(Circulation. 1995;91:2785-2792.)
© 1995 American Heart Association, Inc.
Articles |
Atrial Septal Aneurysm in Adult Patients
A Multicenter Study Using Transthoracic and Transesophageal Echocardiography
From the Division of Cardiology, Hannover Medical School, Germany (A.M., W.G.D., O.L., D.H., P.W.); University Clinic, Munich, Germany (C.A., C.S.); Mayo Clinic, Rochester, Minn (B.K.K.); New York University Medical Center, New York (I.K., R.S.F.); Bikur Cholim Hospital, Jerusalem, Israel (A.K.); German Heart Center, Munich, Germany (K.D.); Academic Hospital, Wolfsburg, Germany (R.E.); Erasmus University, Rotterdam, Netherlands (G.R.S.); Heart Institute, Tel-Hashomer, Israel (Z.V.); University Clinic, Mainz, Germany (R.E.); and Academic Medical Center, Amsterdam, Netherlands (C.A.V.).
Correspondence to Andreas Mügge, MD, Division of Cardiology, Hannover Medical School, Konstanty-Gutschowstr 8, 30625 Hannover, Germany.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Background An atrial septal aneurysm (ASA) is a well-recognized abnormality of uncertain clinical relevance. We reevaluated the clinical significance of ASA in a large series of patients. The aims of the study were to define morphological characteristics of ASA by transesophageal echocardiography (TEE), to define the incidence of ASA-associated abnormalities, and to investigate whether certain morphological characteristics of ASA are different in patients with and without previous events compatible with cardiogenic embolism.
Methods and Results Patients with ASA were enrolled from 11 centers between May 1989 and October 1993. All patients had to undergo transthoracic and transesophageal echocardiography within 24 hours of each other; ASA was defined as a protrusion of the aneurysm >10 mm beyond the plane of the atrial septum as measured by TEE. Patients with mitral stenosis or prosthesis or after cardiothoracic surgery involving the atrial septum were excluded. Based on these criteria, 195 patients 54.6±16.0 years old (mean±SD) were included in this study. Whereas TEE could visualize the region of the atrial septum and therefore diagnose ASA in all patients, ASA defined by TEE was missed by transthoracic echocardiography in 92 patients (47%). As judged from TEE, ASA involved the entire septum in 100 patients (51%) and was limited to the fossa ovalis in 95 (49%). ASA was an isolated structural defect in 62 patients (32%). In 106 patients (54%), ASA was associated with interatrial shunting (atrial septal defect, n=38; patent foramen ovale, n=65; sinus venosus defect, n=3). In only 2 patients (1%), thrombi attached to the region of the ASA were noted. Prior clinical events compatible with cardiogenic embolism were associated with 87 patients (44%) with ASA; in 21 patients (24%) with prior presumed cardiogenic embolism, no other potential cardiac sources of embolism were present. Length of ASA, extent of bulging, and incidence of spontaneous oscillations were similar in patients with and without previous cardiogenic embolism; however, associated abnormalities such as atrial shunts were significantly more frequent in patients with possible embolism.
Conclusions As shown previously, TEE is superior to the transthoracic approach in the diagnosis of ASA. The most common abnormalities associated with ASA are interatrial shunts, in particular patent foramen ovale. In this retrospective study, patients with ASA (especially with shunts) showed a high frequency of previous clinical events compatible with cardiogenic embolism; in a significant subgroup of patients, ASA appears to be the only source of embolism, as judged by TEE. Our data are consistent with the view that ASA is a risk factor for cardiogenic embolism, but thrombi attached to ASA as detected by TEE are apparently rare.
Key Words: aneurysm • embolism • echocardiography • stroke
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Introduction |
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An atrial septal aneurysm (ASA) is a rare but well-recognized cardiac abnormality of uncertain clinical significance.1 2 3 4 5 6 7 ASA has been reported as an unexpected finding during autopsy1 but may also be diagnosed in living patients by echocardiographic techniques.2 ASA formation can be secondary to interatrial pressure differences but may also be a primary malformation involving the region of the fossa ovalis or the entire septum.1 4 ASA may be an isolated abnormality but is often found in association with other structural cardiac abnormalities, eg, mitral valve prolapse8 9 or atrial septal defects.10
Several reports suggest a possible link between ASA and cardiogenic embolism in patients with otherwise unexplained ischemic stroke.4 11 12 13 14 15 16 Hanley and coworkers4 reported clinical events compatible with cardiogenic embolism in 16 (20%) of 80 consecutive patients with ASA; in 4 of these patients, ASA was the only apparent cardiovascular abnormality. Belkin and coworkers12 reported cerebrovascular events compatible with embolism in 10 (28%) of 36 patients with ASA. Using transesophageal echocardiography (TEE) for the detection of ASA, Schneider and coworkers14 observed cerebrovascular events in 12 (52%) of 23 consecutive patients with ASA and noted marked thickening of the atrial septum suggestive of thrombus formation in 9 of the 12 patients. Furthermore, Pearson and coworkers16 noted ASA more frequently in patients who were referred for echocardiographic evaluation of potential sources of embolism (20 of 133 patients; 15%) than in patients who were referred to the echocardiography laboratory for other reasons (12 of 277 patients; 4%).
In the present study, we reevaluated the clinical significance of ASA in a large series of patients. Patients with ASA were recruited from the echocardiography laboratory. The aims of the study were (1) to define morphological characteristics of ASA by use of TEE, (2) to define abnormalities associated with ASA and their incidence, and (3) to investigate whether morphological characteristics of ASA are different in patients with and without previous events compatible with cardiogenic embolism. The present study was not designed to establish ASA as a "novel" source of cardiogenic embolism.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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The centers contributing to this study were selected by the initiating institution (Hannover Medical School) between May 1989 and October 1993. Each of the 11 centers enrolled patients with an ASA detected by echocardiography. The following criteria had to be fulfilled: (1) transthoracic and transesophageal echocardiographic studies had to be performed within 24 hours of each other; (2) ASA was defined as a protrusion of the aneurysm of >10 mm beyond the plane of the atrial septum as measured by TEE (Fig 1
), (3)
echocardiographic images had to be of sufficient quality to allow
precise measurements of morphological characteristics of ASA, and (4)
detailed patient records had to be available. Patients with mitral
stenosis or mitral prosthesis or who had had any cardiothoracic surgery
involving the atrial septum were excluded from the study.
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The patient records were evaluated for history, in particular clinical
events compatible with arterial embolism, cardiac rhythm (ECG), and
history of arrhythmias. The diagnoses of events compatible with
cardiogenic embolism were based on clinical criteria (sudden onset of
symptoms, exclusion of significant [>30% stenosis] carotid artery
disease by Doppler sonography), and technical investigations
(nonhemorrhagic stroke established by computed tomography, peripheral
arterial occlusion established by angiography and/or surgery). The
videotapes were carefully selected by an experienced investigator from
each center. The following parameters were evaluated: length of the ASA
in the plane of the atrial septum (Fig 1
), maximal excursion or
protrusion of the ASA beyond the plane of the atrial septum (Fig
1),
direction of maximal protrusion (into the right or left atrium),
spontaneous oscillation of the ASA during normal cardiorespiratory
cycle, maximal extent of protrusion during oscillation, other
structural abnormalities associated with the atrial septum, presence of
patent foramen ovale (PFO) or atrial septal defect (ASD) (tested either
by color Doppler or contrast echocardiography, Fig 2),
presence of thrombi attached to the ASA, presence of valve
abnormalities, presence of other cardiac abnormalities that might be
potential sources of cardiogenic embolism including the spontaneous
echo-contrast phenomenon, aortic plaques, and intracardiac
thrombi.18 19 A "lone" ASA was defined as
an ASA in
a patient without any other cardiac abnormalities and without a history
of arrhythmias as judged by TEE, ECG, and the patient's records.
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The data were analyzed by univariate ANOVA. The values presented are mean±SD. A value of P<.05 was considered significant.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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A total of 195 patients met the inclusion criteria: 98 men and 97 women, with a mean age of 54.6±16.0 years (range, 18 to 85 years). The indications for the echocardiographic examinations were (n=number of patients): suspicion of cardiogenic embolism and/or intracardiac masses (n=90), congenital heart disease (n=19), valvular heart disease (n=16), infective endocarditis (n=15), aortic dissection (n=10), before cardioversion for atrial fibrillation (n=9), and miscellaneous (n=36).
At the time of the echocardiographic examination, 165 patients (84.6%) were in sinus rhythm, 28 (14.4%) were in atrial fibrillation, and 2 had a pacemaker. The majority of patients for whom detailed information was available had no history of arrhythmias (118 of 180 patients, 65.6%). Overall, atrial tachyarrhythmias were noted in 22.8% of the patients (41 of 180 patients). Among 44 patients with ASA as the only structural abnormality and without a history of coronary artery disease or hypertension, 7 (15.9%) had atrial tachyarrhythmias (atrial fibrillation).
Table 1 summarizes the morphological characteristics of
the ASA as determined by TEE. As judged by TEE, the ASA involved the
entire septum in 100 patients (51.3%) and was limited to the fossa
ovalis in 95 (48.7%). Overall, ASA bulged predominantly toward the
right atrium in 130 patients (66.7%) and toward the left atrium in 65
(33.3%). In 132 patients (67.7%), the septum showed spontaneous
oscillations (between the two atria) during a normal cardiorespiratory
cycle (Table 1).
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ASA was often associated with other cardiac abnormalities, in
particular atrial septal defect, PFO, and mitral valve prolapse (Table
2). In 62 patients (31.8%), ASA was an isolated
structural abnormality, as judged by TEE. In only 37 patients (18.9%)
was the ASA considered a "lone ASA," ie, patients were in sinus
rhythm and had no other cardiac abnormalities and no history of
hypertension or coronary artery disease. Intracardiac thrombi were
found by TEE in 18 patients; thrombi were located within the left
atrium or left atrial appendage in 15 patients and within the left
ventricular cavity in 1 patient after myocardial infarction. In the
remaining 2 patients, thrombotic material appeared to be attached to
the septal aneurysm. In 1 of these 2 patients, ASA involved the entire
septum, and thrombotic material appeared to be attached to the left
atrial side of the septum. In the other, ASA was confined to the fossa
ovalis and was associated with a small type II atrial septal defect; in
this patient, ASA bulged predominantly into the left atrium, and the
thrombotic material appeared to be attached to the right atrial side of
the septum.
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The region of the atrial septum could be clearly visualized by TEE in all patients, thereby allowing the diagnosis of ASA; in contrast, evidence for ASA was not detected by transthoracic echocardiography in 92 patients (47%). In addition, PFO and atrial septal defects were missed by transthoracic echocardiography in 64% and 19% of patients, respectively.
Patients' histories revealed no clinical evidence of cardiogenic
embolism in 108 patients (56%). Forty-three patients (22%) had
suffered a nonhemorrhagic stroke, 24 (12%) transient ischemic attacks,
14 (7%) peripheral arterial embolism, 4 (2%) pulmonary embolism, and
2 (1%) both stroke and peripheral arterial embolism. Clinical events
compatible with embolism had occurred on average 44±78 days (range, 1
to 450 days) before the echocardiographic examination. Table 3
compares several clinical and echocardiographic
characteristics of patients with and without clinical events
potentially due to cardiogenic embolism. The two groups did not differ
with respect to cardiac rhythm at the time of the echocardiographic
examination. Interatrial shunting and intracardiac thrombi were found
more frequently in patients with possible cardiogenic embolism. The two
groups did not differ with respect to several ASA characteristics,
including the predominant side of bulging (right or left atrium),
length of ASA, maximal extent of protrusion, and incidence of
spontaneous oscillation of the ASA (Table 3). It is interesting
to
note, however, that the majority of patients with lone ASA had
experienced a clinical event compatible with arterial embolism (21 of
37 patients, 56.7%) before the echocardiographic examination.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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An aneurysm of the interatrial septum is an infrequent finding in adult patients. ASA formation may be secondary to raised interatrial pressure gradients, producing a bulging septal shift toward the low-pressure side1 ; however, it has been also found in patients with normal atrial pressures,3 suggesting a primary (congenital?) malformation.
Definition Criteria for ASA
The cutoff point between a
slightly redundant atrial septum and an
ASA is somewhat arbitrary. In the present study, we used cutoff
criteria similar to those reported in an autopsy study by Silver and
Dorsey,1 ie, a protrusion of the aneurysm >10 mm beyond
the plane of the atrial septum into either the right or left atrium
(Fig 1). We excluded patients with previous cardiac surgery and
those
with mitral stenosis so as to select predominantly those patients with
a primary ASA. These criteria are slightly different from those used in
previous echocardiographic studies. In the largest series of patients
with ASA diagnosed by transthoracic echocardiography, Hanley and
coworkers4 considered the atrial septum to be aneurysmal
when a dilated portion protruded at least 15 mm beyond the plane of the
atrial septum or when the atrial septum showed phasic excursions during
the cardiorespiratory cycle 
15 mm with the base of the aneurysm 15
mm. In the largest series of cases of ASA diagnosed by TEE, Pearson and
coworkers16 considered a septum aneurysmal when it had an
excursion >10 mm into either the left or right atrium or a sum of the
total excursion into the left or right atrium >10 mm, with a base
width 15 mm. Other authors11 20 21
define ASA as a thin
localized outpouching of the middle portion of the atrial septum, but
not the entire septum, protruding at least 10 mm outside the plane of
the atrial septum. Because a "gold standard" is lacking for
definition of true ASA, one definition appears as arbitrary as the
other. In the present multicenter study, we used a simple and
relatively less restrictive definition to include a large number of
patients with different types of atrial septal redundancy.
Comparison of Transthoracic and Transesophageal
Echocardiography
The transesophageal approach allows almost ideal
imaging of the
interatrial septum. Several authors reported a more detailed and
superior characterization of the atrial septum morphology and pathology
by transesophageal compared with transthoracic
echocardiography.22 23 24 In the present
study, ASA as
defined by TEE was missed by surface (transthoracic) echocardiography
in almost half (47%) of the patients. Thus, the sensitivity for the
detection of ASA appears to be greatly enhanced with the use of TEE.
These results are in agreement with previous reports using both
transthoracic and transesophageal echocardiography. In the first report
on both techniques, ASA was demonstrated only by TEE in 6 of 7
patients.5 In a series of 23 patients communicated by
Schneider et al,14 the surface echocardiogram missed an
ASA in 3 patients. In a series of 32 patients reported by Pearson et
al,16 transthoracic echocardiography missed an ASA in the
majority (62.5%) of patients. It should be mentioned again, however,
that a gold standard is lacking in the detection of ASA. Thus, the
discrepancy between transthoracic and transesophageal echocardiography
may be explained not only by false-negative transthoracic
echocardiographic findings but also by false-positive TEE findings.
Arrhythmias Associated With ASA
Several authors have
suggested an association between ASA and
atrial tachyarrhythmias.25 26 Hanley and
coworkers4 observed atrial tachyarrhythmias in 20 of 80
patients (25%). Using Holter monitoring, Schneider and
coworkers27 reported recently in a preliminary
communication a prevalence of atrial tachyarrhythmias in 26 (52%) of
50 consecutive patients with ASA. In the present study, ambulatory
Holter monitoring was not performed systematically. Information
(patient's history, ECG records) concerning cardiac arrhythmias was
available in 180 patients. In the majority of patients (65%), no
significant arrhythmias were noted. Twenty-eight of 195 patients
(14.4%) were in atrial fibrillation at the time of the
echocardiographic examination. It is unknown whether the redundancy of
the atrial septum itself or ASA-associated structural defects are
related to the pathogenesis of atrial arrhythmias. Overall, a
relatively high prevalence of atrial tachyarrhythmias was noted in the
present study (47 of 195 patients; 24%). This prevalence of atrial
arrhythmias was somewhat less but still relatively high (6 of 37
patients; 16%) in patients without other detectable structural
abnormalities and without a known history of hypertension or coronary
artery disease. This relatively high prevalence of atrial
tachyarrhythmias in patients with ASA cannot as yet be explained and
may be biased by the patient selection criteria. Further studies are
necessary to clarify whether ASA is related to the pathogenesis of
these arrhythmias.
Cardiac Abnormalities Associated With ASA
Several other
cardiac (and noncardiac) abnormalities may be
associated with ASA. As noted in previous
reports,4 10 15
ASA is often associated with other atrial septal defects, in particular
ASD type II and PFO. At autopsy, Silver and Dorsey1 found
a PFO in 8 of 16 patients (50%) with ASA, including 2 patients who
also had a small ASD due to fenestration of the septum primum. Hanley
and coworkers4 noted an ASD in 24 of 49 patients (49%)
examined for atrial shunting; they observed an ASD in all 12 patients
in whom the aneurysm involved the entire septum and in 6 of 8 patients
(75%) in whom an oscillating aneurysm involved the fossa ovalis. Using
TEE, Schneider and coworkers14 demonstrated atrial
shunting in 17 of 22 patients (77%) with ASA. Zabalgoitia-Reyes et
al15 found a small ASD in 1 of 20 patients (5%) and,
using contrast TEE, a PFO in 17 patients (85%) with ASA. In the
present study, interatrial shunting was noted in 106 of 195
patients (54.4%); this shunting was due to a type II ASD in 38
patients, a PFO in 65, and a sinus venosus defect in 3. Interatrial
shunting was noted with a similar frequency in both ASA involving the
fossa ovalis (52 of 95 patients) and involving the entire septum (54 of
100 patients). Whereas a sinus venosus defect or a large ASD can be
easily diagnosed by TEE,22 23 28
differentiation between a
small ASD and PFO may be somewhat arbitrary in selected cases. In
particular, it may be difficult to visualize a small structural defect,
allowing the ASD diagnosis in patients with a highly mobile ASA.
Therefore, the differentiation between PFO and a small ASD was based on
color Doppler TEE demonstrating a continuous interatrial shunting
throughout the cardiac cycle in patients with ASD or an intermittent
right-to-left shunting provoked by Valsalva maneuver in patients with
PFO. These difficulties in a precise anatomic classification of
interatrial shunting, in particular in patients with ASA, may explain
the variation in the frequency distribution of different types of
atrial septal defects in previous
studies.4 14 15
A second type of cardiac abnormality often associated with ASA is mitral valve prolapse.9 21 It has been suggested that the redundancy of the atrial septum and the mitral (and/or tricuspid) valve may be secondary to a similar inherent deficiency in the connective tissue.8 In the present study, a mitral valve prolapse was noted in 20.5% and a tricuspid valve prolapse in 7.2% of the patients. It is interesting to note that 2 of our patients had Marfan's syndrome, 2 additional patients had an aortic dissection, and 1 patient had a sinus of Valsalva aneurysm, supporting the concept of an inherent connective tissue abnormality as a possible cause of ASA.
ASA as a Possible Source of Arterial Embolism
Several authors
have suggested that ASA (isolated or in
combination with other defects) may cause arterial
embolism.11 12 13 14 16
This suggestion is based on clinical
studies demonstrating a statistical association between ASA and
previous ischemic cerebral and/or peripheral embolic events. In fact,
the incidence of clinical events compatible with cardiogenic embolism
appears to be remarkably high in patients with ASA, ranging from 20%
to
52%.4 11 12 14 15
In the present study, 87 of 195
patients (44.6%) with ASA had experienced clinical events compatible
with cardiogenic embolism before the echocardiographic examination.
This high percentage of possible cardiogenic embolism in patients with
ASA is certainly biased by the patient selection criteria.
Nevertheless, the association between ASA and arterial embolism merits
some consideration.
It has been speculated that ASA is a direct source
of thrombus
formation.14 This is supported by anecdotal findings
demonstrating thrombotic material within the aneurysmal sac in patients
at autopsy1 or cardiac surgery.29 In
addition, thrombotic material related to an ASA has occasionally been
visualized by TEE. Schneider et al14 reported a thrombus
in 2 of 23 consecutive patients with ASA; in 1, thrombotic material
appeared to override a PFO, suggesting paradoxical embolism; in the
second, a thrombus was attached to the left atrial side of the
aneurysm. In addition, these authors noted thickening of the atrial
septum in 9 of 12 patients with cerebrovascular events. Pearson et
al16 reported 1 patient (of 32) with a thrombus on the
right atrial side of the aneurysm. In the present study, a mobile
mass suggestive of thrombus formation was visualized by TEE in only 2
of 195 patients. Echocardiographic differentiation between ASA-attached
thrombi and artifacts created by the mobile and bulging part of the
fossa ovalis may be difficult in some patients; a tangential scan
through a mobile ASA may create the false impression of a thrombus (Fig
3). These difficulties in reliably differentiating
between true thrombi and artifact may explain the differences in the
reported incidence of thrombi attached to the ASA. Whether or not the
echo densities that appear attached to an ASA are truly clots, the
overall low incidence would suggest that an ASA on its own is unlikely
to be a common site of thrombus formation. It should be noted, however,
that TEE has a certain limit of resolution for thrombus detection. This
resolution limit has not as yet been defined and may be influenced by
several factors, such as density of the thrombus and its relation to
surrounding blood and tissue. Thus, this study does not exclude the
possibility that small (micro) thrombi are attached to or at least
generated in the region of ASA, subsequently causing cardiogenic
embolism.
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It appears from this (retrospective) analysis that ASA is a risk factor associated with previously occurring events compatible with cardiogenic embolism. This association is certainly biased by the patient enrollment criteria (90 of the 195 patients underwent TEE for suspected cardiogenic embolism). Thus, the present study cannot establish a scientifically proven link between ASA and cardiogenic embolism. Furthermore, it is unclear whether ASA per se could be a risk factor or whether the accompanying cardiac abnormalities are the major determinant for this association. In fact, ASA is often associated with other cardiac abnormalities that are independently recognized causes of cardiogenic embolism, in particular PFO,24 30 31 and, to a lesser extent, mitral valve prolapse.32 33 In the 87 patients with possible cardiogenic embolism, ASA was an isolated finding in 21 patients (24.1%) but was associated with other cardiac abnormalities potentially related to embolism in the remaining 66 patients (75.9%). The present study shows that lone ASA is associated with prior events compatible with cardiogenic embolism, and it appears that this association is more significant when ASA is accompanied by other cardiac abnormalities, in particular those causing interatrial shunting. It can only be speculated that this association with previous embolic events also implies a future risk for cardiogenic embolism. However, to define ASA as a marker of embolic risk, prospective studies with the enrollment of appropriate control groups will be necessary.
A major finding of the present study is that
morphological
characteristics of ASA based on TEE are not helpful for identifying a
subgroup of patients at increased risk of embolism. As shown in Table
3, patients with previous events compatible with cardiogenic
embolism had a higher incidence of left atrial thrombi,
spontaneous echo contrast phenomenon, and PFO compared with patients
without those events; however, patients with and without emboli did not
differ with respect to ASA characteristics such as extent of ASA,
length of ASA, maximal extent of bulging, and incidence of
oscillations. This negative finding indirectly supports the view that
ASA per se is not a direct source of cardiogenic embolism.
To exclude
the possibility that the criteria of ASA definition in the
present study may have caused this negative result concerning the
association of morphological characteristics and incidence of potential
arterial embolism, we reanalyzed our data using the slightly different
criteria proposed by Hanley and coworkers4 (for criteria,
see above). According to these criteria, 138 patients could be included
in the reanalysis. As proposed by Hanley and coworkers, ASAs were
separated into two groups: those in which the aneurysm involved only
the region of the fossa ovalis and those in which the entire atrial
septum was involved. The fossa ovalis ASA type was subdivided according
to the direction of maximal excursion or protrusion during the
cardiorespiratory cycle: type 1, into the right atrium and type 2, into
the left atrium. Type 1 was further subdivided into groups A and B on
the basis of the maximal extent of phasic oscillations of the
aneurysmal membrane occurring during the cardiorespiratory cycle: A,
oscillations <0.5 cm and B, oscillations 0.5 cm. Table 4
summarizes the incidence of possible arterial embolism
in patients classified according to the definition criteria proposed by
Hanley and coworkers. The incidence of possible cardiogenic
embolism appears to be almost equal for all subtypes.
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Although the
overall prevalence of clinical events compatible with
cardiogenic embolism appears to be high in patients with ASA, this
issue should not be overestimated. In recent studies using
TEE,17 34 35 36 37 38 39 40 41 42 43 44 45 46
ASA was found and defined as a possible
source of embolism in 173 of 2037 patients (8.4%) with previous
ischemic stroke and/or peripheral arterial embolism (Table 5).
Since more than half of the patients with ASA had
associated cardiac abnormalities that also could have caused
cardiogenic embolism, the importance of ASA as an independent risk
factor for arterial embolism appears to be questionable in unselected
patients with suspected or proven arterial embolism.
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Limitations and Clinical Implications
The present study has
limitations. First of all, patient
selection was strongly biased by the TEE referral pattern. Thus, the
study did not allow the assessment of the true prevalence of ASA in
unselected patients, the true frequency of associated abnormalities,
and more important, the true prevalence of cerebral ischemia or
peripheral embolism in patients with ASA. Because of a multicenter
design, the same diligence in the echocardiographic examination and
data collection cannot be ensured for all participating centers. In
addition, the diagnosis "cardiogenic embolism" is not a definite
diagnosis in most cases, in particular in patients with cerebral
ischemia. On the one hand, it is difficult to prove a thromboembolic
occlusion of cerebral arteries without invasive techniques; on the
other hand, it is difficult if not impossible to prove a causal
relation between cardiac abnormalities and ischemic stroke, even in the
presence of obvious sources of cardiogenic embolism, eg, intracardiac
thrombi. Furthermore, although significant narrowing of the carotid
arteries was excluded by Doppler sonography, mobile or friable debris
serving as a nidus for cerebral embolism cannot be excluded in selected
patients. Consequently, this study does not allow us to draw
conclusions regarding the pathogenic mechanism of embolism in patients
with ASA. Nevertheless, the data are consistent with the view that the
presence of ASA may be a possible risk factor for cardiogenic embolism.
In summary, although clinical implications are as yet undefined, TEE is
helpful to characterize different types of ASA and to allow a careful
search for additional sources of embolism, in particular for associated
interatrial shunting. The presence of ASA with interatrial shunting may
support the concept of cardiogenic embolism due to paradoxical
embolism. Other morphological characteristics of ASA (length, bulging,
oscillation) appear not to be important for identifying patients at
risk for arterial embolism.
Received October 17, 1994; revision received November 30, 1994; accepted December 18, 1994.
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References |
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