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Cerebrovascular Embolic Events and Atrial Septal Aneurysm: A Clinical and Echocardiographic Correlation

Olivares-Reyes Alexander; Gonzalez Javier; Al-Kamme Ahmad

Cardiology Department, The Brooklyn Hospital Center
Brooklyn, New York, USA.

Abstract
Introduction
Objectives
Material and Methods
Results
Discussion
Conclusions
References

Abstract
Introduction: Several reports suggest that cerebrovascular embolic events (CVEE) may be secondary to cardioembolic origin in approximately 30%, while atrial septal aneurysm (ASA) had been associated to stroke in as high as 62%.
Objectives: The aim of this study is to evaluate the ASA as a risk factor or CVEE.
Material and Methods: we analyzed the paper of ASA as well as other cardiovascular risk factors in the potential pathogenesis of CVEE. For this purpose we evaluated clinical and echocardiographically, 1 1 7 consecutive patients (pts) with ASA and CVEE. All patients had an adequate 2-D echocardiogram. Ninety pts also had a transesophageal echocardiogram, and in 80, saline contrast study was performed. All had a complete neurological evaluation including MRI , CT-Scan, and carotid studies.
Results: Ninety-four pts (80%) had stroke, 23 (20%) had transit ischemic attack (TIA), 24 (21 %) had CVA and TIA concomitantly, 68 (58%) were women, mean age was 69.7 yr. Patients ò 50 yr. represented 91 % (1 07 pts), 99 (85%) had HTN, 93 (79%) had valvular abnormality, 38 (32%) had diabetes mellitus, 37 (32%) had CAD, 32 (27%) had pulmonary HTN, 17 (15%) had heart failure, 15 (13%) had supraventricular tachycardia (SVT), and 9 (8%) had syncope. Only 36 pts (31 %) had ASA as a solo cause of CVEE, while 81 pts (69%) had more than one. Among them, calcified aortic sclerosis 52 %, mitral valve, abnormality 45%, LA enlargement 25%, SVT 13%, LV dysfunction 6%, and interatrial shunt 3%. About the type of ASA, 61 % were mobile, left atrial bulging ASA occurs in 72% vs 28% of right atrial bulging.
Conclusions: The great majority of patients with CVEE had multiple potential CSE. However ASA , per se, can be a solo cause of CSE in about one third of patients with CVEE. Potential CSE seems to have a synergistic effect, at least in the elderly population.

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Introduction:

Several reports suggest that cerebrovascular embolic events (CVEE) may be secondary to cardioembolic origin in approximately 30%, while atrial septal aneurysm (ASA) had been associated to stroke in as high as 62%. The main clinical interest of ASA is its embolic potential. The majority of publications about ASA in the last 10 years have been related to cardiac and peripheral arterial embolism, as well as its association with unexplained stroke. On average, someone in the USA suffers a stroke every 53 seconds; every 3.3 minutes someone dies of one. Stroke is the third most common cause of death in the USA. Each year, 500,000 Americans have a stroke. The annual cost of stroke-related health care is estimated to be about 13.5 billion dollars.

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Objectives:

The aim of this study is to evaluate clinical and echocardiographically the atrial septal aneurysm as a risk factor for cerebrovascular embolic events.

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Material and Methods:

We analyzed the role of ASA as well as other cardiovascular risk factors in the potential pathogenesis of CVEE. For this purpose we evaluated clinical and echocardiographically, 117 consecutive adult patients (pts) which fulfilled the criteria of ASA and cerebrovascular event (CVE). The diagnosis of ASA was made by TTE, TEE or both. All patients had an adequate 2-D echocardiogram (Echo), as well as a complete neurological evaluation including MRI, CT-Scan, and carotid study. All of them were referred to evaluate cardiac source of embolism (CSE).
Statistical analysis. The data were analyzed with Student’s t test and chi-square test. A p value <0.05 was considered significant.

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Results:

From a total of 117 patients with ASA and CVE, 94 (80%) had stroke, 23 (20%) had transient ischemic attack (TIA) , 24 pts (21%) with stroke also had TIA concomitantly. We found 68 women (58%) compared to 49 men (42%), with a ratio of 1.4 : 1. The mean age of this group was 70 years .Patients younger than 50 yr represented a low 9%, while those over 50 yr constituted the majority with 91% (p <0.05). The mean age by gender was 76 yr for women against 64 yr for men. (Table 1) We subdivided these patients with ASA in a group with CVA and another group with TIA, and compared by gender and age. (Table 2). Type of ASA were analyzed utilizing our previously published classification. "Mobile" ASA (types 3RL, 4LR, and type-5) was found in 71 pts (61%), while "fixed" ASA (types 1R and 2L) in 46 pts (39%). Regarding bulging predominance, left bulging ASA (types 2L and 4LR) we found 77 pts (72%), while right bulging ASA (types 1R and 3RL) were 30 pts (28%), p <0.05. (Figure 1). Ten patients from Type-5 ASA were excluded because this type did not have a predominant bulging. Clinical variables associated in these patients were as follow: 99 patients (85%) had HTN, 93 (79%) had some kind of valvular disease, 38 (32%) were diabetics, 37 (32%) had CAD, 32 (27%) had pulmonary hypertension, 17 (15%) had heart failure, 15 (13%) had SVT, (Figure 2) 9 (8%) had history of at least one episode of syncope. Only 36 patients (31%) had ASA as a "solo" possible cause of cardiac source of embolism, while 81 pts (69%) had multiple causes of CSE, p <0.05.

Table 1

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Table 2

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Among the possible cause of CSE, mitral valve pathology (e.g. regurgitation, stenosis, prolapse, calcification, vegetation, etc.) was found in 62 pts (53%), calcific aortic sclerosis in 53 pts (45%), mitral valve calcification in 38 pts (32%), LA enlargement in 29 pts (25%), atrial fibrillation in 14 pts (12%), mitral valve prolapse in 10 pts (9%), and interatrial shunt in 7 pts (6%). Table 3 shows all possible causes of CSE found in our 117 patients.
When we analyzed the potential causes of CSE among our 117 patients, we found that 36 (31%) had only one risk factor (RF) [ASA], 19 (16%) had 2-RF, 33 (28%) had 3-RF, 17 (15%) had 4-RF, 7 (6%) had 5-RF, 2 (2%) had 6-RF, and 3 (3%) had 7-RF. Multiple risk factors for CSE represented a 69% of the total, vs 31% of single risk factor, p <0.05. (Figure 3).

Table 3

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Discussion:

Currently, the association between ASA and CVEE is well accepted although its exact mechanism remains unclear. There are few case reports of paradoxical embolism which is one of the theories for ASA thrombi formation, especially when a PFO is demonstrated in the same patient, Figure 4. In a TEE study, ASA was the second cause of CSE only after intracardiac thrombus. In the present study, ASA alone occurred in about one third of all cases of CSE and possible cause of CVEE. In patients with ASA, the prevalence of clinical CVE range from 20% to 52%, contrasting with 8.4% found in a multicenter study, whereas only 173 of 2,037 patients with previous CVE, had ASA as a possible CSE. We found 23% of patients with CVE (CVA or TIA) and ASA. Regarding the mobility of ASA and CVEE, a French multicenter study using TEE found a significantly higher number of patients with systemic embolic events. We found here that "mobile" ASA were more common 61% vs 39% of "fixed" ASA.
Concerning predominance of the ASA bulging, left side bulging types of ASA were significantly higher than right side bulging types of ASA (72% vs 28%, p < 0.05). The size of the ASA seems to be another risk factor for stroke, as well as the association of possible causes of cardio-embolism such as patients with ASA with PFO, ASD, MVP, etc. Interatrial shunts like ASD or PFO and ASA showed a very high association with stroke, which is as high as 90% of cases.

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Fig.4: A) This is a patient with ASA type 2L and stroke.The TEE
shows bubbles in both atria making evident the presence of a PFO.

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Fig.4: B) This is a patient with ASA and CVEE. The image is a TTE
parasternal short axis view at the level of the great vessels. A big
thrumbus is seen at the left atrial lateral wall and appendage (dotted
area). AO= aorta, IAS= inter atrial septum, LA= left  atrium, RA= right
atrium, RVOT= right ventricular outflow tract.

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Conclusions:

From this study we can conclude: 1) The majority of patients with cerebrovascular embolic events had multiple potential cardiac source of embolism, 2) Atrial septal aneurysm, per se, can be a "solo" cause of cardiac source of embolism in about one third of patients with cerebrovascular embolic events, 3) Potential cardiac source of embolism seems to have a synergistic effect, at least in the elderly population.

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References

1. Olivares-Reyes A, et al. Atrial Septal Aneurysm: A new classification in 205 adults. J Am Soc Echocardiogr 1997;10:644-56.
2. Belkin RN, et al. Atrial septal aneurysm: association with cerebrovascular and peripheral embolic events. Stroke 1987;18:856-62.
3. Zabalgoitia-Reyes M, et al. A possible mechanism for neurologic ischemic events in patients with atrial septal aneurysm. Am J Cardiol 1990; 66:761-64.
4. Pearson AC, et al. Atrial septal aneurysm and stroke: a transesophageal echocardiographic study. J Am Coll Cardiol 1991;18:1223-29.
5. Mas JL, et al. Recurrent cerebrovascular events in patients with patent foramen ovale, atrial septal aneurysm, or both and cryptogenic stroke or transient ischemic attack. Am Heart J 1995;130:1083-88.
6. Mugge A, et al. Atrial septal aneurysm in adult patients: a multicenter study using transthoracic and transesophageal echocardiography. Circulation 1995;19:2785-92.
7. DiPasquale G, et al. Cardioembolic stroke from atrial septal aneurysm. Stroke 1988;19:640-43.
8. Agmon,Y, et al. Frequency of atrial septal aneurysms in patients with cerebral ischemic events. Circulation 1999;99:1942-44.
9. The second report of the Cerebral Embolism Task Force. Cardiogenic brain embolism. Arch Neurol 1989;46:727-43.
10. Cujec B, et al. Transesophageal echocardiography in the detection of potential cardiac sources of embolism in stroke patients. Stroke 1991;22:727-33.
11. Ofelli E, et al. Transesophageal echocardiography in the evaluation of cardiac source of embolus and intracardiac masses. J Invas Cardiol 1992;4:349-58.
12. Husain AM, et al. Transesophageal echocardiography in diagnosing cardioembolic stroke. Clin Cardiol 1995;18:705-08.

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Questions, contributions and commentaries to the Authors: send an e-mail message (up to 15 lines, without attachments) to echo-pcvc@pcvc.sminter.com.ar , written either in English, Spanish, or Portuguese.

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Acknowledgement: We acknowledge the secretarial assistance of JoAnn Natale and Monica Gonzalez.


© CETIFAC
Bioengineering
UNER
Update
Dic/05/1999


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