Summary: A 55-year-old woman with no significant medical history presented
with 1 episode of syncope. Her workup was negative except for a
transthoracic echo cardiogram that suggested the presence of an
atrial mass. Cardiac magnetic resonance imaging (MRI) was
Atrial septal aneurysm
An electrocardiographic-gated segmented fast imaging employing
steady state acquisition (FIESTA) cine sequence (repetition time
4.0, echotime 1.7) in the horizontal long-axis view was used to
evaluate the atria. The MRI shows oscillation of the atrial septum
into both atria throughout the cardiac cycle (Figure 1). The
interatrial septum bulges into the left atrium at end-systole,
moves to the midline at mid-diastole, and bulgesinto the right
atrium at end-diastole. This is diagnostic of an atrial septal
aneurysm (ASA). On MRI, the base of the aneurysm measured 1.9 cm.
Maximum excursion into the right atrium was 1.3 cm and maximal
excursion into the left atrium was 1.6 cm. No atrial thrombi were
seen and no signal voids adjacent to the atrial septum were found
to suggest the presence of a patent foramen ovale (PFO).
Atrial septal aneurysm is a congenital cardiac abnormality that
is characterized by saccular formation of the interatrial septum.
Redundant atrial septal tissue results in bulging of the septum
into either or both atria during the cardiac cycle. The diagnosis
is best established with transesophageal echocardiography (TEE)
since it can be easily missed with transthoracic
echocardiography.1 Diagnostic criteria for ASA
established by Hanley based on the appearance on echocardiography
are: aneurysmal dilatation of the atrial septum protruding at least
1.5 cm beyond the plane of the atrial septum or phasic excursion of
the interatrial septum during the cardiac cycle of at least 1.5 cm
in total amplitude with a diameter at the base of the aneurysm of
at least 1.5 cm.2 The condition can also be described
using the Olivares-Reyes criteria, a classification based on the
extent of excursion into each atrium.3 While the
prevalence of ASA based on autopsystudies is <1%, the prevalence
on TEE in nonselected patients is higher, in the range of 2% to
Atrial septal aneurysm is clinically significant because of its
association with cryptogenic stroke especially when there is a
concurrent PFO. Approximately 70% of patients with ASA also have a
PFO, while PFO is present in only 22% of patients without ASA. In
one study, the combination of ASA and PFO was associated with a
33-fold higher risk of cryptogenic stroke.1 A
meta-analysis has also found that ASA alone or ASA with PFO is
associated with ischemic and cryptogenic strokes in patients <55
years of age. The strongest association is in those patients with
both an ASA and a PFO.4 In patients <45 years of age
with ischemic cerebral events, ASA should especially be suspected
as a cardioembolic source. Mattioli and colleagues5
reported that 86% (43 of 50) of such patients had an ASA as the
only possible etiology while 97% (42 of 43) of these younger
patients with ASA also had a PFO.
Patients with both ASA and PFO who have had a stroke are at
substantial risk for recurrent stroke despite aspirin therapy. Mas
and colleagues6 reported that the risk for recurrent
stroke was 15% for patients with both PFO and ASA compared with
4.2% for patients with neither abnormality. These patients might
benefit from more aggressive therapeutic strategies such as
combination antiplatelet drugs, long-term anticoagulation or
closure of the PFO.6
Proposed mechanisms of stroke include formation of thrombus on
the ASA, paradoxical embolism from a venous source through a PFO
and thrombus formation from an atrial arrhythmia.7
Common maneuvers such as normal inspiration, coughing or Valsalva
can result in transient elevation of right atrium pressures
sufficient to permit paradoxical emboli to pass from the right
atrium to the left atrium via a PFO.8It has been
theorized that in patients with both ASA and PFO, motion of the
fossa ovalis membrane may promote paradoxical shunting by enhancing
the preferential orientation of blood flow from the inferior vena
cava toward the foramen ovale.6 It has also been
suggested that the thickness of an ASA is associated with risk of
embolism. An ASA >5 mm in thickness has been found to have a
higher association with stroke. The increased thickness may
represent thrombotic material that has accumulated on the surface
of the ASA.9 It is possible for an ASA to perforate,
resulting in an interatrial communication that can place the
patient at increased risk for paradoxical
Other reports have also noted that ASAs are also associated with
supraventricular tachyarrhythmias, mitral valve prolapse and
migraines with aura.11-13 The association with
arrhythmia, especially atrial fibrillation, would further increase
the risk of stroke. The association with mitral valve prolapse is
interesting, as it has been suggested that both abnormalities
reflect redundancy of endocardial tissue.12 Up to 28% of
patients who suffer from migraines with an aura have an ASA. One
explanation for this relationship is that a PFO (associated with
the ASA) would allow trigger substances for migraines (vasoactive
chemicals) in the venous blood to bypass the pulmonary filter and
enter the systemic circulation.14
On cine bright-blood MRI sequences, ASA can be easily diagnosed.
The phasic excursion of the atrial septum throughout the cardiac
cycleis readily apparent. If present, a signal void extending from
the ASA into the left atrium would also indicate an associated PFO.
Contrast-enhanced dynamic MRI with Valsalva has also recently been
shown to be useful in the diagnosis of ASA and PFO.15 If
echocardiography is inconclusive for the diagnosis of an ASA, MRI
is the imaging study of choice for further evaluation.
Atrial septal aneurysm is a congenital cardiac abnormality
characterized by oscillation and aneurysmal bulging of atrial
septal tissue into either or both atria during the cardiac cycle.
Roughly 70% of patients can also have a PFO, placing them at
increased risk of cryptogenic stroke. Atrial septal aneurysm is
easily recognized with cine bright-blood MRI sequences.
- Cabanes L, Mas JL, Cohen A, et al. Atrial septal aneurysm and
patent foramen ovale as risk factors for cryptogenic stroke in
patients less than 55 years of age. A study using transesophageal
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- Hanley PC, Tajik AJ, Hynes JK, et al. Diagnosis and
classification of atrial septal aneurysm by two-dimensional
echocardiography: Report of 80 consecutive cases. J Am Coll
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- Olivares-Reyes A, Chan S, Lazar EJ, et al. Atrial septal
aneurysms: A new classification in two-hundred five adults. J
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- Overell JR, Bone I, Lees KR. Interatrial septal abnormalities
and stroke: A meta-analysis of case control studies.
- Mattioli AV, Aquilina M, Oldani A, et al. Atrial septal
aneurysm as a cardioembolic source in adult patients with stroke
and normal carotid arteries. A multicentre study. Eur Heart
- Mas J, Arquizan C, Lamy C, et al. Recurrent cerebrovascular
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- Lamy C, Giannesini C, Zuber M, et al. Clinical and Imaging
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- Wu LA, Malouf JF, Dearani JA, et al. Patent foramen ovale in
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- Mattioli AV, Aquilina M, Oldani A, et al. Frequency of atrial
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- Ewert P, Berger F, Vogel M, et al. Morphology of perforated
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- Morelli S, Voci P, Morabito G, et al. Atrial septal aneurysm
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- Belkin RN, Kisslo J. Atrial septal aneurysm: Recognition and
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- Carerj S, Narborne MC, Zito C, et al. Prevalence of atrial
septal aneurysm in patients with migraine: An echo cardiographic
study. Headache. 2003;43:725-728.
- Wilmhurst PT, Nightingale S, Walsh KP, Morrison WL. Effect on
migraine of closure of cardiac right-to-left shunts to prevent
recurrence of decompression illness or strokeor for haemodynamic
reasons. Lancet. 2000;356:1648-1651.
- Mohrs OK, Petersen SE, Erkapic D, et al. Diagnosis of patent
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