A myxoma is the most common primary tumor of the heart. It has been reported as the source of a cardiogenic embolism. Therefore, it is important for clinicians to detect the myxoma early via echocardiography to prevent complications, such as syncope, sudden death, and cerebral embolic ischemic stroke. This report presents the case of a 54-year-old female whose clinical manifestation of atrial myxoma was an ischemic stroke. Atrial myxoma was later confirmed as the cause of her symptoms via transesophageal echocardiography

BD Le

Dion F Graybeal

E Hofmann

G Bajraktari

G Hirose

G Rescigno

M Ozaydin

Minwook Yoo

English

PubMed

Springer - Publisher Connector

BioMed CentralCases Journal
ssOpen AcceCase Report
An echocardiographic-confirmed case of atrial myxoma causing 
cerebral embolic ischemic stroke: a case report
Minwook Yoo* and Dion F Graybeal
Address: Department of Neurology, University of Texas Southwestern Medical Center, Dallas, Texas, USA
Email: Minwook Yoo* - newmachine@dreamwiz.com; Dion F Graybeal - dion@utsouthwestern.edu
* Corresponding author    
Abstract
A myxoma is the most common primary tumor of the heart. It has been reported as the source of
a cardiogenic embolism. Therefore, it is important for clinicians to detect the myxoma early via
echocardiography to prevent complications, such as syncope, sudden death, and cerebral embolic
ischemic stroke. This report presents the case of a 54-year-old female whose clinical manifestation
of atrial myxoma was an ischemic stroke. Atrial myxoma was later confirmed as the cause of her
symptoms via transesophageal echocardiography.
Background
Cerebral infarction induced by cardiogenic embolism is
observed in about 20% of stroke patients. Of those
patients, atrial fibrillation is responsible for over 50% of
the cardiogenic emboli, while myxomas are observed in
only 0.5% of emboli [1]. Atrial myxomas are a very rare
source of cardiogenic embolism. Although they are usu-
ally asymptomatic, myxomas can develop lethal compli-
cations without warning because of their ability to
embolize. This report describes a patient who presented
with a left-sided hemiparesis. The cause of the patient's
right cerebral infarction was a left atrial myxoma which
was detected by transesophageal echocardiography (TEE).
Case presentation
A 54-year-old Caucasian female presented to the emer-
gency room with a 4 day history of left-sided weakness.
The patient stated that she was at home when she sud-
denly felt a sharp pain in her left hand that radiated to her
neck. She then lost consciousness and collapsed to the
floor. It was not until 4 days later that her friend con-
vinced her to go to the hospital. The patient had a medical
history of longstanding hypertension, obstructive sleep
apnea, hypothyroidism, and depression. She had been a
smoker for 25 years. Her mother also had hypertension
and her father had a myocardial infarction at the age of
56. Her height was 161.5 cm and her weight was 127.3 kg.
The patient's vital signs were as follows: blood pressure,
153/104 mm Hg; heart rate, 101 beats/minute; respiratory
rate, 18/minute; and body temperature, 36.6°C (98.0°F).
She was alert and oriented, had left facial paralysis, slight
dysarthria and right-sided tongue deviation, but no dys-
phasia. On cardiac examination, the carotid impulse was
normal without a bruit. Her heart had a regular rate and
rhythm, and there were normal S1 and S2 heart sounds
without murmurs. An EKG showed a normal sinus
rhythm. Range of motion was limited to 30° for the left
upper and lower extremities. She had 1/5 motor strength
on the left side, but 5/5 motor strength on the right side.
The deep tendon reflexes were 2+ bilaterally. Her sensa-
tion was intact bilaterally. The Babinski and Hoffman
signs were both negative. All her laboratory results were
normal. A chest X-ray showed a normal cardiac silhouette
with no signs of pulmonary edema. A non-contrast com-
Published: 18 August 2008
Cases Journal 2008, 1:96 doi:10.1186/1757-1626-1-96
Received: 18 May 2008
Accepted: 18 August 2008
This article is available from: http://www.casesjournal.com/content/1/1/96
© 2008 Yoo and Graybeal; licensee BioMed Central Ltd. 
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), 
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Page 1 of 5
(page number not for citation purposes)
Cases Journal 2008, 1:96 http://www.casesjournal.com/content/1/1/96puted tomography (CT) scan of the brain revealed multi-
ple low density areas in the right frontal and parietal
lobes. Our stroke team started her on intravenous
heparin. Metoprolol (Toprol-XL) and furosemide (Lasix)
were administered to stabilize her blood pressure. The fol-
lowing day, magnetic resonance imaging (MRI) of the
brain demonstrated an acute infarction in the distribution
of the right middle cerebral artery (MCA; Figure 1). On the
Axial T1-weighted MRI shows acute infarcts in the right caudate body, and the frontal and parietal lobesFigure 1
Axial T1-weighted MRI shows acute infarcts in the right caudate body, and the frontal and parietal lobes. (A), 
The diffusion weighted image (DWI) presents an abnormal signal corresponding to the restricted diffusion in the right hemi-
sphere. (B), MRA shows no aneurysm, stenosis, or abnormal flow in the visualized vessels of the Circle of Willis, the carotid 
arteries, and the vertebral arteries. (C).Page 2 of 5
(page number not for citation purposes)
Cases Journal 2008, 1:96 http://www.casesjournal.com/content/1/1/96third day of hospitalization, the patient underwent a TEE.
A TEE was chosen since the less invasive transthoracic
echocardiography (TTE) showed negative imaging for a
cardiogenic embolic source. In addition, the patient was
obese and the TTE did not provide a comprehensive
image. The TEE identified a 4.3 cm × 1.3 cm mass in the
left atrium. A cardiac catheterization showed no signifi-
cant coronary artery disease. The patient was thus diag-
nosed with a right MCA ischemic infarction and a left
atrial myxoma. On the 13thhospital day, the patient
underwent successful surgical excision of the myxoma
(Figure 2). The biopsy confirmed the diagnosis of
myxoma. The patient recovered without any complica-
Transesophageal echocardiography shows a mobile mass in the left atrium, which does not obstruct the mitral valveFigur  2
Transesophageal echocardiography shows a mobile mass in the left atrium, which does not obstruct the mitral 
valve. (A), After performing cardiopulmonary bypass, the retractor allows visualization of the left atrium, and the atrium is 
then opened by a blade. The myxoma is attached from the atrial septum. (B), LA myxoma: tan and jelly-like tissue with an 
aggregate measurement of 6 cm × 1.5 cm. (C).Page 3 of 5
(page number not for citation purposes)
Cases Journal 2008, 1:96 http://www.casesjournal.com/content/1/1/96tions and was discharged on the 20th day of hospitaliza-
tion.
Discussion
A myxoma is the most common primary tumor of the
heart. Primary cardiac neoplasms are rare, with incidences
ranging from 0.001–0.3% in autopsy series. Benign
tumors account for 75% of primary neoplasms and malig-
nant tumors account for 25%. Myxomas compromise 30–
50% of primary cardiac tumors [1]. The majority of myxo-
mas are sporadic, but 7% of patients have a genetic muta-
tion that is inherited in an autosomal dominant manner.
Familial myxoma has been well-described as the Carney
complex, characterized by hyperpigmentation, cutaneous
myxomas, and endocrine adenomas. This tumor is three
times more common in females than in males and gener-
ally occurs between the third and sixth decades, with an
average age of presentation at 43 years [2].
Myxomas originate from the mesenchymal cells of the
septal endocardium. They are gelatinous with a smooth or
lobulated surface and are usually white, yellow, or brown
in color. They can present as villous, papillary, sessile, or
pedunculated-type growths. Approximately one-half of
the cases of myxomas are pedunculated tumors, and these
are irregular and more likely to result in emboli because
of the mobility of this type of tumor [3]. Sixty to 75% of
cardiac myxomas develop in the left atrium, most of
which are from the atrial septum near the fossa ovalis.
Most other myxomas develop in the right atrium. Fewer
than 20 cases of myxomas arising from the right or left
ventricle have been reported [4]. Myxomas produce a vas-
cular endothelial growth factor that stimulates angiogen-
esis and tumor growth and an increased expression of
interleukin-6 [5].
A myxoma may be completely asymptomatic until it
grows large enough to obstruct the mitral or tricuspid
valve or fragments that give rise to emboli. Because they
are intravascular and friable, myxomas account for most
cases of tumor emboli [1]. Embolism occurs in about 30–
40% of patients with myxomas. The site of embolism is
dependent upon the location of the myxoma (left or right
atrium) and the presence of an intracardiac shunt. This is
not surprising, given the degree of motion that can be seen
on echocardiography and angiography, as the myxoma
swings on a small pedicle with each cardiac contraction
[6]. Intermittent acute obstruction of the mitral orifice has
been reported to produce syncope and even sudden death.
Some myxomas produce generalized symptoms resem-
bling an autoimmune disorder, including fever, weight
loss, digital clubbing, myalgias, and arthralgias. These
patients may have an immune reaction to the neoplasm,
as elevated levels of interleukin-6 and elevated levels of
antimyocardial antibodies have been described [5].
The emboli that occur are either a tumor fragment that is
released from the myxoma or a blood clot that is formed
on the surface of the myxoma. These resulting emboli can
result in infarction, as occurred in our patient. More pre-
cisely, it has been reported that 45% of patients with
myxomas have neurologic manifestations resulting from
embolization [7]. This embolization includes pulmonary
embolism, myocardial infarction, mesenteric infarction,
retinal artery occlusion, spinal cord ischemia, and stroke
[2-7]. Right-sided myxomas cause pulmonary emboliza-
tion, but left-sided myxomas usually cause systemic
embolization. Ischemic infarction of the brain is respon-
sible for the majority of cases of systemic embolization.
The MCA is frequently affected by this type of infarction
because of the MCA's dominant blood flow [8]. In cases
in which frontal or parietal infarction is suspected in a
patient with myxoma, the MCA territory should be thor-
oughly investigated.
Usually, the diagnosis is readily established by two-
dimensional echocardiography, which is considered the
gold standard. TEE may be useful when transthoracic find-
ings are equivocal or confusing. MRI has been of value in
diagnosis, providing excellent cardiac definition. Cardiac
catheterization is not necessary in the majority of cases,
but may be necessary when other cardiac disease is sus-
pected or if other diagnostic studies are equivocal. TTE has
a sensitivity of 95% and the sensitivity is nearly 100% [9].
Whether performing TTE or TEE, echocardiography is able
to evaluate the location, size, shape, and movement of
myxomas. TTE or TEE may also show other cardioembolic
sources, such as a patent foramen ovale, mitral valve cal-
cification, or aortic atherosclerosis. Prompt resection is
required after the diagnosis, even in asymptomatic
patients. It is important that myxomas should be excised
with negative margins because any remnant can aggravate
an infarction. The recurrence rate is 1~3% after surgery
[10]. Therefore, all patients with myxomas are recom-
mended to undergo long-term follow-up with echocardi-
ography. This patient described herein, who was morbidly
obese with a BMI of 48.8 kg/m2, is representative of a
growing medical problem in the United States. With
stroke patients, physicians use TTE routinely when they
search for cardiogenic embolic sources. But, in using TTE
exclusively, myxomas in the obese will frequently be
missed.
Conclusion
This case demonstrates the importance of investigating
the possibility of cardiogenic source in stroke, as our
patient developed cerebral infarction that was caused by
an atrial myxoma. It is important that clinicians consider
using echocardiography in stroke patients. Treating the
atrial myxoma can prevent a cardioembolic stroke and its
complications. In conclusion, TEE, as compared to TTE,Page 4 of 5
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has many more advantages when physicians search for a
cardiogenic embolic source in obese stroke patients. In
addition, because obesity has sharply increased in the
United States, the importance and use of TEE will increase
over time as physicians encounter obese patients with car-
diogenic emboli.
Abbreviations
MCA: Middle Cerebral ArteryP; CT: Computed Tomogra-
phy; MRI: Magnetic Resonance Imaging; TEE: Trans-
esophageal Echocardiography; TTE: Transthoracic
Echocardiography.
Competing interests
The authors declare that they have no competing interests.
Authors' contributions
MY and DG were involved in the clinical assessment and
writing the case report. All authors read and approved the
final manuscript.
Consent
Full written consent was received for the manuscript to be
published.
Acknowledgements
I would like to extend my thanks to Michael A. Wait, M.D., the surgeon 
who excised the myxoma. I would also like to express my appreciation to 
Craig Litz, M.D., the pathologist who performed the analysis of the myxoma 
biopsy.
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An echocardiographic-confirmed case of atrial myxoma causing cerebral embolic ischemic stroke: a case report

Crossref

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An echocardiographic-confirmed case of atrial myxoma causing cerebral embolic ischemic stroke: a case report

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