DOI:10.2214/AJR.04.1989
AJR 2007; 188:W21-W24
© American Roentgen Ray Society
Calcified Chronic Pericardial Fat Necrosis in Localized Lipomatosis of Pericardium
Bae Young Lee1 and
Kyung Sup Song1
1 Both authors: Department of Radiology, St. Paul's Hospital, Medical College,
The Catholic University of Korea, 620-56 Jeonnong-dong, Dongdaemun-gu, Seoul
130-709, Korea.
Received December 31, 2004;
accepted after revision May 29, 2005.
Address correspondence to K. S. Song.
WEB
This is a Web exclusive article.
Keywords: cardiopulmonary imaging • coronary arteriography • MDCT • radiologic-pathologic correlation
Introduction
Pericardial fat necrosis is an infrequent clinical entity first reported by
Jackson et al. [1] in 1957.
Only 19 cases have been reported in the English-language literature
[1-3].
In all reported cases, patients presented with a sudden onset of chest pain
and fatty masses without calcification. On routine radiography, most
pericardial fat necrosis was interpreted as a juxtacardiac mass. CT findings
have been reported in three cases as fat-attenuation masses
[1-3].
However, our patient complained of long-standing pitting edema of the leg and
intermittent dizziness without chest pain. On radiography, eccentric
overgrowth of pericardial fat with fat necrosis was noted, and calcified
flecks were seen around the pericardial fat necrosis. These unique clinical
and radiologic findings have not been reported in the literature.
Case Report
A 47-year-old man was admitted to our institution, presenting with
intermittent dizziness and pitting edema of the leg for several years. His
height was 169.5 cm and his weight was 64 kg. No history of previous infection
or trauma was noted. On physical examination, the patient's heart rate was 70
beats per minute and his blood pressure was 120/80 mm Hg. His heart sound was
normal without murmur or pericardial rub. Mild pitting edema of the legs was
noted. Engorgement of the neck veins was not detected. Pulmonary function test
results were normal. A 24-hour Holter monitoring test revealed paroxysmal
atrial tachycardia. Chest radiographs showed an ill-defined mass with a
calcific rim at the right-side base of the cardiac silhouette (Figs.
1A and
1B). Transthoracic and
trans-esophageal echocardiography revealed a 5-cm ovoid pericardial solid mass
with a calcified rim compressing the right heart.
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Fig. 1A —47-year-old man who presented with intermittent dizziness and
pitting edema of leg for past several years. Posteroanterior (A) and
lateral (B) chest radiographs show ovoid mass at right side of cardiac
silhouette (arrows).
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Fig. 1B —47-year-old man who presented with intermittent dizziness and
pitting edema of leg for past several years. Posteroanterior (A) and
lateral (B) chest radiographs show ovoid mass at right side of cardiac
silhouette (arrows).
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Unenhanced and contrast-enhanced 16-MDCT (LightSpeed 16, GE Healthcare) of
the chest was performed with 1.25-mm slice acquisitions. ECG gating was not
performed. MDCT showed a 6 x 5 cm unenhanced solid mass, measuring 40-50
H, with peripheral calcified flecks and a few tiny fat densities. This mass
showed broad contact to the wall of the right atrium. Eccentric thickening of
the pericardial fat was noted along the right atrium and ventricle, and this
thickening was also prominent in the right atrioventricular groove. The right
atrium and ventricle were compressed by focal deposition of the pericardial
fat and solid mass with calcified flecks. Pericardial fat thickening was not
noted around the left side of the heart. Mild thickening of the interatrial
septum was noted (Fig. 1C).
Initially, we overlooked a few tiny fat densities, so we excluded the
possibility of a mass of fatty composition. Our preoperative diagnosis was
complicated pericardial cyst or other pericardial neoplasm.
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Fig. 1C —47-year-old man who presented with intermittent dizziness and
pitting edema of leg for past several years. Contrast-enhanced axial CT scan
shows large chronic fat necrosis with peripheral calcified flecks (thick
arrows) abutting right atrium. Tiny fat densities are noted in this mass
(thin arrows). Focal intrapericardial fat thickening
(arrowheads) is noted in right side of heart, predominantly in
atrioventricular groove. Compressed right atrium and ventricle are noted.
Thickened interatrial septum is seen (open arrows).
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After median sternotomy, marked adhesion of the pericardium was noted at
the solid mass with calcified flecks. This mass firmly attached to right
atrium, and the margin between this mass and the pericardial fat was
indistinct. When the mass was incised, it was found to be filled with
brown-colored sludge and peripheral calcified flecks
(Fig. 1D). Debulking surgery of
this mass including adjacent fat was performed. Complete removal of this mass
was not performed because of severe adhesion and the possibility of rupture of
the right atrium. Histology revealed hyalinized fibrous tissue and adipose
tissue with calcification and old hemorrhage
(Fig. 1E). The pathologists
reported chronic fat necrosis with calcification. There was no evidence of
malignancy.
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Fig. 1D —47-year-old man who presented with intermittent dizziness and
pitting edema of leg for past several years. Intraoperative findings with
incision of mass reveal green- to brown-colored central necrotic materials and
yellowish fat around necrotic materials. Severe adhesion of pericardium
covering this mass is seen.
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Fig. 1E —47-year-old man who presented with intermittent dizziness and
pitting edema of leg for past several years. Histology shows hyalinized
fibrous tissue with calcifications (arrows) and old hemorrhage in
peripheral portion (lower half) and adipose tissue in central portion (upper
half). (H and E, x40)
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Pericardial tamponade developed after surgery. Follow-up cardiac 16-MDCT
was performed with ECG-gating and 0.625-mm slice acquisition for the
evaluation of tamponade and remnant mass. Small remnant calcified mass and
thickening of the pericardial fat were seen with cardiac tamponade. The
previously noted passive compression of the right atrium and ventricle had
improved, although pericardial tamponade had developed. The right coronary
artery (RCA) was running through thickened pericardial fat with a tortuous
course, and some branches of the RCA supplied the thickened pericardial fat
pad and remnant calcified mass. The thickened interatrial septum of fat
attenuation is shown in Figures
1F and
1G. A pericardial window was
made, and the hematoma was removed. At 4 weeks after surgery, pitting edema
and dizziness had subsided. The patient was discharged in stable
condition.
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Fig. 1F —47-year-old man who presented with intermittent dizziness and
pitting edema of leg for past several years. Postoperative oblique sagittal
multiplanar reconstruction image shows right coronary artery and its branches
(arrows), which supply remnant calcified fat necrosis
(arrowheads) and lipomatosis.
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Fig. 1G —47-year-old man who presented with intermittent dizziness and
pitting edema of leg for past several years. Postoperative contrast-enhanced
axial CT scan shows large pericardial effusion (white arrows) and
small remnant calcified fat necrosis (arrowheads). Relatively low
density in thickened interatrial septum (open arrows) is seen (-50 to
30 H). Right atrium and ventricle are less compressed compared with
preoperative CT scan (C).
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Discussion
The previously reported 19 cases of pericardial fat necrosis have a unique
clinical feature characterized by the sudden onset of severe chest pain
[1-3].
Symptoms may mimic those of myocardial infarction or pulmonary embolism. Only
two patients suffered pain for 1 year
[1,
3], and the duration of
symptoms of the other patients was several days to weeks. However, our patient
did not complain of chest pain, and the duration of symptoms of edema and
dizziness was several years. With some exceptions including our patient, most
patients were moderately obese. All the reported cases were adults from 23 to
67 years old. ECG results were normal in all except two patients; one showed
resolving pericarditis and the other showed right bundle branch block
[3], but our patient showed
paroxysmal atrial tachycardia.
In the reported cases, most radiologic findings were seen as juxtacardiac
masses on chest radiographs. CT scans in three cases showed large
fat-attenuation components and MR imaging in one case also showed fat signal
mass
[1-3].
The typical pathologic features of fat necrosis can be seen elsewhere in
the body and are common in the breast and epiploic appendices. Morphologic
changes are dependent on the duration of the lesion and the stage of
inflammation. Histologically, the central necrotic fat cells are surrounded by
lipid-filled macrophages and neutrophilic infiltrations. Within days,
progressive fibroblastic proliferation, increased vascularity, and lymphocytic
and histiocytic infiltration wall off the necrosis. Consecutively central
necrotic fat cells have disappeared and been replaced by foamy, lipid-laden
macrophages. Later, foreign body giant cells, calcium salts, and blood
pigments appear, and eventually the focus is replaced by scar tissue
[3].
Most portions of the mass in our patient revealed soft-tissue attenuation
(40-50 H), and only a few tiny fat-attenuation foci and peripheral
calcifications were seen. These findings have not been reported in pericardial
fat necrosis until now. In the other organs, such as epiploic appendices,
similar findings of calcified chronic fat necrosis can be found in the
literature [4,
5]. Chronic infarction of
epiploic appendices usually goes unrecognized clinically and undergoes aseptic
fat necrosis. Infarcted epiploic appendices gradually transform into
heterogeneous masses with calcification
[4,
5]. We postulate that the mass
in our patient could be a result of aseptic chronic fat necrosis as is the
case with epiploic appendix. In addition, the symptoms of our patient were of
long duration.
Primary cardiac fatty masses include lipoma and lipomatous hypertrophy of
the interatrial septum. Lipomas are encapsulated fatty tumors that frequently
arise from the epicardial surface, usually from a broad pedicle, and grow into
pericardial space. They may also arise from the endocardium and grow into any
of the cardiac chambers. Lipomatous hypertrophy is fatty deposition of the
interatrial septum with septal enlargement to a thickness of more than 2 cm in
the transverse dimension at the level of the fossa ovalis. In contrast to
lipoma, lipomatous hypertrophy of the interatrial septum is not encapsulated
and is caused by an increased number of adipocytes
[6].
In our patient, the lipomatous overgrowth of the pericardial fat along the
right heart was noted without encapsulation, and mild thickening of the
interatrial septum was also seen. In previous reports concerning cardiac
lipomatosis, this kind of lipomatosis was reported in two cases
[7,
8]. The case reported by Akhtar
et al. [7] revealed lipomatosis
without thickening of the interatrial septum. Another case described by
Myerson et al. [8] revealed
lipomatosis combined with mild thickening of the interatrial septum (9 mm in
the transverse dimension). The thickness of the interatrial septum in our case
is 8 mm. At 41 to 60 years of age, the average thickness of the interatrial
septum is 3.5 mm [9], so
thickening of the interatrial septum is normal. Fat accumulation in the septum
may play a role in the development of arrhythmia
[9], so this lipomatous
infiltration of the septum may be the cause of paroxysmal atrial tachycardia
in our case.
The pathogenesis for pericardial fat necrosis remains unknown. The first
possibility is torsion. In two patients, pedicle was reported
[3], leading to the presumption
that acute torsion was the underlying phenomenon. The second possibility is a
Valsalva maneuver. Straining or heavy lifting may trigger a Valsalva maneuver
that could lead to a rapid rise in venous pressure accompanied by a drop in
cardiac output and arterial pressure. Later when venous pressure falls, there
is a momentary increase in systemic arterial pressure. These rapid changes in
intravascular pressure may cause hemorrhage into the loosely supported adipose
tissue of the pericardium [2].
The third possibility is a preexisting structural abnormality of the adipose
tissue, such as lipoma, hamartoma, or lipomatosis. This structure would be
particularly vulnerable to the trauma of the beating heart and moving
diaphragm [2]. In our case,
lipomatosis along the right heart and a mass closely abutting the right atrium
and diaphragm were present. Branches from the RCA supplied the mass and
lipomatosis. We postulate this third theory may offer a reasonable explanation
for the pericardial fat necrosis of our case. Other predisposing factors are
obesity, severe pancreatitis, and trauma
[1-3].
Unlike previously reported cases, the mass in this case showed severe
adhesion, so removal of the mass was difficult. In the previously reported 19
cases, the masses were easily removed.
Pericardial fat necrosis has been infrequently reported, but most cases are
acute and all cases have reported severe chest pain. However, the patient in
our case had long-standing symptoms for several years without chest pain.
Calcified chronic pericardial fat necrosis in localized lipomatosis of the
pericardium has not been reported previously.
References
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- Chipman CD, Aikens RL, Nonamaker EP. Pericardial fat necrosis.
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- Inoue S, Fujino S, Tezuka N, et al. Encapsulated pericardial fat
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- Osadchy A, Shapiro-Feinberg M, Zissin R. Strangulated small bowel
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BJR 2001;74:1062
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- Araoz PA, Mulvagh SL, Tazelaar HD, Julsrud PR, Breen JF. CT and MR
imaging of benign primary cardiac neoplasms with echocardiographic
correlation. RadioGraphics2000; 20:1303
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- Akhtar A, D'Cruz IA, Ramanathan KB, Umpierrez M. Diffuse locally
invasive lipomatosis of the pericardium.
Echocardiography2003; 20:173
-177[CrossRef][Medline]
- Myerson SG, Roberts R, Moat N, Pennell DJ. Tamponade caused by
cardiac lipomatous hypertrophy. J Cardiovasc Magn
Reson 2004;6:565
-568[CrossRef][Medline]
- Reyes CV, Jablokow VR. Lipomatous hypertrophy of the cardiac
interatrial septum. Am J Clin Pathol1979; 72:785
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Introduction
Case Report
