Stroke. 1996;27:1424-1426
(Stroke. 1996;27:1424-1426.)
© 1996 American Heart Association, Inc.
Aneurysm of the Left Sinus of Valsalva
An Unusual Source of Cerebral Embolism
Claudia Stollberger, MD;
Rainald Seitelberger, MD;
Christof Fenninger, MD;
Christian Prainer, MD
Jorg Slany, MD
the Zweite medizinische (C.S., C.F., J.S.) und neurologische (C.P.) Abteilung der Krankenanstalt Rudolfstiftung; and Abteilung fur Herz-und Thoraxchirurgie (R.S.), Allgemeines Krankenhaus, Vienna, Austria.
Correspondence to Dr Claudia Stollberger, Krankenanstalt Rudolfstiftung, Juchgasse 25, A-1030 Vienna, Austria.
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Abstract
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Background Aneurysm of the ascending aorta is rarely reported
as the source of emboli. We report a patient with a minor stroke
in whom a saccular aneurysm of the left sinus of Valsalva was
diagnosed as the presumed source of cerebral embolism.
Case Description A 49-year-old right-handed woman presented 10 days after sudden onset of right-sided hemiparesis. Her history was uneventful apart from an acute inflammation of the subcutaneous tissue in the right leg 20 years earlier. A diastolic murmur was heard best over the third left intercostal space. Results of duplex ultrasound investigation of the cerebral vessels, chest x-ray, and electrocardiography and biochemical and hematological variables were normal. CT of the brain showed a small hypodense area in the left frontal region. Transthoracic and transesophageal echocardiography detected moderate aortic regurgitation and a saccular aneurysm originating from the left sinus of Valsalva. The aneurysm had calcified walls and contained thrombotic material. Surgical closure of the aneurysm with a pericardial patch was performed to prevent recurrent embolism and rupture. Coaptation of the aortic valves was achieved, and no residual aortic regurgitation could be detected.
Conclusions We conclude that an unruptured sinus of Valsalva aneurysm should be included in the list of sources of embolism. Transthoracic echocardiography establishes the diagnosis. Transesophageal echocardiography provides additional information about the origin and size of the aneurysm and presence of thrombotic material. Surgical closure of the aneurysm prevents rupture and recurrent embolism and possibly corrects aortic regurgitation.
Key Words: aorta aneurysm cerebral embolism echocardiography sinus of Valsalva
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Introduction
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Aneurysm of the ascending aorta is rarely reported as the source
of emboli.
1 Aneurysms of the sinus of Valsalva (SOV), the portion
of the ascending aorta immediately behind the aortic valve cusps,
are an uncommon abnormality.
2 3 SOV aneurysms have been reported
as the presumed source of embolism in only two cases.
4 5 We
observed a patient with a minor stroke in whom a saccular aneurysm
of the left SOV was diagnosed as the presumed source of cerebral
embolism.
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Case Report
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A 49-year-old right-handed woman presented 10 days after sudden
onset of right-sided hemiparesis. Her history was uneventful
apart from an acute inflammation of the subcutaneous tissue
in the right leg 20 years earlier. On clinical examination,
mild motor and sensory deficits predominantly affecting the
face and the right arm were present. Blood pressure was 105/60
mm Hg. A diastolic murmur was heard best over the third left
intercostal space. Results of duplex ultrasound investigation
of the cerebral vessels, chest x-ray, electrocardiography, and
biochemical and hematological variables (including the lipid
profile and VDRL) were within normal limits. CT of the brain
showed a small hypodense area in the left frontal region. Transthoracic
echocardiography showed normal chamber dimensions. Left ventricular
systolic function was normal. The cardiac valves were normal,
without thickening or vegetation. Moderate aortic regurgitation
was seen by color-flow imaging and by continuous-wave Doppler.
Beneath the left coronary ostium, a cavity was detected. Color
Doppler showed flow within the cavity. Transesophageal echocardiography
(TEE) delineated this cavity as a saccular aneurysm, originating
from the left coronary SOV (Fig 1

). The aneurysm had a diameter
of 25 mm and calcified walls. Its orifice measured 8 mm. Echodense
structures, suggestive of a thrombus, were seen within the aneurysm.
No other cardiac source of embolism was identified with TEE.
Cardiac catheterization confirmed the diagnosis of a circumscribed
aneurysm of the aortic root. Coronary angiography showed normal
coronary arteries. Impending recurrent embolism from the thrombus,
as well as rupture of the aneurysm, was feared. At surgery (Fig
2

), the orifice of the aneurysm was located between the left
coronary ostium and the left coronary commissure. Thrombotic
material was removed from the aneurysm. The orifice of the aneurysm
was closed with an autologous pericardial patch. The aneurysm
was left in place. As a consequence of the closure of the orifice,
coaptation of the aortic valves was achieved, and no residual
aortic regurgitation could be detected with intraoperative TEE.
The postoperative course was uneventful. At 15-month follow-up,
the patient remains asymptomatic and without any neurological
deficit. No signs of aortic regurgitation have been detected
on clinical or echocardiographic examination.

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Figure 1. Transesophageal picture of the ascending aorta, just distal to the valvular plane. An aneurysm (A) originates from the left sinus of Valsalva (arrow). Echodense structures within the aneurysm indicate thrombotic material. LA indicates left atrium; RV, right ventricle; and AO, aortic root.
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Figure 2. Intraoperative site after opening of the aortic root. 1 indicates left coronary ostium; 2, orifice of the aneurysm; and 3, left coronary cusp of the aortic valve.
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Discussion
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The ascending aorta is a well-recognized source of emboli.
6 In the presented case, the SOV, the portion of the aorta immediately
behind the aortic valve cusps, was the presumed source of embolism.
To our knowledge, this is the first description of an unruptured
aneurysm of the left SOV as an embolic source, whereas both
other SOVs have been reported previously as sources for embolism.
4 5 SOV aneurysms originate from the right (90%), from the noncoronary
SOV (8%), or rarely (2%) from the left coronary SOV.
2 The prevalence
of unruptured SOV aneurysms is difficult to assess because they
rarely cause symptoms and may even be missed at necropsy.
3
Aneurysmal dilatation of the SOV can be caused by infective endocarditis, subsequent abscess formation, and development of a mycotic aneurysm.7 The acute inflammation of the subcutaneous tissue in the history of the patient presented might have served as an entrance for clinically silent endocarditis. The heavily calcified walls of the aneurysm and its location in the left SOV favor that hypothesis; however, the normal valves contradict that explanation.8 A further possibility is formation of the aneurysm due to congenital absence of the media of the aorta.9 We consider this possibility unlikely, since the aneurysm of our patient had a small orifice and calcified walls, both rare findings in congenital aneurysms of the SOV.2 Still less likely is formation of the aneurysm due to degeneration. Degenerative dilatation of the SOV affects all three SOVs to a similar degree, whereas in the presented case the aneurysm was confined to the left SOV. Additionally, arteriosclerosis, a history of hypertension, signs of Marfan's or Ehlers-Danlos syndrome, or laboratory evidence of syphilitic infection were all absent.3 At surgery, the orifice of the aneurysm was closed with a patch. This procedure restored the normal function of the aortic valve, eliminating aortic regurgitation. That effect has already been reported in another case.5
We conclude that an unruptured sinus of Valsalva aneurysm should be included in the list of sources of embolism.10 Transthoracic echocardiography establishes the diagnosis. TEE provides additional information about origin and size of the aneurysm and presence of thrombotic material. Surgical closure of the aneurysm prevents rupture and recurrent embolism and possibly corrects aortic regurgitation.
Received December 22, 1995;
revision received March 18, 1996;
accepted March 22, 1996.
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