J Neurol (1995) 242 : 689-694
© Springer-Verlag 1995

H. P. Mattle
D. Maurer
M. Sturzenegger
C. Ozdoba
R. W. Baumgartner
G. Schroth

Received: 7 December 1994
Received in revised form: 23 February 1995
Accepted: 27 February 1995

H. P. Mattle (N~) • D. Maurer M. Sturzenegger • R. W. Baumgartner
Department of Neurology,
University of Bern, Inselspital,
CH-3010 Berne, Switzerland
C. Ozdoba • G. Schroth
Department of Neuroradiology,
University of Bern, Inselspital,
CH-3010 Berne, Switzerland

Cardiac myxomas: a long term study

Abstract From 1980 to 1992 we
followed 12 patients with cardiac
m y x o m a s for an average of 4.4 years
(8 m o n t h s - l l years). Presenting
s y m p t o m s were neurological in four
patients (hemiparesis, aphasia, visual
field deficits, progressive dementia
or vertigo), progressive dyspnoea in
six, pulmonary embolism in one, and
peripheral arterial or renal emboli in
three. The diagnosis was suspected
clinically in 11 patients. It was confirmed by echocardiography in ten
and by thoracic CT in one. All these
patients had cardiac surgery. One
diagnosis was made at autopsy; the
patient died unexpectedly during
surgery for emboli to the leg arteries.
At follow-up, two additional patients
had died, one from myocardial infarction and one from rhabdomyosarcoma. Only one of the nine surviving
patients had recurrent s y m p t o m s after cardiac surgery. His dementia

Introduction
Cardiac m y x o m a is a rare cause of stroke or peripheral
emboli. W h e n diagnosed early surgical resection of the
m y x o m a generally cures the condition. However, in rare
cases there are progressive s y m p t o m s in spite of surgical
resection of the m y x o m a . We recently observed such a patient with progressive dementia after surgical removal of
an atrial m y x o m a . In order to find out whether his clinical
and neuroradiological findings were different from those
of other m y x o m a patients, we performed a clinical and,

continued to progress. The patients
without new s y m p t o m s after cardiac
surgery had normal M R I o f the brain
or residual ischaemic lesions. M R I
of the patient with progressive dementia showed multiple cerebral lesions with a bright centre and a dark
rim on T 1- and T2-weighted spinecho images. On CT there were
m a n y calcified lesions. CT, M R angiography and contrast angiography
revealed multiple fusiform aneurysms. The rare occurrence o f progressive neurological symptoms after
m y x o m a resection with multiple
cerebral lesions and aneurysms
should suggest m y x o m a metastases
to the brain.
K e y w o r d s Cardiac m y x o m a •
Aneurysm • Dementia. Computed
tomography - Magnetic resonance
imaging

when possible, also neuroradiological follow-up of all the
patients with cardiac m y x o m a s at our institution.

Subjects and methods
From 1980 to 1992 we identified 12 patients with cardiac myxomas at the University Hospital in Berne, Switzerland. All myxomas were proven by histology.
All charts were reviewed. At initial presentation all 12 patients
underwent clinical examinations, 12-lead electrocardiography
(ECG), chest roentgenography, and complete blood count; in nine
patients erythrocyte sedimentation rate (ESR) was recorded. In ten

690

patients echocardiography was performed, in one patient echocardiography and cardiac CT. Of four patients with neurological presentation, two had cranial CT and one cranial MRI initially. In one
of them cranial CT, cerebral angiography and MRI were performed 3 years after diagnosis and surgical resection of the myxoma.
In December 1992 we performed clinical follow-up examinations in seven of the nine surviving patients. The two additional
living patients were interviewed by phone. The information they
gave was confirmed by the family physician, who also performed
the clinical examination. Cranial MRI was performed in five patients. One patient with a cardiac pacemaker and a patient with a
myxoma of the right ventricle did not have MRI at follow-up.

Results
The average age of the 12 patients at diagnosis was 54
years (range: 37-74). There were nine women and three
men. Mean follow up of the surviving patients was 4.4
years (range: 8 months to 11 years). Ten m y x o m a s were
situated in the left atrium, one in the right atrium and one
in the right ventricle.
Presenting symptoms are given in Table 1. They were
neurological in four patients (hemiparesis, aphasia, visual
field deficits, progressive dementia or vertigo) and general in eight. General symptoms were progressive dyspnoea in six patients, pulmonary embolism in one, and peripheral arterial or renal emboli in three.
The history of the four patients presenting with neurological signs was as follows.
Patient 2, a 48-year-old woman was found comatose at
home in 1991. She was admitted to a regional hospital,
where a diagnosis of myocardial infarction was made on
ECG. In addition, there was right hemiplegia, left oculomotor palsy and bilateral leg ischaemia. Arterial pulses of
the legs were absent. She was referred to our hospital for
further investigation and treatment. The right hemiplegia
and left oculomotor palsy were considered signs of a midbrain lesion causing the coma. Laboratory investigations
ruled out a metabolic cause of the coma. Cranial CT was
normal. Aortic aneurysm was excluded by CT angiography. Contrast angiography showed a large thrombus at the
aortic bifurcation. She was taken to the operating room
and died in ventricular fibrillation during surgery. Autopsy of the heart was performed. It showed a 2 cm by 3
cm by 3 cm left atrial m y x o m a originating from the interatrial septum, and there were multiple myxomatous emboli in the coronary arteries. The abdominal aorta was occluded by a thrombus containing myxomatous material.
Patient 4, a 72-year-old woman, suffered from dyspnoea on exertion and was in atrial fibrillation. In November 1990, she experienced transient vertigo. On the same
day motor aphasia and right facial paresis occurred, which
cleared within 2 days. Investigations for the cause of the
transient neurological deficits showed a left atrial mass on
echocardiography.
Patient 7 experienced a first episode of vertigo at age
51 years. One year later she suffered transient dysarthria

and paraesthesias in the right arm. In the same year a
transient right sensorimotor hemisyndrome occurred. Investigations including CSF examination, cerebral arteriography and transthoracic echocardiography were normal.
One year later vertigo, transient hearing loss and spontaneous nystagmus recurred compatible with Meni~re's disease. At age 55 she suffered embolic retinal ischaemia on
the right. Cerebral MRI showed multiple small foci of increased signal on T2-weighted images compatible with ischaemic changes. Repeat CSF examination showed intrathecal immunoglobulin production. Repeat echocardiography demonstrated a tumour in the left atrium, which
was confirmed by cardiac CT and turned out to be a myxoma on surgery. When she was seen at age 58 she seemed
to be depressed and complained of mild positional vertigo
and imbalance. On examination she had a residual partial
visual field deficit on the right and mild tetrahyperreflexia. MRI showed the same (probably ischaemic) nonspecific changes as 3 years previously.
Patient 9 was a 49-year-old farmer. He and his wife
had observed progressive mnestic and mental changes
since age 44. Four and 5 years later there were two
episodes with transient right hemiparesis and aphasia and
agraphia. There was also an episode of mild renal insufficiency and microhaematuria, and there was lower leg pain
and transient claudication on two occasions. A systemic
vasculitis was suspected and ruled out. Echocardiography
showed a left atrial mass, which was considered to be a
m y x o m a causing recurrent emboli to the brain, kidneys
and the legs. The m y x o m a was resected. Three years later
there was an acute event with disorientation, failure to
recognize familiar surroundings, motor aphasia and motor
incoordination. CT, MRI, and cerebral arteriography
showed multiple calcified cerebral lesions and multiple
fusiform aneurysms (Fig. 1). When he was seen at age
54 he was demented. According to his wife the dementia
had continuously progressed over the last few years.
He showed aphasia, agraphia, alexia, decreased constructional ability and spatial disorientation. He needed help
when dressing and found his way only in the familiar surroundings of his farm.

General and laboratory findings
Cardiac auscultation was abnormal in ten patients (systolic murmur in ten, additional diastolic murmur in two
and mitral valve opening snap in one). ESR was normal in
one patient, slightly elevated in three (8-15 m m / l s t h),
moderately elevated in five (30-55 m m / l s t h), and highly
elevated in one (over 100 m m / l s t h). There was anaemia
in 4 of 12 patients. A chest radiograph was normal in six
patients. Four patients showed ventricular enlargement,
one left atrial enlargement and three signs of pulmonary
congestion. There were non-specific ECG changes in 8 of
the 12, and one patient was in atrial fibrillation.

Multiple ischaemic changes
in both hemispheres,
unchanged since surgery
Dead at follow-up
Multiple myxomatous
lesions and calcifications,
multiple fusiform
aneurysms
Normal
Not performed
Small nonspecific vascular
changes in both
hemispheres

No recurrent symptoms or signs,
Residual monocular visual field
deficit, residual slight
tetrahyperreflexia, imbalance, depression
Died 5 months after surgery
because of myocardial infarction
Further progressive dementia,
tetrahyperreflexia

No recurrent symptoms, no signs
No recurrent symptoms, no signs
No recurrent symptoms, no signs

Echocardiography,
after negative
echocardiography
3 years previously
Echocardiography
Echocardiography

Echocardiography

Left atrium

Right atrium
Left atrium

Left atrium

Right ventricle Echocardiography

Recurrent vertigo, recurrent left
and right hemiparesis, right
hemianopia

Progressive dyspnoea on exertion,
orthopnoea, chest pain

Progressive dementia, recurrent
transient ischaemic attacks,
emboli to the renal and leg arteries

Progressive dyspnoea on exertion,
palpitations

Pulmonary embolism

56

74

49

37

54

42

8

9

10

11

12

Progressive dyspn0ea on exertion,
chest pain, phlebothrombosis and
pulmonary embolism when diagnosis
was made

Left atrium

Thoracic CT

7

Normal

No recurrent symptoms or signs,
slight left hemiparesis

Echocardiography

Left atrium

Ischaemia left leg

41

6

Dead at follow-up

Died 3 years after surgical
resection of the myxoma due to
rhabdomyosarcoma occluding the
lung veins

Echocardiography

Left atrium

Dyspnoea, peripheral edema

41

5

Not performed

No recurrent symptoms, no signs

Echocardiography

Left atrium

Transient ischaemic attack, motor
aphasia and right facial paresis,
dizziness

72

4

Not performed

No recurrent symptoms or signs,
pacemaker, paroxysmal
positioning vertigo

Echocardiography

Left atrium

Progressive dyspnoea on exertion,
dizziness, chest pain

74

3

Dead at follow-up

Died at surgery for leg ischaemia

Autopsy

Left atrium

Right hemiparesis, coma,
myocardial infarction, recurrent
emboli to the leg arteries

48

2

Not performed

No recurrent symptoms, no signs

Echocardiography

Left atrium

Progressive dyspnoea on exertion

57

1

Follow-up MRI

Diagnosis by

Location of
the myxoma

Clinical manifestation

Patient

Age at
diagnosis
(years)

Follow-up 1993

Table 1 Overview of 12 patients with cardiac myxomas

v,D

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Fig. i a-f Patient 9, with progressive dementia, shows multiple lesions in all cerebral lobes on MRI (1.5 T). Tl-weighted (a) and
T2-weighted (b) spin-echo images demonstrate areas with hyperintense signal in both occipital lobes surrounded by a rim of signal
loss, more pronounced on T2-weighted than on Tl-weighted images. e In the frontal and parietal lobes there are additional lesions
and signs of old infarctions, d CT demonstrates that the areas of
signal loss are due to calcifications, e On angiography there are
multiple large and small fusiform aneurysms, which were also
seen on MR angiography (f)
The diagnosis was suspected clinically in 11 patients.
It was confirmed by echocardiography in ten and by thoracic CT in one. In patient 7 the m y x o m a was discovered
only at the second echocardiographic examination because of persisting dizziness and recurrent left and right
hemiparesis. All these patients had cardiac surgery for resection of the myxoma. Diagnosis was made at autopsy in
patient 2, who died unexpectedly at surgery for emboli to
the leg arteries.
At follow-up, two additional patients had died, one
from myocardial infarction and one from rhabdomyosarcoma. Only one of the nine surviving patients (no. 4) had
recurrent symptoms after cardiac surgery. He came to our
attention because of progressive dementia.

Neuroradiological findings
The patient with progressive dementia showed multiple
cerebral lesions on cranial MRI (Fig. 1). On both T1- and
T2-weighted spin-echo images the lesions had a bright
centre and a dark rim. They turned out to be calcified
on CT and were presumably metastatic myxomatous tumours. MRI and contrast angiography demonstrated multiple fusiform aneurysms. Two patients without new
symptoms after cardiac surgery had normal MRI of the
brain. One woman with persistent dizziness and dysequilibrium after cardiac surgery (Patient 3) had multiple hyperintense areas in both hemispheres on T2-weighted
spin-echo images. Another woman without neurological
symptoms or signs showed similar changes, which were
regarded as residual, presumably lacunar ischaemic lesions.

Discussion
Cardiac myxomas lead to constitutional, cardiac (usually
obstructive) or embolic symptoms and signs [1-8].
Constitutional signs may include low-grade fever,
weight loss, anaemia, elevated ESR, leucocytosis and hypergammaglobulinaemia [9]. They mimic disorders such

693

as rheumatic diseases, polymyositis and other connective
tissue disorders, polyarteritis nodosa and systemic amyloidosis [10-14]. Pathogenetic theories include a possible
systemic or immunological response to serum proteins
produced by the myxoma or proteins released into the circulation by damaged tumour fragments. Autoantibodies
have been found, whose levels diminished after excision
of a myxoma [15]. Finally, there is strong evidence that
myxomas produce interleukin-6 (IL-6), causing constitutional symptoms [16]. S6guin and coworkers [17] demonstrated, that IL-6 is produced by myxoma cells and that elevated IL-6 levels in patients with constitutional symptoms return to normal after resection of the myxomas
[17]. Constitutional symptoms in our patients disappeared
after resection of the myxomas except in the patient with
progressive dementia whose ESR remained high.
In our series, one-third of the myxomas initially manifested with features of embolism to the brain, half with
cardiovascular signs and the rest with pulmonary or leg
embolism. The proportion with neurological manifestations may be higher, since patients referred to hospital
with cardiovascular symptoms were not seen by a neurologist initially. Three years after surgical resection of a left
atrial myxoma one patient died of rhabdomyosarcoma occluding the lung veins. Reviewing the pathology specimens no malignancy of the myxomatous material was detected. One additional patient showed progressive neurological symptoms after cardiac surgery. His initial presentation was with emboli to the renal and leg arteries and dementia. After surgical resection of the myxoma the dementia progressed further to such a degree that he became
completely dependent on his family, and his son had to
take care of the farm. All the other patients remained free
of symptoms or had only residual neurological symptoms
or signs.
The several modes of neurological presentation of cardiac myxoma include embolic infarction, aneurysm formation, and subarachnoid and primary intraparenchymal
haemorrhage [18]. Even fulminant brain necrosis from
atrial myxoma showers has been reported [19]. In addition, both benign and the rare malignant cardiac myxomas
can cause metastases to the brain [20-23]. Among 56 primary cardiac tumours in a Japanese series, one case had
evidence of intracranial metastasis, and among 1518 cases
of intracranial metastases only one originated in the heart
[24] The neurological presentation may lead to the diagnosis of the cardiac myxoma, or neurological signs may
occur only months or years after resection of the cardiac
tumour and indicate continuation of the disease [18, 25].
Myxoma metastases sometimes remain within the vessels, and sometimes invade and transgress the arterial
walls [26]. For this reason both vascular and mass lesions
may occur and result in highly variable neuroradiological
findings. Angiography can show occlusions of cerebral
vessels or aneurysms [14, 18, 25, 27-39]. They resemble
mycotic aneurysms, are typically multiple and are located

distal to the circle of Willis. They can grow rapidly [40].
CT of a cerebral myxoma metastasis was first reported by
Desouza and coworkers [26]. CT showed an enhancing
mass. On later CT hyperdense or hypodense lesions or lesions with heterogeneous density and homogeneous or
ring-like contrast enhancement were reported [22, 23, 33,
41, 42]. Perifocal oedema is sometimes present [22, 33].
The hyperdense lesion reported by Frank e~ al. [41]
showed haemorrhage on histological examination. However, most often CT shows ischaemic infarcts [43]. Infarcts, mostly of the lacunar type, are also the most frequent findings on MRI [43]. In one patient multiple
aneurysms were seen on MRI [37]. Two of the five MR
scans at follow-up of our patients showed non-specific
changes in the white matter, presumably representig a microangipathy. Two scans were normal.
A patient with multiple episodes of neurological symptoms and signs, ischaemic and haemorrhagic infarctions
on CT and multiple aneurysms on angiography was reported by Michael et a1.[33]. The neurological manifestations occun'ed after she had been symptom-free for 20
months after myxoma resection. MRI revealed multiple
areas of subacute and chronic haemorrhages, surrounded
by oedema, and comprising abnormally dilated vessels.
Open brain biopsy revealed a typical aneurysm, haemorrhage and nodules of myxoma within an area of infarction. These authors considered the MRI appearance to
be non-specific, showing oedema, and/or haemorrhage
and/or vascular dilatations around the lesions, indistinguishable from primary or metastatic vascular tumour or
cerebral vascular malformations with haemorrhage. Our
patient 4 seems to be identical to this patient. He also
showed episodes of progressive neurological symptoms
and signs after the cardiac myxoma had been removed.
CT revealed hyperdense enhancing and non-enhancing lesions, some representing calcified lesions and some vascular dilatations. On angiography there were multiple
fusiform aneurysms beyond the circle of Willis, mostly of
middle cerebral artery branches. The Tl-weighted spinecho images showed multiple areas of hyperintense signal
surrounded by signal loss. T2-weighted and proton density images showed that the areas of hyperintensity were
still present but less hyperintense. The hyperintense signal was similar to the signal of fat. The surrounding area
of signal loss was more pronounced than on Tl-weighted images. Time-of-flight MR angiography showed the
larger aneurysms seen on contrast-enhanced angiography
but failed to demonstrate the tiny aneurysms.
In conclusion, the findings of our series of patients
with cardiac myxomas and literature reports show that
most patients are symptom-free after removal of the myxoma. They show normal or non-specific abnormalities on
neuroimaging studies. However, a few patients harbour
locally invasive and progressive metastases and may develop progressive neurological symptoms and signs.
These patients are probably characterized by multiple

694

a ne u ry s m s on angiography, multiple m a s s e s on CT, and
m u l t i p l e lesions on M R I with a h y p e r i n t e n s e centre surr o u n d e d by a r i m o f signal loss. It m a y be w o r t h w h i l e to
p e r f o r m f o l l o w - u p e x a m i n a t i o n s and n e u r o i m a g i n g stud-

ies in patients with cardiac m y x o m a s . H o w e v e r , h o w to
treat patients with cerebral m y x o m a metastases and
w h e t h e r radio-therapy and c h e m o t h e r a p y are beneficial is
still u n k n o w n .

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