A 30-year-old man, recently relocated from Pakistan, presented to the emergency department with a 4-week history of exertional breathlessness and central chest pain. He also had a 2-month history of fever and weight loss.

His electrocardiogram showed sinus tachycardia with T-wave inversion in leads V4–6 (Panel A). C-reactive protein was elevated but with normal serum troponin levels. Computed tomography pulmonary angiography excluded pulmonary embolism but showed pleural and pericardial effusion (Panel B). No pericardial calcification and enhancement were found. Echocardiography showed a bright pericardium (Panel C) with pericardial effusion and dilated inferior vena cava.

Cardiovascular magnetic resonance (CMR) revealed severe pericardial thickening (Panel D), septal bounce, and inspiratory septal flattening consistent with ventricular interdependence (see Supplementary data online, Video S1). Mobility of the lateral left ventricular walls and right ventricular free wall was limited by pericardial attachment, resulting in biventricular systolic impairment (see Supplementary data online, Video S2). The pericardium showed an increased signal on T2-weighted short tau inversion recovery (T2-STIR) sequences (Panel E), suggesting active inflammation, with associated circumferential late gadolinium enhancement (Panel F).

Constrictive pericarditis of presumed tuberculous origin was deemed the most likely diagnosis, and the patient was started on anti-tuberculous treatment. Considering the signs of pericardial inflammation, corticosteroids and colchicine were added and pericardiectomy was deferred. Pleural aspirate was negative but results from pleural biopsy later confirmed mycobacterial infection.

At 4-month follow-up, CMR showed only minimal pericardial thickening (Panel G) and no pericardial inflammation (Panels H and I). Constrictive physiology had resolved (see Supplementary data online, Video S3) and systolic function normalized.

Tuberculosis is the most common aetiology for constrictive pericarditis in endemic areas. CMR can help in distinguishing acute from chronic forms, guiding optimal treatment and subsequent monitoring of treatment response.

Supplementary data are available at European Heart Journal - Cardiovascular Imaging online.

Funding: None declared.

Consent: Written informed consent was obtained.

Data availability: No new data were generated or analysed in support of this article.

Author notes

Victor Voon and Mohammed Y Khanji contributed equally to this work.

Conflict of interest: None declared.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact [email protected] for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact [email protected].

Supplementary data