Abstract
Abstract Introduction The objective of this case report is to highlight the difficulties in establishing the proper management in some patients with chronic constrictive pericarditis (CCP). Case Description A 67 year-old-man with a long history of COPD (stage D), coronary heart disease, diabetes mellitus type 2, prostate cancer treated with local radiotherapy and hormonotherapy, was admitted due to progressive fatigue and dyspnoea on exertion,. Three months before he was hospitalised in pulmonary ward because of sudden onset of severe dyspnoea with mild leg oedema, and unusually weak response for typical COPD treatment was observed. At this time local lab test revealed moderately elevated CRP (43.6 mg/l), ESR (36 mm) and NT-proBNP (483 pg/ml). CT scan was performed to exclude pulmonary embolism. No pericardial calcifications were noted. Physical examination showed obesity (33 kg/m2), heato-jugular reflux and mild ankle oedema. Chest auscultation revealed normal lungs sounds and muffled heart sounds. Pleural effusion was excluded and no ascites nor hepatomegaly was found. Echocardiography revealed typical changes for CCP prominent septal bounce during inspiration, annulus reversus (TDI e` lat 16 cm/sek; e` med 18 cm/sek), annulus paradoxus (E/e` 8), normal LV function, dilated vena cava inferior (VCI). MRI showed thickened pericardium (5mm) particularly near the right ventricle (RV) and thick layer of fatty tissue (15 mm) localised in pericardium, next to the RV free wall. RV was compressed (fig.1). LVEF was 63%, EDV 117 ml, SV 74 ml, SVi 33 ml/m2, LV mass 78 g; RV EF 71%, EDV 72 ml/m2, right atrium enlargement was found (38 cm2), while left atrium was of normal size (22 cm2). VCI and hepatic veins were dilated (29 mm and 13mm respectively. Fig 1. MRI – thickened pericardium containing thick fatty tissue causin with RV compression After diuretic uptitration, the dyspnoea improved to NYHA I/II. Due to clinical improvement heart team decided to continue medical treatment. Due to comorbidities (DM, COPD, obesity), the risk of pericardiectomy was considered high. Three month later the patient was hospitalized due to sudden dyspnoea and subsequent cardiac arrest. Despite cardiopulmonary resuscitation the patient died in ICU. CCP was confirmed in autopsy. Discussion The diagnosis of CCP remains challenging. In this case the presentation was not fully typical. There was no clear precipitating factor, the history was relatively short and the symptoms and signs mild. CT scan did not show pericardial calcifications. Although TTE revealed typical features of CCP and MRI confirmed compression of the right ventricle, the heart team did not confirm the need for pericardiectomy, which is treatment of choice in progressive CCP. Abstract P1484 Figure. Fig.1
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