Ann Thorac Surg 2001;71:1672-1673
© 2001 The Society of Thoracic Surgeons
Case report
Three-year follow-up of an atrial septal aneurysm
Tadashi Shinohara, MDa,
Tamizo Kimura, MDb,
Hiroshi Yoshizu, MDb,
Fumitaka Ohsuzu, MDa
a Department of Internal Medicine, National Defense Medical College, Saitama, Japan
b Department of Surgery, National Defense Medical College, Saitama, Japan
Accepted for publication June 6, 2000.
Address reprint requests to Dr Shinohara, Internal Medicine, National Defense Medical College, 3–2 Namiki, Tokorozawa, Saitama, 359–8513, Japan
e-mail: srg1512{at}gr.ndmc.ac.jp
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Abstract
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This is a 3-year follow-up of a gradually ballooning atrial septal aneurysm (ASA) which developed a spontaneous echo contrast and later a mobile thrombus in the aneurysm. This clearly demonstrates one of the pathogenetic mechanisms of systemic thromboembolism associated with ASA. In view of the risk of systemic thromboembolism or the need for lifelong anticoagulation treatment, the aneurysm was excised and an atrial septal patch was fashioned to close the resultant defect.
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Introduction
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An atrial septal aneurysm (ASA) is thought to be a rare anomaly of the atrial septum that is usually diagnosed incidentally by transthoracic echocardiography (TTE) [1]. With the advent of transesophageal echocardiography (TEE), which provides an excellent high-resolution imaging of interatrial septum, ASA has been recently recognized as a potential cause of systemic thromboembolism [2]. One of the possible mechanisms of systemic thromboembolism associated with ASA is thrombus formation in the aneurysm. We herein describe a 3-year follow-up case of large ASA that revealed a spontaneous echo contrast followed by the development of a mobile thrombus in the aneurysm.
A 32-year-old man was given a diagnosis of paroxysmal atrial fibrillation in 1987. He had no history of congenital heart disease or stroke. He had been followed at 6 month intervals by electrocardiography and TTE, and had received antiarrhythmic and antiplatelet medication.
On June 18, 1996, TTE revealed left atrial dilatation and a right atrial mass, which was confirmed to be an ASA protruding into the right atrium by TEE. The aneurysm wall appeared to be continuous and a Doppler flow analysis did not reveal any shunt flow across the atrial septum. No thrombus was identified in the aneurysm.
About 3 months later, the ASA had gradually ballooned and a spontaneous echo contrast was seen to arise from the bottom of the aneurysm. His electrocardiogram revealed chronic atrial fibrillation, however, the patient remained asymptomatic. Routine biochemical analyses and chest radiograph gave normal results.
On July 13, 1998, TEE revealed a mobile thrombus, measuring 7 mm in diameter and 16 mm in length, which was attached to the left side of the thin-walled pouch of the aneurysm (Fig 1). No thrombus was identified in the left appendage. The patient refused to undergo early surgery, and thus, in line with the patient’s wishes, warfarin administration was started. Six months later, no intraaneurysmal thrombus was identified by TEE. The spontaneous echo contrast subsequently persisted in the aneurysm despite the use of adequate anticoagulation therapy. The patient’s full understanding of the risk of a systemic thromboembolism and the need to continue lifelong anticoagulation treatment led to a decision to choose surgical treatment.
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Fig 1. Transesophageal echocardiography showing a mobile thrombus attached to the left side of the thin-walled pouch of the aneurysm. LA, left atrium; RA, right atrium.
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On January 26, 1999, surgery was performed through the right atrium and a large aneurysm was found bulging into the right atrium. The aneurysm was excised and an atrial septal patch was then placed and attached to close the resultant defect. The excised aneurysm contained no thrombi. There were no abnormalities observed except for the ASA. No postoperative complications occurred and his electrocardiogram returned to a normal sinus rhythm. The patient is now being followed by the oral administration of aspirin 80 mg/d and disopyramide 300 mg/d at our outpatient clinic.
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Comment
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We documented the process of thrombus formation in the ASA throughout the 3-year follow-up course of the present case. The unique aspect of this case lies in the identification of a gradually ballooning aneurysm and then the spontaneous echo contrast rising from the bottom of the aneurysm, followed by a mobile thrombus in the large aneurysm. The pathogenetic mechanism of thrombus formation, in the present case, is probably due to the stagnation of blood in the large aneurysm along with poor contraction during chronic atrial fibrillation.
Lifelong warfarin is administered to most patients with stroke or intraaneurysmal thrombi associated with ASA, but this treatment is also associated with serious complications such as hemorrhaging. At least in young and middle-aged patients, it seems reasonable to consider other treatments. The surgical risk of ASA is comparable with that of an atrial septal repair, which has a mortality approaching 0% in patients under 45 years of age [3]. Therefore, when no specific contraindications are present, surgery seems safer than lifelong anticoagulation and may thus be considered as an alternative treatment in patients with atrial arrhythmias and/or intraaneurysmal thrombi associated with ASA for the prevention of systemic thromboembolism.
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References
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Hanley P.C., Tajik A.J., Hynes J.K., et al. Diagnosis and classification of atrial septal aneurysm by two-dimensional echocardiography: report of 80 consecutive cases. J Am Coll Cardiol 1985;6:1370-1382.[Abstract]
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Gallet B., Malergue M.C., Adam C., et al. Atrial septal aneurysm: a potential cause of systemic embolism. Br Heart J 1985;53:292-297.[Abstract/Free Full Text]
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Murphy J.G., Gersh B.J., McGoon M.D., et al. Long-term outcome after surgical repair of isolated atrial septal defect. N Engl J Med 1990;323:1645-1650.[Abstract]
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Abstract
Introduction
