for an exploratory diagnosis of TCP in right-sided heart failure patients with pericardial effusion.
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