PMC9905231_01
Physical examination revealed pitting edema of the lower extremities and abdominal distension (A). Chest radiology showed a pleural effusion (B). Electrocardiography (ECG) at admission indicated the diagnosis of atrial fibrillation (AF) [heart rate (HR), 134 bpm] with low voltage in all leads (C). Echocardiography showed left (D) and RA enlargement (E), and a normal LV chamber. Cardiac computed tomographic angiography of the pulmonary arteries excluded pulmonary embolism (F). LV, left ventricle; RV, right ventricle; LA, left atrium; RA, right atrium; AAO, ascending aortic artery; MPA, main pulmonary artery; DAO, descending aortic artery.
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F1
A physical examination revealed distended jugular veins, abdominal distension, pitting edema of both lower extremities (Figure 1A), decreased breath sounds in the right lower lung, and a grade II/VI systolic murmur at the apex of the heart. Chest radiology revealed a right-sided pleural effusion and cardiac enlargement (Figure 1B). T-wave changes was confirmed on electrocardiography (ECG) (Figure 1C). Transthoracic echocardiography (TTE) revealed left atrial (LA) and right atrial (RA) enlargement (LA, 51 mm; RA, 53 mm), mild mitral and tricuspid regurgitation, decreased LV systolic function (LVEF, 45%), diastolic dysfunction, and a normal LV size (42 mm) (Figures 1D, E). Pulmonary embolism was excluded using computed tomography angiogram (CTA) (Figure 1F).
Tissue Doppler imaging (TDI) using echocardiography revealed that e' = 18.4 m/s (medial) > 14.4 m/s (lateral) in the mitral valve (A,B). Significant respiratory variation of mitral or tricuspid peak E velocity was indeterminable due to atrial fibrillation (AF) (C). Paradoxical septal motion during respiration was not observed (D). The inferior vena cava (IVC) was dilated without inspiratory collapse (E). Pulmonary artery pressure was elevated according to the velocity of tricuspid regurgitation (F).
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F2
A repeat TTE revealed mitral lateral annulus e' velocity (14.4 cm/s) < mitral medial annulus e' velocity (18.4 cm/s) using tissue Doppler imaging (TDI) (Figures 2A, B). We were unable to determine significant respiratory variation of mitral and tricuspid peak E velocity due to the AF (Figure 2C). Paradoxical septal motion during respiration was not observed (Figure 2D). The IVC was dilated without inspiratory collapse (Figure 2E). The pulmonary artery pressure (~30 mmHg) was elevated according to the velocity of the tricuspid regurgitation (Figure 2F).
Cardiac computed tomographic angiogram of four-chamber view (A) and volume rendering views (B) showed calcified annular constrictive pericarditis (ACP) trapping both ventricles (red arrows). Spontaneous conversion from atrial fibrillation (AF) to sinus rhythm as the calcified pericardial ring was severed (C). Complete pericardiectomy was performed and revealed a thickened pericardium with calcification embedded in the atrioventricular (AV) groove (D). Pathological examination of the pericardial tissue indicated fibrotic tissue with calcification (E).
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F3
ACP was diagnosed using further CT scan analysis, which showed a thickened and calcified pericardial ring around each AV groove with minimal pericardial calcification; however, radiological pericardial thickening and calcification were not observed on chest X-ray (CXR) (Figures 3A, B). AV groove was revealed. As the calcified pericardial ring was severed, spontaneous conversion to sinus rhythm was observed (Figure 3C). A large amount of fat was observed on the surface, confirming the diagnosis of ACP (Figures 3D, E).