Ann Thorac Surg 1996;62:1190-1192
© 1996 The Society of Thoracic Surgeons
Case Report
Surgical Elimination of an Atrial Septal Aneurysm Causing Cerebral Embolism
Jon Aksnes, MD,
Harald L. Lindberg, MD, PhD,
Halfdan Ihlen, MD, PhD
Cardiothoracic and Cardiologic Units, The National Hospital, University of Oslo, Oslo, Norway
Accepted for publication May 1, 1996.
 |
Abstract
|
|---|
Atrial septal aneurysms have been recognized as sources of arterial embolism. An intraatrial aneurysm was demonstrated in the fossa ovalis of a 45-year-old woman who suffered an episode of cerebral embolism. The disorder is rarely treated surgically. Most patients with this condition are given life-long anticoagulation, a treatment that may have serious complications. As an alternative treatment with possible lower risk, we removed the aneurysm surgically.
|
Introduction
|
|---|
A patent foramen ovale is recognized as the level of right-to-left shunting of paradoxical emboli [1]. Aneurysms in the fossa ovalis have only recently been recognized as a source of systemic arterial embolism [2, 3]. Nonsurgical treatment of this condition implies life-long anticoagulation, which has serious complications [4]. Only a few cases of surgical resections of atrial septal aneurysms have been reported [5, 6]. We present a case with arterial embolism that caused cerebral infarctions, most probably originating from an atrial septal aneurysm, and describe an operative treatment for the condition.
A 45-year-old female doctor had been fit all her life, and had experienced no difficulties daily performing a considerable load of work. She had no family history of atherosclerosis and had never noticed any episodes of heart palpitations. She experienced a sudden onset of rotary vertigo, nausea, dysarthria, loss of right field of vision, and ataxia as well as paresis of the right upper extremity. All symptoms declined over the next several weeks with no sequelae.
Investigation with computed axial tomography and magnetic resonance imaging demonstrated an infarction of the right cerebellar hemisphere and a possible cortical infarction of the left cerebral hemisphere, and confirmed the diagnosis of cerebral embolism. Angiography could not demonstrate irregularities in extracranial or intracranial vessels. Electrocardiographic registration during 48 hours showed sinus rhythm with episodes of bradycardia; paroxysmal cardiac arrhythmias were not detected. Transthoracic echocardiography showed a suspicious abnormality in the fossa ovalis, confirmed by transesophageal technique to be a septal aneurysm bulging from the left to the right atrium (Fig 1
). The aneurysm wall seemed to be continuous (see Fig 1), and Doppler flow analysis did not reveal any shunt flow across the atrial septum. No thrombus was detectable in the aneurysm sac. The heart valves functioned normally and had no structural abnormalities.
View larger version (31K):
[in this window]
[in a new window]
|
Fig 1. . Transesophageal echocardiography showed a septal aneurysm in the fossa ovalis. There was no detectable thrombus in the aneurysm sac, which was seen bulging from the left to the right atrium.
|
|
Initially the patient was given dextran followed by warfarin to prevent new embolic events. Supported by the cardiac surgeon, the patient's own professional judgment of life-long warfarin administration subsequently brought operative treatment into consideration. Eight months after the initial embolic episode she came to operation. We used an inframammary skin incision and a median sternotomy. Complete normothermic extracorporeal circulation was used with bicaval vein cannulation. Through a right atrial incision on a beating heart and with a 1
-minute cross-clamp of the aorta, the aneurysm was closed. A pursestring suture was inserted that eliminated the fossa ovalis with the aneurysm. The tip of the aneurysm was resected. It contained no thrombus material and had a pinpoint opening allowing a small leakage of blood. A postoperative transesophageal echocardiographic examination after weaning from bypass could not demonstrate any abnormalities in the atrial septum (Fig 2). No postoperative complications occurred, and the patient was discharged from the hospital after a week.
View larger version (38K):
[in this window]
[in a new window]
|
Fig 2. . Postoperative transesophageal echocardiography showed no rest abnormalities in the atrial septum.
|
|
|
Comment
|
|---|
Cerebral embolism is most frequently caused by arteriosclerosis of precerebral vessels or supraventricular arrhythmia. Structural abnormalities in the left side of the heart have been found more frequently in patients suffering cerebral embolism without ipsilateral carotid stenosis [3]. In many cases of cerebral embolism, however, the source is never detected despite thorough examination.
With the improvement of transesophageal echocardiographic techniques, atrial septum aneurysms have been recognized as sources of cerebral embolism [2]. Aneurysms in the atrial septum have been detected more frequently in patients with unexplained stroke than in patients examined for other reasons [2]. Atrial septum aneurysms have been detected more frequently in stroke patients without ipsilateral carotid stenosis than in patients with ipsilateral carotid lesion [3]. Prospectively, patients with atrial septum aneurysms have had a higher recurrent stroke rate compared with others [3].
The mechanism for embolism still remains uncertain because shunt flow that could indicate paradoxical embolization was detected in 70% of stroke patients with atrial septum aneurysms [2]. Another possibility is thrombus formation due to stagnation of blood in the thin-walled pouch with poor contraction, similar to the left atrium that does not empty with proper contractions during atrial fibrillation. The latter is supported by studies demonstrating that in 85% of stroke patients with aneurysms, the main pouching of the aneurysm was into the right atrium [2]. The aneurysm also had a thinner wall, but contained thrombus only in 1 case [2]. In our case the shunt flow that would otherwise prevent blood stagnation was small, and a significant paradoxical embolization through the pinpoint opening was not possible.
Warfarin medication is given to most stroke patients with atrial septal aneurysm, but this treatment has serious complications [7]. Studies have shown that the cumulative incidence of serious bleeding increased almost linearly with the length of medication from 12% after 1 year to 40% after 8 years [4]. The anticoagulation must be life-long, and at least in young and middle-aged patients, it seems reasonable to consider other treatment options. The surgical procedure that is performed through the right atrium is feasible. The operative risk is comparable with that of atrial septal repair, which has a mortality approaching 0% in patients less than 45 years of age [8]. The expected risk of embolic episodes due to the suture in the fossa ovalis will be comparable with that in young patients undergoing atrial septal repair, shown to be 0% in a 30-year follow-up study [8]. Thus, when no specific contraindication is present, operation seems safer than life-long anticoagulation and should, in our opinion, be considered as the treatment of choice.
|
Footnotes
|
|---|
Address reprint requests to Dr Aksnes, Surgical Department A, Rikshospitalet, 0027 Oslo, Norway.
|
References
|
|---|
- Pell ACH, Hughes D, Keating J, Christie J, Busuttil A, Sutherland GR. Brief report: fulminating fat embolism syndrome caused by paradoxical embolism through a patent foramen ovale. N Engl J Med 1993;329:926–9.[Free Full Text]
- Pearson AC, Nagelhout D, Castello R, Gomez CR, Labovitz AJ. Atrial septal aneurysm and stroke: a transesophageal echocardiographic study. J Am Coll Cardiol 1991;18:1223–9.[Abstract]
- Comess KA, DeRook FA, Beach KW, Lytle NJ, Golby AJ, Albers GW. Transesophageal echocardiography and carotid ultrasound in patients with cerebral ischemia: prevalence of findings and recurrent stroke risk. J Am Coll Cardiol 1994;23:1598–603.[Abstract]
- Fihn SD, McDonell M, Martin D, et al. Risk factors for complications of chronic anticoagulation: a multicenter study. Ann Intern Med 1993;118:511–20.[Abstract/Free Full Text]
- Angelini P, Wilansky P, Gaos C, Montazavi A, Boncompagni E, Cooley DA. Prolapsing large aneurysm of the atrial septum simulating a right atrial mass. Cathet Cardiovasc Diagn 1992;26:122–6.[Medline]
- Kondo T, Iwasaki T, Hiramatsu K, et al. Partial resection of atrial septal aneurysm with multiple fenestrations: a case report. Angiology 1988;39:838–42.
- Landefeld CS, Beyth RJ. Anticoagulant-related bleeding: clinical epidemiology, prediction, and prevention. Am J Med 1993;95:315–28.[Medline]
- Murphy JG, Gersh BJ, McGoon MD, et al. Long-term outcome after surgical repair of isolated atrial septal defect. N Engl J Med 1990;323:1645–50.[Abstract]
Related Article
-
Invited Commentary
- Paolo Angelini
Ann. Thorac. Surg. 1996 62: 1192.
[Extract]
[Full Text]
Top
Abstract
Introduction
