Human Pathology (2008) 39, 1064–1071

www.elsevier.com/locate/humpath

Original contribution

Hamartomas of mature cardiac myocytes:

report of 7 new cases and review of literature
Michael E. Fealey a , William D. Edwards MD b,⁎, Dylan V. Miller MD b ,
Shaji C. Menon MD c , Joseph A. Dearani MD d
a
Mayo Work Study Program, Mayo Clinic, Rochester, MN 55905, USA
b
Division of Anatomic Pathology, Mayo Clinic, Rochester, MN 55905, USA
c
Division of Pediatric Cardiology, Mayo Clinic, Rochester, MN 55905, USA
d
Division of Cardiovascular Surgery, Mayo Clinic, Rochester, MN 55905, USA

Received 22 August 2007; revised 19 November 2007; accepted 21 November 2007

Keywords:
Summary Only 8 cases of hamartomas of mature cardiac myocytes have been reported. The aim of the
Hamartoma of mature
study was to describe 7 new cases and provide clinicopathologic correlation. Our anatomical pathology
cardiac myocytes
database was searched for all cases of cardiac hamartoma, of which 7 represented mature myocyte type.
Medical records were reviewed for clinical information, and microscopic slides were evaluated for
extent of characteristics. Five males and 2 females ranged in age from 6 months to 74 years (mean,
23 years). There were 11 ventricular hamartomas (8 left free wall, 2 right free wall, 1 septum). Death in
3 infants was unrelated to incidental hamartomas discovered at autopsy. A 10- and 16-year-old were
asymptomatic but had abnormal electrocardiogram (ECG) results, which led to detection of cardiac
masses by imaging studies. Two adult males had only mild coronary disease angiographically. The
57-year-old, who died suddenly, had a 7-year history of abnormal ECG results. The 74-year-old, who
died after aortic surgery, had a 3-year history of chest discomfort. Their hamartomas were identified at
autopsy and contributed to sudden death in 1. Microscopically, all hamartomas were involved by
myocyte hypertrophy and disarray, without inflammation or calcification. Myocyte vacuolization and
venular dilatation occurred only in the pediatric cases, and interstitial adipose tissue only affected
1 adult. In conclusion, hamartomas of mature cardiac myocytes may be detected at any age. They
primarily affect males, arise predominantly in the left ventricle, are asymptomatic, may have nonspecific
ECG findings, and rarely may be associated with sudden death. Microscopic findings in infants differ
from older patients.
© 2008 Published by Elsevier Inc.

1. Introduction

Hamartomas of mature cardiac myocytes are rare and, to

our knowledge, have been reported in only 8 patients [1-6].
⁎ Corresponding author. As such, their clinicopathologic spectrum is not yet well
E-mail address: edwards.william@mayo.edu (W. D. Edwards). defined in the literature. In addition, these hamartomas share

0046-8177/$ – see front matter © 2008 Published by Elsevier Inc.

doi:10.1016/j.humpath.2007.11.014
Hamartomas of mature cardiac myocytes 1065

in common several features with other cardiac tumors,
making their clinical diagnosis arduous. Herein, we describe
the clinical and pathologic findings in 7 new cases.
2. Materials and methods
2.1. Study group
The Mayo Clinic anatomical pathology database was
searched for all cases with cardiac hamartoma, from which
7 hamartomas of mature cardiac myocytes were identified
and formed the study group. An eighth case had been
previously reported [3]. The project was approved by the
Mayo institutional review board.
2.2. Clinical findings
From medical records and from the descriptions of
surgical and biopsy procedures, the following information
was obtained from each of the 7 cases: patient's sex, age when
cardiac tissue was obtained, results of electrocardiogram
(ECG) and imaging studies, and intraoperative findings.
3.1.2. Clinical findings
The 2 oldest patients had no apparent cardiac symptoms.
However, abnormal ECGs eventually lead to the discovery of
their cardiac hamartomas. The 16-year-old female with
anorexia and bulimia had deep inverted T waves in leads II,
III, and aVF. During a sports physical examination, the ECG
in the 10-year-old male showed premature atrial complexes,
left axis deviation, and ST depression and T-wave inversion
in the lateral chest leads. During subsequent cardiac
evaluation, both echocardiography and magnetic resonance
imaging (MRI) were performed in both patients and
demonstrated relatively large ventricular masses (Table 1),
which were obtained from the biopsy in the 16-year-old and
surgically excised in the 10-year-old.
In contrast, the 3 infants all presented with some form of
respiratory distress. The 14-month-old boy had double inlet
left ventricle, transposed great arteries, mitral stenosis, and
coarctation of the aorta, for which he had undergone a
Norwood procedure. The 6-month-old girl had congenital

2.3. Pathologic findings

Microscopic slides of resected cardiac tissues were

reviewed for each case (by W. D. E., D. V. M., M. E. F.).
Cardiac lesions were evaluated for extent of myocyte
hypertrophy, myocyte disarray, and interstitial fibrosis,
adiposity, vascularity, and inflammation. Extent was deter-
mined semiquantitatively as absent, mild, moderate, or
marked, as previously described [7].

3. Results

Five cases were pediatric (b18 years old) and 2 repre-

sented adults (≥18 years old). Patients ranged from 6 months
to 74 years of age (mean, 23 years; median, 10 years). The
male-to-female ratio was 5:2.
Hamartomas arose solely from the left ventricle, right
ventricle, and ventricular septum with occurrence rates of 73%,
18%, and 9%, respectively. Tissue was derived from autopsy in
71.4% and from surgical and biopsy procedures in 14.3% each.

3.1. Pediatric group

3.1.1. General findings

Ages ranged from 6 months to 16 years with a mean of
5.6 years and a median of 1.2 years. There were 3 males and
2 females. Six ventricular hamartomas originated from the
left free wall, 2 from the right free wall, and 1 from the
septum. Tissue was obtained from autopsy in three and from
surgical or biopsy procedures in two.
Fig. 1 Gross appearance of hamartomas. A, Ill-defined fibrotic
lesion is in the anterior wall of the left ventricle in a 6-month-old
baby boy. B, Solitary poorly defined fibrotic region is present in the
inferoseptal wall of the left ventricle in a 57-year-old man.
1066 M. E. Fealey et al.

Fig. 2 Microscopic features of hamartomas in autopsy tissue from infants. A, Prominent myocyte disorganization in 6-month-old male. B
and C, Tissue from 6-month-old female. Nodular appearance at low power (B) and myocyte disarray at high power (C). D, Two subepicardial
nodules with prominent dilated venules in a 14-month-old male. (All, hematoxylin-eosin; A ×25, B ×10, C ×50, D ×10).

auditory abnormalities and had developed pneumonia.
Lastly, the 6-month-old boy had been born 10 weeks
prematurely and had developed respiratory distress; he also
had a bicuspid aortic valve and required surgical closure of a
patent ductal artery. All 3 cardiac hamartomas were
discovered incidentally at autopsy and were unrelated to
the cause of death. None had extracardiac hamartomas.
3.1.3. Pathologic findings
In one infant, the multiple hamartomas were grossly
visible and bulged from the epicardial surface (Fig. 1A).
They formed ill-defined, pale white-tan, somewhat firm
lesions that protruded slightly from the cut surface.
In all patients, histologic sections showed features typical
for hamartomas of mature cardiac myocytes (Figs. 2 and 3).
Of the 9 hamartomas identified among the 6 pediatric patients,
6 were ill-defined microscopically and 3 (in the 6-month-old
female and 14-month-old male) formed distinct nodular
structures with markedly dilated venules (Figs. 2B-D).
All 5 patients exhibited myocyte hypertrophy (Table 2).
Myocyte disarray (haphazard, herringbone, or whorled type)
was present in 4 patients. The fifth patient, who did not have
apparent myocyte disarray, had only small biopsy tissues
available, making some microscopic categories difficult to
evaluate. Myocyte vacuolization was observed in four. The
interstitium was fibrotic in all 5 patients but was not involved
by adiposity, inflammation, or calcification. Dilated venules
occurred in 4 patients and thickened arteries in 1.
3.2. Adult group
3.2.1. General findings
The 2 men in this group were 57 and 74 years of age. Both
hamartomas were identified at autopsy and arose in the left
ventricular free wall.
3.2.2. Clinical findings
The 74-year-old patient had a 2- to 3-year history of
exertional chest discomfort, although an ECG was normal
and coronary angiography showed only mild disease. The
day after repair of an aortic arch aneurysm, he underwent
emergency surgical repair of an acute aortic dissection. He
developed a perioperative myocardial infarction and died
2 weeks later of multiple organ system failure.
Hamartomas of mature cardiac myocytes
Fig. 3 Microscopic features of hamartomas in childhood and
adolescence. A and B, Surgical tissue from 10-year-old male.
Myocyte disorganization (A) and focal pericellular interstitial
fibrosis (B). C, Myocyte hypertrophy, interstitial fibrosis, and dilated
venule in right ventricular endomyocardial biopsy tissue from
16-year-old female. (All, hematoxylin-eosin; A ×25, B ×50, C ×50).
The 57-year-old who died suddenly had a 7-year history
of abnormal ECGs characterized by marked ST-T wave
changes. However, a recent coronary angiogram was
normal, and an echocardiogram showed no regional wall
motion abnormalities.
1067
3.2.3. Pathologic findings
The hamartoma in the 57-year-old had a gross ill-defined
fibrotic appearance (Fig. 1B). In contrast, the lesion in the
74-year-old was not apparent grossly but was incidentally
detected microscopically.
Both hamartomas formed irregular subepicardial lesions
characterized by moderate myocyte hypertrophy and by
haphazard and herringbone patterns of disarray (Fig. 4). The
57-year-old also showed whorled or pinwheel patterns, as
well as moderate interstitial fibrosis and focal interstitial
adipose tissue. There was no myocyte vacuolization, dilated
venules, thick-walled arteries, calcification, or inflammation
in either case (Table 2).
4. Discussion
4.1. Background
Masses of the heart include metastatic lesions, primary
malignancies, benign neoplasms, hamartomas, nonneoplas-
tic growths, and infectious processes [8-13]. Despite their
diversity, cardiac masses all may have similar cardiovascular
effects, including obstruction, arrhythmia, and pulmonary
or systemic embolization. Benign and nonneoplastic
masses generally have good prognosis when surgically
excised [8,14-16].
Hamartomas consist of disorganized tissue indigenous to
the organ [12]. They generally have the same growth rate as
their surrounding tissues and rarely extend into them. The
origin of hamartomas is still unknown, but their composition
suggests congenital anomalous development.
4.2. Cardiac hamartomas
Within the heart, several distinct types of hamartomas
have been described [17]. Rhabdomyomas are most
commonly diagnosed in childhood, may be associated with
tuberous sclerosis, and tend to regress over time. Histocytoid
(oncocytic) cardiomyopathy presents in infancy or early
childhood as tachyarrhythmia, sudden death, or heart failure;
primarily affects females; and tends to regress over time.
Some cardiac hemangiomas that contain mature fat, fibrous
tissue, and myocytes are also probably best categorized
as hamartomas.
Hamartoma of mature cardiac muscle was, to our
knowledge, first described in 1988 by Tanimura et al [5].
Three additional cases were reported in 1998 by Burke et al
[1]. Although it has been described as well demarcated, in
our experience, poorly-defined lesions were the rule [1].
Lesions are characterized by disorganized myocytes that also
underwent hypertrophy and by variable interstitial fibrosis
and adiposity [1-6]. Myocyte disorganization or disarray
includes 3 patterns: (1) haphazard, (2) herringbone, and (3)
whorl or pinwheel.
1068 M. E. Fealey et al.

4.3. General findings
Overall, published data exist for 15 patients with hamar-
tomas of mature cardiac myocytes, including our 7 new cases
and 8 previously reported ones (Table 3) [1-4,6]. Ages
ranged from 6 months to 74 years (mean, 28 years; median,
24 years). Among the 15 patients, 40% were pediatric
(b18 years of age) and 60% were adults. Interestingly, the
male-to-female ratio was 4:1.
4.4. Location of hamartomas
Lesions arose primarily in the left ventricular free wall
(62%). Other sites included the septum (15%), right
ventricular free wall (15%), and right atrium. This distribu-
tion pattern may simply represent a reflection of the relative
amount of myocardium in each of the affected areas.
4.5. Pediatric group
Of the 8 previously reported cases, only 1 was not an
adult. A 9-year-old boy died suddenly and unexpectedly and,
at autopsy, was found to have multiple ventricular and atrial
hamartomas [1]. He had no history of cardiac symptoms.
In contrast, pediatric patients accounted for 71% of our
cases. Of these, 3 were infants and 2 were preadolescent and
adolescent. The 3 infants had respiratory distress due to
underlying pulmonary or cardiac disease. All 3 patients died,
and at autopsy, their cardiac hamartomas were discovered
incidentally. The 2 older patients were asymptomatic, and their
ventricular hamartomas were discovered only after clinical
evaluation for abnormal ECGs detected during a sport physical
examination and during treatment of bulimia and anorexia.
For all 6 pediatric cases, ages ranged from 6 months to
16 years (mean, 6 years; median, 5 years) (Tables 1 and 3).
The male-to-female ratio was 2:1. Of the 17 hamartomas in
this group, 11 (65%) arose from the left ventricular free wall
and 3 (18%) each from the ventricular septum and right
ventricular free wall. None originated in the atrial walls.
Death occurred in three but was considered unrelated to the
cardiac hamartoma or coexistent ECG findings.
4.6. Adult group
In addition to the 7 previously reported cases of cardiac
hamartomas in adults, the current study provides 2 new cases
[1-6]. Among these 9, ages ranged from 22 to 74 years
(mean, 42 years; median, 33 years) (Tables 1 and 3).
Interestingly, the male-to-female ratio was 8:1. All hamarto-
mas in this group were solitary, with 5 in the left ventricular
free wall, 2 in the ventricular septum, and 1 each in the right
ventricular free wall and right atrium.
Three patients were asymptomatic, and sudden death
occurred in another. In the remaining 5 patients, 3 had
palpitations, 2 had syncope/light-headedness, 2 had dyspnea,
and 1 had exertional chest discomfort. Four patients had a
history of atherosclerosis or its risk factors.
ECG abnormalities of various types were present in
7 patients. Of the 7 in whom echocardiography had been
performed, a cardiac mass was identified in 6. Three patients
had undergone MRI, and myocardial masses were detected
in all 3.
Six of the 9 patients had surgical resection of their cardiac
lesions and all have done well postoperatively. Only after
removal of the masses was their hamartomatous nature
discovered. Of the 3 patients who died and underwent autopsy

Table 1 Clinical features in 7 patients with hamartoma of mature cardiac myocytes

Pediatric (≤17 y) Adult (≥18 y)
Age 6 mo 6 mo 14 mo 10 y 16 y 57 y 74 y
Sex Male Female Male Male Female Male Male
Clinical None None None None None Sudden
Exertional
manifestation deathchest
discomfort
ECG findings Sinus None Sinus tachycardia, dilated Lat ST- and Deep inverted T ST-T Normal sinus
tachycardia RA, biventricular T-wave depression waves, inf leads changes, inf- rhythm
hypertrophy (see text) lat leads
Echocardiography Mild LVH Normal Congenital anomalies 5 × 3-cm LV mass 8 × 9-cm RV Mild LVH None
mass
Cardiac MRI or None None None LV mass RV mass None 3-cm asc ao
CT aneur
Location of NA NA NA LV lat RV inf NA NA
masses
No. of masses NA NA NA 1 1 NA NA
Asc ao aneur indicates ascending aortic aneurysm; inf, inferior; lat, lateral; LV, left ventricle; LVH, left ventricular hypertrophy; NA, not applicable; RA,
right atrium; RV, right ventricle.
Hamartomas of mature cardiac myocytes 1069

examination, none had detection of a cardiac mass antemortem.
In two, the cause of death was unrelated to the hamartoma.
However, in the 57-year-old male in our series, death
might be attributable to his hamartoma, which involved
the inferolateral aspect of the left ventricle from base to apex
and microscopically contained appreciable fibrosis and
myocyte disorganization. The heart was otherwise unaf-
fected by significant coronary atherosclerosis or by other
areas of fibrosis. In addition, his electrocardiogram had
shown marked ST-T wave changes in the distribution of this
relatively large lesion.
4.7. Microscopic features
The histologic abnormalities identified in the current
series are similar to those described by others [1-6]. These
include myocyte hypertrophy and disorganization, as well as
interstitial fibrosis and adiposity, and thick-walled arteries. In
addition, we observed myocyte vacuolization and dilated
venules. In keeping with previously reported features, none
of our cases displayed gross or microscopic calcification.
Unique to our series was an apparent difference between the
microscopic constellation of findings in the pediatric age
group compared with the adults.
Only in the pediatric age group were vacuolated myocytes
and dilated venules observed. Moreover, in 2 of the infants,
the hamartomas formed distinct subepicardial nodules that
appeared well demarcated both grossly and microscopically.
In contrast, only in the adult age group was interstitial
fat detected.
4.8. Differential diagnosis
The microscopic features described above, though
nonspecific individually, are characteristic of localized
hamartomas of mature cardiac myocytes when seen together.
However, they are also characteristic of hypertrophic
cardiomyopathy and must be distinguished from this more
diffuse cardiac disorder [7]. Burke et al [1] have suggested
that the whorl/pinwheel form of disarray, which is commonly

Fig. 4 Microscopic features of hamartomas in adults. A and B, Autopsy tissue in 57-year-old male. Myocyte hypertrophy and interstitial
fibrosis in a whorled pattern (A) and interlacing of myocyte bundles that underwent hypertrophy in a herringbone pattern (B). C and D,
Myocytes show several whorled patterns of disarray (C) and myocyte bundles arranged in a zigzag herringbone pattern (D) in autopsy tissue
from 74-year-old male. (All, hematoxylin-eosin; A ×25, B ×25, C ×25, D ×50).
1070 M. E. Fealey et al.

Table 2 Pathology features in 7 patients with hamartoma of mature cardiac myocytes

Pediatric (≤17 y) Adult (≥18 y)
Age 6 mo 6 mo 14 mo 10 y 16 y 57 y 74 y
Sex Male Female Male Male Female Male Male
Source A A A S B A A
Location LV-A mid, LV-IS LV-IS LV-A LV-AL/IL base to RV-I LV-IS base to LV-AS
apex, VS mid, RV-A mid apex
Hypertrophy Mild Moderate to Moderate Moderate to Moderate to Moderate to Moderate to
severe to severe severe severe severe severe
Myocyte Haphazard Haphazard, Haphazard Haphazard, None (small Haphazard, Haphazard,
disarray herringbone, herringbone, specimen) herringbone, herringbone
whorl whorl whorl
Vacuolated Yes Yes Yes Yes No No No
myocytes
Interstitial Mild Mild Mild Moderate to Moderate to Moderate to None
fibrosis severe severe severe
Interstitial fat No No No No No Yes No
Thick No No No Yes NA (none in No No
arteries specimen)
Dilated No Yes Yes Yes Yes No No
venules
Calcium No No No No No No No
Inflammation No No No No No No No
A indicates autopsy; B, biopsy; S, surgery; VS, ventricular septum; AL, anterolateral; AS, anteroseptal; IL, inferolateral; IS, inferoseptal.

seen in hypertrophic cardiomyopathy, is not a feature of
hamartomas of mature cardiac myocytes. However, this
pattern was identified in 3 of our 7 cases.
Among autopsy cases, myocardium adjacent to hamarto-
mas is normal in otherwise normal hearts and is hyper-
trophied in those with chronic heart disease. Thus,
heart weight is not necessarily helpful for distinguishing
between hearts with localized lesions and those with a
diffuse cardiomyopathy. Nevertheless, differentiation bet-
ween hamartomas and hypertrophic cardiomyopathy is

Table 3 Features of 8 previously reported hamartomas of mature cardiac myocytes

Reference (1) (1) (6) (1) (2) (4) (3) (5)
no.
Age (y) 9 22 24 28 33 33 41 68
Sex Male Male Male Male Male Male Female Male
Clinical None None None Syncope Palpitations, Dyspnea, Palpitations None
manifestation light- palpitations
headedness
ECG findings NM Repolarization Rare Non- None Deep inverted T PSVT, Low
changes, inf APC and conducted P waves, inf-lat palpitations voltage
leads VPC waves, WPW leads
Echocardi- None 5-cm mass Mass RA mural Transmural 4.5 × 5.5-cm Septal mass NM
ography mass LV mass mass
MRI or CT NM None None NM 4.5 × 3.1 × Intramural mass 4.8-cm None
4.4-cm LV mass, no
mass calcium
Location of LV ant, LV lat, RV VS RA LV lat, mid LV inf-lat VS LV
masses LV inf, MV-PM (2), to apex apex ⁎
VS, RV, RA ⁎
No. of masses 8⁎ 1 1 1 1 1 1 1⁎
Tissue source A S S S S S S A
(1) indicates Burke et al; (2), Dinh et al; (3), Gilman et al; (4), Martinez-Quesada et al; (5), Tanimura et al; (6), Sturtz et al; ant, anterior; APC, atrial premature
contractions; MV-PM, mitral valve papillary muscles; NM, not mentioned; PSVT, paroxysmal supraventricular tachycardia; VPC, ventricular premature
contractions; WPW, Wolf-Parkinson-White preexcitation syndrome.
⁎ This information was determined at autopsy and not clinically.
Hamartomas of mature cardiac myocytes
usually straightforward in either nonhypertrophied or hyper-
trophied hearts.
However, when smaller surgical or biopsy specimens
represent the only available tissue for evaluation, particularly if
removed from the ventricular septum, distinction of hamar-
toma from hypertrophic cardiomyopathy may be impossible
microscopically. In such cases, the two may be differentiated
only in light of clinical findings and imaging studies.
Hamartomas may also be confused with cardiac
fibromas. Both benign masses tend to be solitary noninfil-
trating lesions. However, fibromas are generally poorly
vascularized and focally calcified, whereas hamartomas of
mature cardiac muscle are noncalcific and may be highly
vascularized, with dilated venous channels [4]. Although
both have a whorled appearance, this is because of
fibroblasts and collagen in fibromas and is because of
myocyte disarray in hamartomas.
Cardiac rhabdomyomas may also have a gross appearance
similar to hamartomas of mature cardiac muscle. Neither
represent a calcified lesion. Microscopically, however, myo-
cytes in rhabdomyomas are diffusely vacuolated and contain
abundant glycogen, whereas myocytes in hamartomas are
hypertrophied and display only focal areas of vacuolization.
4.9. Summary
Hamartomas of mature cardiac myocytes show no
predilection for age at detection. They have a slow growth
rate, and their relative size is probably established in utero. The
development of ECG and other clinical manifestations may be
related primarily to the size of the hamartoma. Their prevalence
in the left ventricle likely explains the frequent occurrence of
nonspecific ECG abnormalities among patients with large
hamartomas. Echocardiography, electrocardiography, and CT
imaging have been helpful in visualizing their location and
size, as well as their lack of calcification. Because their
vascularity is variable, angiography may be difficult to
interpret. Currently, the only means to establish a diagnosis
of hamartoma is by microscopic examination.
1071
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