Eternal Hospital, Jaipur-India
Clinical History
A 60-year-old woman without diabetes or hypertension was admitted with symptoms of mild cough, dyspnea, and non-specific chest pain. On evaluation, she had blood pressure of 110/78 mmHg, pulse 98 bpm, pulse oxygen saturation 98% on room air, and was afebrile. Physical examination was normal, including heart sounds. Lab assays revealed anemia (Hemoglobin 9.2 g/dl, normal range 12.3 to 15.3 g/dL) with elevated C-reactive protein (CRP) level (230 mg/L, normal <3 mg/L) and elevated erythrocyte sedimentation rate (ESR) which was 118mm/hour (normal range 0-30 mm/hour). Further laboratory examination was within normal limits.
Twelve lead electrocardiogram (ECG) demonstrated normal sinus rhythm. Transthoracic echocardiogram revealed mild to moderate circumferential pericardial effusion with a large hyperechoic mass measuring approximately 60 x 35 mm (Figure 1) in the posterior pericardial space with thickened and irregular pericardial surface. All cardiac chambers were normal in size. There was significant respiratory variation of mitral (Figure 2) and tricuspid (Figure 3) valvular Doppler inflow velocity suggesting tamponade physiology.
In view of the elevated CRP and ESR, with pericardial effusion, the possibility of tubercular pericarditis was considered and contrast enhanced chest computed tomography (CT) was conducted to evaluated for pulmonary involvement. The presence of pericardial mass also prompted cardiovascular magnetic resonance (CMR) to better characterize the mass. Tuberculin purified protein derivative skin test was positive, but sputum was negative for acid fast bacilli (AFB).
CT chest showed small bilateral pleural effusions with sub-segmental atelectasis, scattered mediastinal lymphadenopathy, however no areas of consolidation of nodules characteristic of pulmonary tuberculosis were seen. Moderate to large pericardial effusion with mild peripheral enhancement and a non-enhancing, fat density 5.7 x 3.5 cm mass in the pericardial space, attached to visceral pericardium was diagnosed as a probable lipoma (Figure 4). CMR was advised to better characterize the mass.
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| Figure 1. Echocardiogram short axis (left) and 4-chamber (right) demonstrating large pericardial effusion and large posterior pericardial mass (arrow). | |
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| Figure 2. Mitral valve inflow Doppler with significant respiratory variation across the mitral valve. |
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| Figure 3. Tricuspid valve inflow Doppler with significant respiratory variation across the tricuspid valve. |
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| Figure 4. Computed tomography without (left) and with (right) intravenous contrast demonstrating homogenous, discrete fat density left posterior pericardial mass and pericardial effusion. | |
CMR Findings
CMR performed with and without contrast on a 3T Ingenia scanner (Philips Healthcare, Best, Netherlands) revealed large circumferential pericardial effusion (Figure 5), with left posterior pericardial mass with similar appearance as fat. Tissue characterization demonstrated T1 and T2 hyperintensity to myocardium with appearance similar to fat, with near complete suppression of the mass by fat suppression (Figures 6 and 7). Diffusion weighted images and apparent diffusion coefficient (ADC) maps did not suggest restricted diffusion as would occur with high grade malignancy or abscess (Figure 8). Multi-echo Dixon fat water separation images (Figure 8, lower image) suggested the mass was composed predominantly of fat. Late enhancement images identified no definite enhancement of the mass. There was pericardial thickening and enhancement on post contrast images, suggesting pericarditis (Figure 9). Septal motion did not suggest pericardial constrictive physiology.
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| Figure 5. Axial cine (left) and short axis (right) balanced steady state free precession single shot with a large pericardial effusion, left posterior pericardial mass and pleural effusion present. | |
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| Figure 6. Pre-contrast axial T1-weighted black blood fast spin echo without (left) and with (right) fat saturation demonstrate lipomatous left posterior pericardial mass. | |
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| Figure 7. T2 weighted black blood short axis without (left) and with fat saturation (right) demonstrated lipomatous left posterior pericardial mass. | |
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| Figure 8. Diffusion weighted images (DWI, top) and ADC map (middle) did not identify restricted diffusion that would suggest high grade malignancy or abscess. There is T2 shine due to pericarditis and pericardial fluid attributed to probable tuberculosis. Multi-echo Dixon fat water separation (bottom) suggests the hypo-intense mass is fat containing. |
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| Figure 9. Post contrast phase sensitive inversion recovery (PSIR) short axis image showing pericardial thickening and enhancement, suggesting pericarditis. |
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| Figure 10. Follow-up CT depicts 1 cm decrease in mass dimensions and reduced pericardial thickening and effusion. Decrease in size of lipoma is attributed to shifts in pericardial hemodynamics with reduced effusion size. | |
Conclusion
Based on the baseline CT and CMR findings, a diagnosis of pericardial lipoma with concurrent mild pericarditis was made, and patient was advised surgical excision of the mass. She was also advised antitubercular therapy for associated pericarditis, which was presumed to be tubercular.Patient however declined surgery and agreed to undergo antitubercular therapy. She underwent follow up echocardiography one month later, and it showed the mass was now smaller with markedly reduced size of pericardial effusion. Chest CT was done to confirm these changes, which confirmed interval resolution of bilateral pleural and pericardial effusion, and mild persistent enhancing pericardial thickening. These findings were in keeping with the diagnosis of tubercular pericarditis which improved secondary to antitubercular therapy.
The fatty mass was also smaller measuring 5.0 x 2.5 cm (Figure 10). This was likely due to malleable nature of the pericardial lipoma, which was now compressed by the decreased pericardial space owing to decrease in pericardial effusion. Lipomas are soft masses, which due to the fat component of the lesion can be deformed by outside pressure and redistributed in the pericardial space. Large lesions can cause mass effect on heart; however, this was not the issue in our case as the lesion was relatively small. The patient continues to be in follow up with significant improvement.
Perspective
This case emphasizes the role of multimodality imaging for cardiac masses and associated pathologies, as pericarditis in this case. Four pathological stages of tuberculous pericarditis are recognized: (1) fibrinous exudation with initial polymorphonuclear leukocytosis, relatively abundant mycobacteria, and early granuloma formation with loose organization of macrophages and T cells; (2) serosanguineous effusion with a predominantly lymphocytic exudate with monocytes and foam cells; (3) absorption of effusion with organization of granulomatous caseation and pericardial thickening caused by fibrin, collagenases, and ultimately, fibrosis; and (4) constrictive scarring: the fibrosing visceral and parietal pericardium contracts on the cardiac chambers and may become calcified, encasing the heart in a fibrocalcific skin that impedes diastolic filling and causes the classic syndrome of constrictive pericarditis.[1-2]
This case likely reflects stage 3, where organization of caseous material led to enhancing pericardial thickening. The preexisting lipoma in the pericardial space appeared to be larger on initial examination, and it diminished in size on follow up studies with improvement in pericardial effusion.[3-4] Several reports have described initial misdiagnosis of caseous tuberculosis as a variety of tumors.[1-2] Caseation may contain fatty acids and cholesterol byproducts that may fat suppress on MRI and could be mistaken for lipoma and careful evaluation is warranted in such cases. In our case, the initial diagnosis of lipoma was correct. The lesion was relatively small and patient was symptomatic due to the pericardial effusion. Upon institution of anti-tubercular medical therapy, there was improvement in clinical condition as well radiological findings.
This case is an excellent example to the many facets of tuberculosis, which remain an important health problem in endemic countries. The presentation can be atypical, with delayed diagnosis as in our case. However, multimodality imaging, follow up examination and good clinical correlation helped to support the diagnosis. Tissue diagnosis remains the gold standard, but is invasive and many patients may opt for non-surgical follow up as in our case.
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References
- Yoon SA, Hahn YS, Hong JM, Lee OJ, Han HS. Tuberculous pericarditis presenting as multiple free floating masses in pericardial effusion. J Korean Med Sci. 2012 Mar;27(3):325-8.
- Mayosi BM, Burgess LJ, Doubell AF. Tuberculous pericarditis. Circulation. 2005 Dec 6;112(23):3608-16.
- Bardakci H, Altintas G, Unal U, Kervan U, Arda K, Birincioglu L. Giant cardiac lipoma: report of a case. J Card Surg. 2008 May-Jun;23(3):254-6.
- Grande AM, Minzioni G, Pederzolli C, Rinaldi M, Pederzolli N, Arbustini E, Viganò M. Cardiac lipomas. Description of 3 cases. J Cardiovasc Surg (Torino). 1998 Dec;39(6):813-5.
Case Prepared by:
Eddie Hulten, MD, MPH, FACC, FACP, FSCMR, FSCCT, FASNC
Cases of SCMR, Editorial team
Brown University Health Cardiovascular Institute
Rhode Island, the Miriam and Newport Hospitals
Warren Alpert Medical School, Brown University
