ORIGINAL CONTRIBUTION

Central Nervous System Manifestations

of Cardiac Myxoma
Vivien H. Lee, MD; Heidi M. Connolly, MD; Robert D. Brown Jr, MD

Background: Neurologic complications can be the ini-
tial manifestation of atrial myxoma. Prompt diagnosis is
of paramount significance to prevent recurrent compli-
cations.
Objective: To identify patients with neurologic com-
plications attributed to atrial myxoma.
Design, Setting, and Patients: With institutional re-
view board approval, we retrospectively reviewed the
medical records of 74 consecutive patients with patho-
logically confirmed cardiac myxoma at the Mayo Clinic
from January 1, 1993, through December 31, 2004.
Main Outcome Measures: Discharge and follow-up
modified Rankin score.
Results: Nine of the 74 patients with cardiac myxoma
(12%) presented with neurologic manifestations in the
setting of atrial myxoma. Mean age was 48.5 years (range,
17-70 years). There were 6 females and 3 males. Among
patients with myxoma and neurologic symptoms, ische-
mic cerebral infarct was the most common neurologic
manifestation (8 patients [89%]). No patients had con-
comitant cardiac symptoms. The size of the atrial myxoma
was variable, with a mean diameter of 2.7 (range, 0.4-
6.5) cm. Most of the atrial myxomas causing neurologic
symptoms demonstrated a mobile component on trans-
esophageal echocardiography (8 patients [89%]). Two
patients (22%) had pathologic evidence of systemic myxo-
matous emboli. One patient with intracerebral hemor-
rhage had pathologically confirmed intracranial meta-
static myxoma and myxoma-induced aneurysmal
dilatation.
Conclusions: Neurologic complications are associated
with cardiac myxoma in some patients with myxoma and,
when they occur, frequently present with cerebral in-
farction. The mobility, not the size, of the myxoma ap-
pears to be related to embolic potential. Potential de-
layed neurologic complications relevant to patients with
tumor embolization include myxoma-induced cerebral
aneurysm and myxomatous metastasis, which can mimic
the clinical picture of central nervous system vasculitis
or infective endocarditis.
Arch Neurol. 2007;64(8):1115-1120

Author Affiliations:
Department of Neurology
(Drs Lee and Brown) and
Division of Cardiovascular
Diseases (Dr Connolly), Mayo
Clinic College of Medicine,
Rochester, Minnesota. Dr Lee is
now with the Department of
Neurologic Sciences, Rush
University Medical Center,
Chicago, Illinois.
M
YXOMAS ARE GENER -
ally thought to origi-
nate from multipoten-
tial mesenchymal cells
of the endocardium.1
Cardiac myxomas are the most common
primary cardiac tumor in adults, repre-
senting as many as 83% of all primary tu-
mors of the heart.2 Myxomas are particu-
larly frequent from the third to the sixth
decades of life and show a 2:1 female pre-
dominance.3-6 Most myxomas occur in the
left atrium (83%-88%).2,5,7 Although the
occurrence of atrial myxoma is normally
sporadic, as many as 7% of cases are fa-
milial, with the most notable condition
being Carney syndrome, an autosomal
dominant complex of cutaneous and car-
diac myxomas, pigmentation, and endo-
crine abnormalities.8,9 Transesophageal
echocardiography (TEE) has proved su-
perior to transthoracic echocardiography
in the diagnosis and characterization of
cardiac mass lesions.10-12 In general, the
outcome after cardiac myxoma resection
is favorable, with a 20-year survival rate
of 85%, and the recurrence rate of atrial
myxoma after resection is low (5%).3,7
As many as 10% of patients with atrial
myxoma present with no symptoms. 3
However, in most patients, left atrial myxo-
mas produce symptoms via the following
3 principal mechanisms: obstruction of the
mitral valve, systemic embolization (pe-
ripheral or cerebral), and constitutional
symptoms. The most common initial
symptom that provokes the diagnosis is re-
lated to mitral valve obstruction and can
include dizziness, palpitations, dyspnea,
and congestive heart failure.3 Obstruc-
tive cardiac symptoms are the provoking
symptoms in approximately 50% of pa-

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 Table 1. Clinical Features of Patients With Atrial Myxoma and Neurologic Manifestations a

Medical Treatment

Patient Postoperative mRs at

No./Sex/ (Length of Discharge/Follow-up
Age, y Medical Conditions Neuroimaging Preoperative Therapy) Delay b (Length of Follow-up)
1/F/70 Hyperlipidemia CT: right MCA infarct Warfarin Warfarin sodium 47 d 1/0 (11 y)
(1 mo)
2/F/70 Hypertension, MRI: left frontoparietal None Warfarin 68 d 1/0 (11 y)
hyperlipidemia infarct (6 mo)
TCD and CUS: negative
findings
3/F/48 None MRI: left occipital and Aspirin Warfarin 16 d 0 (NA)
parietal infarcts
4/M/17 None MRI: right MCA infarct None None 2d 3/NA (17 mo)
Angiogram: occlusion of
right MCA (M2)
5/F/20 Carney syndrome, smoker MRI: right MCA infarct Aspirin Warfarin 1.4 y 1/0 (2 y)
Angiogram: negative finding
6/M/45 Hypertension, CT: right parietal infarct None Aspirin 60 d 4/3 (11 mo)
hyperlipidemia, CT angiogram: negative
smoker, atrial fibrillation finding
7/F/41 None MRI: right frontal Aspirin Aspirin 2.3 y 1/0 (11 mo)
hemorrhage and chronic
right occipital infarct
Angiogram: 3-mm left ICA
aneurysm
8/F/79 Hypertension, MRI: right basal ganglia None Aspirin 7d 4 (NA)
hyperlipidemia, infarct
diabetes mellitus, MR angiogram: left PCA
coronary disease with stenosis
9/M/42 None CT: right occipital and None Warfarin 4d 3/3 (8 mo)
cerebellar vermis with (3 mo)
hypoattenuation

Abbreviations: CT, computed tomography; CUS, carotid ultrasonography; ICA, internal carotid artery; M2, first branch of the middle cerebral artery (MCA);
MR, magnetic resonance; MRI, MR imaging; mRs, modified Rankin score; NA, not available; PCA, posterior cerebral artery; TCD, transcranial Doppler.
a None of the patients showed obstructive cardiac symptoms of light-headedness, palpitations, or dyspnea.
b Indicates delay from symptoms onset to atrial myxoma resection.

tients, but may be present at any time in as many as
70%.3,6,7 Constitutional symptoms (eg, fever, fatigue, and
weight loss) are the provoking symptoms in 50% but can
be present at any time in as many as 58%.3,6,7 Systemic
embolization is the provoking symptom in 16%, but may
be present at any time in as many as one-third of pa-
tients.3,6,7 Neurologic symptoms have been reported in
26% to 45% of patients, with embolic cerebral infarct being
the most frequently observed event.3,13,14 We report the
largest descriptive clinical case series of neurologic com-
plications related to atrial myxoma seen during an 11-
year period at the Mayo Clinic.
METHODS
Using the pathology database of biopsy and autopsy speci-
mens, we searched for the diagnosis myxoma and then con-
firmed a cardiac origin in 74 patients. With institutional re-
view board approval, we reviewed medical records to identify
patients who underwent neurologic testing (computed tomog-
raphy or magnetic resonance imaging of the brain, magnetic
resonance angiography, or cerebral angiography) or neuro-
logic consultation. One of us (V.H.L.) reviewed the medical rec-
ords to identify patients with neurologic complications attrib-
utable to cardiac myxoma. Two patients with neurologic
complications were excluded. The first patient had a possible
amaurosis of the right eye in the setting of a right atrial myxoma
without intracardiac shunt. The second patient had an intra-
cranial mass that was pathologically confirmed to be myxoma
without evidence of an atrial mass.
We identified 74 consecutive patients with pathologically
proved cardiac myxoma who underwent cardiac myxoma re-
section at the Mayo Clinic from January 1, 1993, through De-
cember 31, 2004. Transesophageal echocardiography was per-
formed on all patients before surgery. The mean age was 59.1
(range, 12-92) years, with a female predominance (43 pa-
tients [58%]). The left atrium (LA) was the most commonly
observed location of cardiac myxomas (60 patients [81%]), fol-
lowed by the right atrium (8 [11%]) and the ventricles (5 [7%]).
RESULTS
We identified central nervous system complications of
cardiac myxoma in 9 patients (12%), including 6 fe-
males and 3 males (Table 1). The mean age at the time
of cardiac tumor resection in patients with neurologic
complications was 48.5 years (range, 17-79 years). Four
patients had no significant prior medical conditions. In
the remaining 5 patients, the following stroke risk fac-
tors were present: hyperlipidemia (n=4), hypertension

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 A B

Figure 1. Neuroimaging studies in case 7. A, Axial cranial computed tomography without contrast medium demonstrates a right frontal intraparenchymal
hemorrhage. B, Gadolinium-enhanced axial T1-weighted cranial magnetic resonance image shows blood components of varying ages and a thin enhancing rim.

(n = 3), active tobacco use (n = 2), paroxysmal atrial fi- NEUROIMAGING

brillation (n=1), diabetes mellitus (n = 1), and coronary
artery disease (n = 1). One patient was diagnosed as hav-
ing Carney syndrome (case 5).
CLINICAL PRESENTATION
In 7 patients with atrial myxoma who developed neuro-
logic complications (78%), the provoking neurologic
symptoms were the initial manifestation. Only 2 pa-
tients had the following neurologic events preceding the
provoking neurologic symptom: patient 2 had a history
of transient ischemic attack and patient 7 had a history
of stroke and seizure. None of the patients with atrial
myxoma and neurologic symptoms presented with car-
diac symptoms.
Only 2 patients (cases 7 and 9) had evidence of
pathologically confirmed systemic embolization of
myxomatous emboli. Patient 7 (Figure 1) had a prior
presumptive diagnosis of central nervous system vascu-
litis empirically treated with corticosteroids and cyclo-
phosphamide; she then subsequently developed head-
ache and left hemiparesis owing to a right frontal
intracerebral hemorrhage. Case patient 9 with patho-
logically confirmed myxomatous embolization
(Figure 2), presented with lower back pain and acute
weakness of the bilateral lower extremities owing to an
acute infrarenal aortic thrombus. He also developed
splenic and renal emboli and underwent aortic embo-
lectomy, bilateral transfemoral thromboembolectomy, and
bilateral lower extremity fasciotomies.
Neuroimaging was performed on all patients with neu-
rologic complications related to cardiac myxoma. Three
patients had only computed tomography studies avail-
able; in 6 patients, magnetic resonance imaging studies
were also available. Neuroimaging findings were consis-
tent with ischemic cerebral infarction in 8 patients and
intracerebral hemorrhage in 1 patient. Six patients (67%)
had single-vessel territory ischemic events on neuroim-
aging findings. Only 3 patients (33%) had neuroimag-
ing results that showed involvement of multiple vascu-
lar territories distinctive for a proximal embolic source
(cases 3, 7, and 9).
Case 7 involved the only patient with intraparenchy-
mal hemorrhage confirmed on computed tomography and
magnetic resonance imaging of the brain (Figure 1). The
patient in case 7 also had unusual magnetic resonance
imaging findings, including multiple punctate areas of
hemosiderin outside the area of the initial hemorrhage,
and details of this case have been previously pub-
lished.15 A cerebral angiogram in case 7 demonstrated a
3-mm wide-necked left internal carotid artery aneu-
rysm arising proximal to the left ophthalmic artery in the
region of the distal cavernous left internal carotid ar-
tery. There was also mild luminal irregularity with a more
focal zone of dilatation involving 2 distal branches of the
left middle cerebral artery in the region of the posterior
aspect of the sylvian fissure. Cerebral angiogram data were
available in 1 additional patient (case 4) and were unre-
markable.

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Figure 2. Cranial axial computed tomography (CT) without contrast medium
in case 9. The CT shows a 12-mm ovoid focus of decreased attenuation
within the right occipital lobe suggestive of metastatic myxoma lesions.
TRANSESOPHAGEAL ECHOCARDIOGRAPHY
Transesophageal echocardiography results were avail-
able in all 9 patients (Table 2). Eight patients (89%)
had mobile or highly mobile masses. All 9 patients with
neurologic manifestations had myxomas originating in
the atrium. The size of the atrial myxoma was variable,
with a mean diameter of 2.7 cm (range, 0.4-6.5 cm). Three
patients had unusual echocardiographic features, includ-
ing frondlike projections and a multilobulated appear-
ance. Eight of the atrial myxomas causing neurologic
symptoms (89%) demonstrated a mobile component on
TEE. All patients had a normal or a mildly reduced ejec-
tion fraction (ⱖ40%). In 3 patients, the atrial mass pro-
lapsed through the mitral valve during diastole, but none
of the patients demonstrated inflow obstruction of the
mitral valve. Multiple TEEs were necessary before a di-
agnosis was reached in 1 patient (case 7).
PATHOLOGICAL FINDINGS
All patients had pathologically confirmed cardiac myxoma.
Additional features noted on cardiac pathological exami-
nation included an organized thrombus in 2 patients (cases
3 and 8) and myxoma with focal hemorrhage in 1 pa-
tient (case 6). Only 2 patients (cases 7 and 9) had evi-
dence of pathologically confirmed systemic emboliza-
tion of myxomatous material. Pathological examination
of the right frontal lesion in case 7 showed myxomatous
proliferation inside the vascular lumen associated with
aneurysmal dilatation. Despite atrial myxoma resec-
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tion, the patient subsequently developed metastatic le-
sions in the pelvis and proximal femur, confirmed by re-
sults of a sacrum biopsy 10 months later. In case 9,
pathological examination of the infrarenal segment of the
aorta demonstrated embolic myxoma aggregate.
OUTCOME
All patients underwent successful surgical resection of the
cardiac myxoma. The median time from the onset of neu-
rologic symptoms to resection was 47 days (range, 2-848
days). The longest delay in diagnosis occurred in case 7,
who was presumed to have central nervous system vascu-
litis. Preoperative medical treatment included warfarin so-
dium in 1 patient and aspirin in 3. After surgical resec-
tion, 5 patients received warfarin and 3 received aspirin.
The duration of warfarin therapy was unknown in 2 pa-
tients and ranged from 1 to 6 months in the remaining 3
patients (Table 1). On hospital discharge, the mean modi-
fied Rankin score was 2 (range, 0-4). Information regard-
ing the length of follow-up after hospital discharge was un-
available in 2 patients; and follow-up ranged from 8 months
to 11 years in the remaining patients. A follow-up modi-
fied Rankin score was available in 6 patients, who had a
mean score of 1 (range, 0-3). No deaths were recorded. Pa-
tient 1 had asymptomatic recurrence of myxoma 5 years
after her initial presentation and underwent a second atrial
myxoma resection.
COMMENT
We present herein, to our knowledge, the largest clini-
cal series of central nervous system neurologic sequelae
of atrial myxoma. The ages and sex of the patients with
cardiac myxoma were consistent with those of previ-
ously reported series, with a female predominance be-
tween the third and sixth decades of life.3 Because our
series was based on a search of the pathology database,
we included all consecutive atrial myxoma resections per-
formed, including asymptomatic presentations. Com-
pared with other series that have reported neurologic
symptoms in 26% to 45% of patients with atrial myxoma,
the rate of central nervous system complications in our
series was lower (9/74 [12%]).3,13,14 In our series, no pa-
tients demonstrated symptoms related to mitral valve ob-
struction or constitutional effects, suggesting that pa-
tients with atrial myxoma who develop neurologic
complications may lack concomitant cardiac symp-
toms. Thus, neurologic symptoms can represent the ini-
tial clinical manifestation in patients with atrial myxoma.
All of the patients in our series had a normal or mildly
reduced ejection fraction, and none of the patients dem-
onstrated inflow obstruction of the mitral valve, which
was in concordance with the lack of cardiac obstructive
symptoms clinically.
In our series, ischemic cerebral infarction was the most
common neurologic complication, and the mobility, not
the size, of the myxoma appears to be related to embolic
potential. Histologically, 41% of cardiac myxomas have
surface thrombi, and systemic embolization most likely
is related to myxoma surface thrombus.16 Fibrotic and
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 Table 2. Transesophageal Echocardiography Features

Ejection
Prolapse Fraction,
Patient No. Myxoma Attachment Description Into MV % Size, cm
1 Posterolateral wall of left Multilobulated, Yes 65 2.1 ⫻ 1.1
atrium multifronded, highly
mobile
2 Junction of LAA and Highly mobile No 60 0.8 ⫻ 0.8
pulmonary veins
3 Atrial septum (fossa ovalis) Small stalk, mobile No 65 2.7 ⫻ 2.5
4 Atrial septum Large, mobile Yes 53 3.5 ⫻ 2.4
5 Multiple chambers (left Multiple masses, mobile ... 65 ...
atrium)
6 Atrial septum Multilobulated, highly No 50 3.5 ⫻ 2.0
mobile
7 Atrial septum, inferior Sessile mass with frondlike No 65 0.4 ⫻ 0.7
aspect mobile projections
8 Atrial septum Not available No 60-65 2.0
9 Atrial septum (fossa ovalis) Large, highly mobile Yes 40-45 6.5 ⫻ 2.5

Abbreviations: LAA, left atrial appendage; MV, mitral valve (during diastole); ellipses, data not available.

nonthrombotic tumors are more likely to be found in older
patients.16 Surgical resection of atrial myxoma is cura-
tive in most patients, and continued systemic or cere-
bral embolization after tumor removal is rare.13,17,18 Al-
though surface thrombus embolization may be the
suspected mechanism, only one-third of the patients in
our series had multiple vascular territory involvement on
neuroimaging. Surgical resection is considered cura-
tive, and medical management alone may be ineffective.
In a case series of 5 patients with atrial myxoma and stroke,
cerebral embolization recurred in 2 patients before sur-
gical resection, despite anticoagulation therapy.13 Al-
though anticoagulation therapy may reduce the risk of
emboli due to thrombus, it would be mechanistically in-
effective in preventing emboli from fragments of the myxo-
matous tumor.
Only 2 patients (22%) showed evidence of systemic
myxomatous tumor embolization. Although rare, myxo-
matous tumor emboli have been demonstrated histologi-
cally in a variety of locations, including the coronary ar-
teries, common iliac arteries, kidney, spleen, pancreas, liver,
and brain.3,7,19,20 Compared with nonembolic myxomas,
embolic tumors are more likely to have a surface throm-
bus and myxoid frondlike projections.16 After acute myxo-
matous emboli, there are 2 potential neurologic compli-
cations: myxomatous emboli may invade the vessel walls,
inducing cerebral aneurysmal formation, or embolic im-
plants may metastasize and form space-occupying
lesions.
Intracranial aneurysms are a rare complication of myxo-
matous emboli.3,20,21 Pathologically proved myxomatous em-
boli have been demonstrated in the cerebral ves-
sels,3,19,20,22,23 as was evident in case 7. Histologically, 23%
of myxomas have mitotic activity and myxomatous em-
boli can demonstrate continued growth within ves-
sels.16,24 Myxomatous tumor cells can penetrate the vessel
wall at the site of final lodgment, and tumor emboli can
infiltrate via subintimal growth, leading to weakening of
the arterial wall and subsequent aneurysm formation.25,26
This complication can be delayed, and pathologically proven
intracranial aneurysms have been reported 5 years after suc-
cessful left atrial myxoma resection.27
Aneurysm formation associated with embolized atrial
myxoma is not caused by blood-flow dynamics but by
myxomatous tumor invasion into the vessel wall. Thus,
cerebral aneurysm associated with atrial myxoma has been
described as having angiographic features similar to those
of septic emboli, including multiplicity, peripheral loca-
tion, and fusiform appearance.27-30 In case 7, a cerebral
angiogram demonstrated focal dilatations in 2 distal
branches of the left middle cerebral artery consistent with
myxoma-related aneurysms and a 3-mm aneurysm in the
distal cavernous left internal carotid artery of uncertain
significance.
Case 7 also illustrated the second rare complication
of myxomatous tumor emboli known as metastatic
myxoma. Metastatic cardiac myxoma has been docu-
mented in the lung, bones, and soft tissue.31 Metastatic
myxoma is infrequent, and intracranial metastatic car-
diac myxoma is even less common, limited to single case
reports in the literature.31-33 As illustrated by case 7, sur-
gery may not preclude delayed neurologic sequelae and
metastatic myxoma is a complication that can present long
after cardiac myxoma resection. Rarely, these masslike
lesions may precede the diagnosis of the cardiac myxoma
by as long as 22 months.34 There is no definitive treat-
ment for metastatic cardiac myxoma, although there is
an isolated case report of treatment with irradiation and
chemotherapy (doxorubicin hydrochloride and ifos-
famide) with a 10-year remission.31
Atrial myxoma is a rare but potentially curable cause
of stroke. Neurologic complications associated with atrial
myxoma most frequently include cerebral infarct due to
thrombus. Rarely, neurologic complications may be due
to embolized tumor fragments. Patients with embolized
myxomatous tumor represent a minority of patients with
cardiac myxoma and appear to be at increased risk for pe-
ripheral systemic embolization and delayed neurologic com-

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 plications. Potential neurologic sequelae relevant to pa-
tients with tumor embolization include myxoma-induced
aneurysmal formation and myxomatous metastasis. Cere-
bral angiography should be considered in patients with em-
bolic cerebral infarction associated with atrial myxoma, es-
pecially in the setting of pathologically confirmed
myxomatous emboli elsewhere. In addition to being evalu-
ated for myxomatous intracranial aneurysms, this subset
of patients should be monitored for the potential develop-
ment of metastatic myxoma.
Accepted for Publication: January 18, 2007.
Correspondence: Vivien H. Lee, MD, Department of Neu-
rologic Sciences, Rush University Medical Center, 1725
W Harrison St, Ste 1121, Chicago, IL 60612 (vivien_lee
@rush.edu).
Author Contributions: Study concept and design: Brown.
Acquisition of data: Lee, Connolly, and Brown. Analysis
and interpretation of data: Lee, Connolly, and Brown. Draft-
ing of the manuscript: Lee. Critical revision of the manu-
script for important intellectual content: Connolly and
Brown. Statistical analysis: Brown. Obtained funding:
Brown. Administrative, technical, and material support: Lee.
Study supervision: Connolly and Brown.
Financial Disclosure: None reported.
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