(Circulation. 1999;99:1942-1944.)
© 1999 American Heart Association, Inc.
Brief Rapid Communication |
Frequency of Atrial Septal Aneurysms in Patients With Cerebral Ischemic Events
Presented in part at the 47th Annual Scientific Session of the American College of Cardiology, Atlanta, Ga, March 29–April 1, 1998.
From the Division of Cardiovascular Diseases and Internal Medicine (Y.A., B.K.K., F.G., J.B.S.) and Departments of Neurology (I.M., D.O.W.) and Health Sciences Research (J.P.W., J.D.S., W.M.O., J.L.C., D.O.W.), Mayo Clinic and Mayo Foundation, Rochester, Minn.
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Abstract |
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Background—Atrial septal aneurysm (ASA) is a putative risk factor for cardioembolism. However, the frequency of ASA in the general population has not been adequately determined. Therefore, the frequency in patients with cerebral ischemic events, compared with the frequency in the general population, is poorly defined. We sought to determine the frequency of ASA in the general population and to compare the frequency of ASA in patients with cerebral ischemic events with the frequency in the general population.
Methods and Results—The frequency of ASA in the population was determined in 363 subjects, a sample of the participants in the Stroke Prevention: Assessment of Risk in a Community study (control subjects), and was compared with the frequency in 355 age- and sex-matched patients undergoing transesophageal echocardiography in search of a cardiac source of embolism after a focal cerebral ischemic event. The proportion with ASA was 7.9% in patients versus 2.2% in control subjects (P=0.002; odds ratio of ASA, 3.65; 95% CI, 1.64 to 8.13, in patients versus control subjects). Patent foramen ovale (PFO) was detected with contrast injections in 56% of subjects with ASA. The presence of ASA predicted the presence of PFO (odds ratio of PFO, 4.57; 95% CI, 2.18 to 9.57, in subjects with versus those without ASA). In 86% of subjects with ASA and cerebral ischemia, transesophageal echocardiography did not detect an alternative source of cardioembolism other than an associated PFO.
Conclusions—The prevalence of ASA based on this population-based study is 2.2%. The frequency of ASA is relatively higher in patients evaluated with transesophageal echocardiography after a cerebral ischemic event. ASA is frequently associated with PFO, suggesting paradoxical embolism as a mechanism of cardioembolism. In patients with cerebral ischemia and ASA, ASA (with or without PFO) commonly is the only potential cardioembolic source detected with transesophageal echocardiography.
Key Words: aneurysm • cerebral ischemia • echocardiography
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Introduction |
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An association between atrial septal aneurysm (ASA) and focal cerebral ischemic events (stroke and transient ischemic attack) has been suggested.1 2 Nevertheless, the role of ASA as a risk factor for cerebral ischemia is poorly defined. This is the result of variable echocardiographic definitions of ASA3 and the lack of adequate nonselected control groups in previously published studies. Specifically, the frequency of ASA in a large nonselected population has not been determined. Therefore, the relative frequency of ASA in patients with cerebral ischemic events is unknown.
The Stroke Prevention: Assessment of Risk in a Community (SPARC) study is a community-based study evaluating the prevalence of potential risk factors for stroke in the population. The purpose of the present study was to compare the frequency of ASA in the SPARC population, assessed with transesophageal echocardiography (TEE), with its frequency in a group of patients undergoing TEE after a cerebral ischemic event. An association between ASA and cerebral ischemia was established. Possible mechanisms of cardioembolism are considered.
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Methods |
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Study Populations
SPARC Study
The SPARC study was designed to estimate the prevalence of potential risk factors for cerebral ischemia in the population. The resources of the Rochester Epidemiology Project were used to enumerate the Olmsted County population
45
years old.4 The SPARC sampling process was designed to
randomly select 580 subjects, stratified by sex and 5 age subgroups (45
to 54 years, 55 to 64 years, 65 to 74 years, 75 to 84 years, 85
years). Of the 1475 Olmsted County residents selected, 230 were
ineligible according to predefined exclusion criteria (terminal
illness, dementia, significant functional disability, or esophageal
disease precluding TEE) and 609 refused to participate in the study. In
all, 636 subjects participated in a home interview, 48 of whom dropped
out of the study. The final SPARC study sample consisted of 588
subjects (47% of those eligible) who were evaluated with TEE, carotid
ultrasonography, and ambulatory blood pressure monitoring. TEE was
performed successfully in 581 of the SPARC participants.
Control Group
The control group of the present study consisted of 363
subjects randomly selected for review from the SPARC TEE database.
Patient Group
The patient group consisted of 355 patients in whom TEE
was performed in search of an embolic source after a focal cerebral
ischemic event (stroke or transient ischemic attack)
clinically compatible with cerebral embolism. These patients were
identified through the Mayo Clinic Echocardiography
Laboratory computerized database and were matched with the control
group by age and sex.
Transesophageal Echocardiography
All TEE studies (control and patient groups) were
performed during the same 2-year period (June 1993 to August
1995). TEE was performed according to standard practice
guidelines. Briefly, esophageal intubation was performed with the
patient in the fasting state and in the left lateral decubitus
position, after premedication with topical anesthesia
(lidocaine) and sedation (intravenous midazolam and
meperidine, as clinically indicated). Commercially available
ultrasonographic instruments (Acuson XP-128 equipped with a biplane
5-MHz transesophageal probe and Hewlett Packard Sonos
1500/2500 with an OmniPlane probe) were used for cardiac
imaging. The heart and thoracic aorta were scanned for the presence of
potential embolic sources.2 The interatrial septum (IAS)
was viewed primarily in the transverse midesophageal 4-chamber view and
the longitudinal biatrial/bicaval view.
Echocardiographic Definitions
Atrial Septal Aneurysm
ASA was defined according to criteria previously published by
Hanley et al5 : (1) diameter of the base of the
aneurysmatic portion of the IAS measuring 15 mm and
either (2) protrusion of the IAS, or part of it, 15 mm beyond
the plane of the IAS or (3) phasic excursion of the IAS during the
cardiorespiratory cycle 15 mm in total amplitude (Figure 1
).
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Patent Foramen Ovale
A patent foramen ovale (PFO) was defined as a right-to-left
interatrial shunt diagnosed by intravenous injections of
agitated saline with the patient at rest and with
provocative maneuvers (cough or release of Valsalva or
both).
For the present study, all TEEs were reviewed systematically by an observer blinded to the initial diagnoses, with offline measurements of ASA dimensions. Any discrepancies between the initial and review diagnoses were settled by a third observer blinded to all previous diagnostic data.
Statistical Analysis
The frequency of ASA in each group and the frequency of PFO
among those with or without ASA were estimated and studied by
multivariate logistic models. An estimate of the ratio
of the odds of ASA among the patients to that among the control
subjects and associated 95% CI, adjusted for age and sex, was obtained
from the multivariate logistic model. Similarly, the
ratio of the odds of PFO among those with ASA to the odds among those
without ASA with associated 95% CI, adjusted for group, age, and sex,
was also estimated from a multivariate logistic model.
If the CIs failed to include the integer 1, there was a significant
association (P
0.05).
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Results |
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Prevalence of ASAs
The proportions with ASA in the patient and control groups and in the various age subgroups are shown in Figure 2
. Overall, 7.9% of the patient group
(28 of 355 patients) and 2.2% of the control group (8 of 363
subjects) had ASA (P=0.002). The odds of ASA were 3.65
greater (95% CI, 1.64 to 8.13) in patients than in control subjects
after adjustment for minor age and sex differences between study
groups.
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Additional Cardiac Sources of Embolism
Right-to-left interatrial shunting through a PFO was detected in
56% of subjects with ASA. The presence of ASA was a predictor of the
presence of PFO. The odds of PFO were 4.57 greater (95% CI, 2.18 to
9.57) in subjects with ASA than in those without ASA. Among subjects
with ASA, nearly the same proportions of patients and control subjects
had PFO (P=0.70). TEE did not identify thrombi in any of the
ASAs. Alternative potential cardiac or aortic sources (or both) of
embolism in patients with ASA are presented in the
Table. Importantly, in 24 of the 28
patients with ASA (86%), no alternative cardiac source of embolism was
identified.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The present study demonstrated a significantly higher proportion of ASA in patients referred for TEE after a cerebral ischemic event than is present in the general population. This finding suggests that ASA is a risk factor for cerebral ischemia. ASA is frequently associated with right-to-left interatrial shunting. Therefore, paradoxical embolism is a probable mechanism of cardioembolism in a large subgroup of patients with ASA.
Frequency of ASA
The rate of ASA detection with
echocardiography varies from 0.22% in consecutive
transthoracic studies5 to significantly higher
rates by TEE, the diagnostic technique of
choice.6 The frequency of ASA is highly variable among
TEE studies, reflecting differences in study populations as well as in
ASA definition.3 Although any cutoff in ASA definition is
arbitrary, the 15-mm cutoff adopted in the present study provides
relatively high specificity for ASA diagnosis. According to this
definition, the proportion of ASA in the general population is low
(2.2%) and similar to a 1% proportion noted in a large autopsy
series.7 This figure is lower than those of smaller
population-based studies, which reported frequencies of 4.5% (no
quantitative definition of ASA)8 and 13% (15-mm ASA
definition).9
ASA and Cerebral Ischemia
A possible relationship between ASA and cerebral ischemia
was suggested initially by retrospective observations of the high
frequency of preceding cerebral ischemic events in patients
with an echocardiographic diagnosis of
ASA.10 This was confirmed subsequently in 2 multicenter
studies.11 12 In addition, studies comparing the
proportion of ASA in patients with cerebral ischemia with its
proportion in those undergoing TEE for miscellaneous clinical
indications have found a relatively high prevalence of ASA in
association with cerebral ischemia.13 However, the
control groups of such studies were highly prone to selection bias. Our
study allowed an estimation of the relative frequency of ASA in
patients with cerebral ischemia in comparison with a sample of
the general population undergoing TEE.
Right-to-left shunting through a PFO (permitting paradoxical embolism),11 thrombus formation in the ASA,1 associated mitral valve prolapse,14 and supraventricular arrhythmias1 are the potential mechanisms of cardioembolism associated with ASA. Our data support only the first mechanism, although undiagnosed transient atrial arrhythmias as well as small or rapidly resolving thrombi in ASAs cannot be excluded.
Clinical Implications
Clinical follow-up data have suggested that ASA is associated with
an increased risk of stroke recurrence.15 However,
the optimal therapeutic regimen for secondary prevention and possibly
primary prevention of stroke in subjects with ASA remains to be
determined.
In summary, our study estimated the frequency of ASA in the general population, confirmed an association between ASA and cerebral ischemic events, and suggested that paradoxical embolism is a mechanism of cardioembolic stroke in patients with ASA.
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Acknowledgments |
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This study was supported in part by a grant from the National Institute of Neurological Disorders and Stroke, National Institutes of Health (NS-06663).
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Footnotes |
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Reprint requests to Bijoy K. Khandheria, MD, Mayo Clinic, 200 First St SW, Rochester, MN 55905.
Received December 31, 1998; revision received February 18, 1999; accepted February 22, 1999.
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