Ann Thorac Surg 2002;73:291-294
© 2002 The Society of Thoracic Surgeons
Case report
Aortic arch replacement for recurrent cerebral embolization
Gilead Lancaster, MDd,
Constantinos J. Lovoulos, MDa,
Michael Moussouttas, MDb,
Andrew H. Goldstein, MDa,
Dana Leifer, MDb,
Pierre B. Fayad, MDb,
Drew Olsen, MDc,
John A. Elefteriades, MD*a
a Section of Cardiothoracic Surgery, Yale University School of Medicine, New Haven, Connecticut, USA
b Section of Neurology, Yale University School of Medicine, New Haven, Connecticut, USA
c Department of Pathology, Yale University School of Medicine, New Haven, Connecticut, USA
d Department of Cardiology, Danbury Hospital, Danbury, Connecticut, USA
Accepted for publication May 14, 2001.
* Address reprint requests to Dr Elefteriades, Section of Cardiothoracic Surgery, Yale University School of Medicine, 121 FMB, 333 Cedar St, New Haven, CT 06510, USA
e-mail: john.elefteriades{at}yale.edu
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Abstract
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Replacement of the aortic arch for atheroma with cerebral embolization is in its infancy. The appropriateness of such intervention is controversial. Over a 10-month period, a 58-year-old woman suffered multiple debilitating cerebral vascular accidents manifested by motor, sensory, and memory deficits and documented by computed tomographic scanning and magnetic resonance imaging. Carotid and vertebral arteries were free of arteriosclerotic disease. Transesophageal echocardiography demonstrated two large atheromas with friable, pedunculated forms, one in the aortic arch and one in the very proximal descending thoracic aorta. Transcranial ultrasound revealed recurrent cerebral microembolic events. Cerebrovascular events continued, and the atheromas increased in size, despite treatment with Coumadin and aspirin. Under deep hypothermic arrest, the segment of the aortic arch harboring the atheroma was excised and replaced with a Dacron graft. Repeat transcranial ultrasound revealed cessation of embolic signals. All cerebrovascular events ceased. No further anticoagulation therapy was required. The patient has made substantial recovery from the preoperative deficits and continues to do well 1 year after aortic arch replacement. Resection of mobile aortic arch atheromas is likely to become increasingly important in the future as transesophageal echocardiography leads to their more common identification as a cause of cerebral ischemic events.
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Introduction
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Carotid endarterectomy is widely applied for patients with cerebral vascular symptoms and arteriosclerotic disease of the carotid arteries. Although a similar rationale may be applied for patients with cerebral symptoms and atheromas in the aortic arch, direct surgical attack on the aortic arch specifically for the treatment of cerebral ischemic events remains in its infancy. The intent of such a surgical approach is to remove atherosclerotic material that embolizes to the cerebral circulation.
We report the case of a 58-year-old woman with a history of hypertension, diabetes, and recurrent cerebral ischemic events. The first ischemic episode occurred 10 months before admission to Yale and consisted of left hemiparesis and memory impairment. Some clinical recovery was noted. A computed tomographic scan demonstrated a right lacunar infarction, and the patient was treated with aspirin. One month later, the patient again developed left hemiparesis, this time accompanied by dysphagia. Computed tomographic scan demonstrated only old left caudate and putamen lacunar infarctions, and warfarin was added to the aspirin. Duplex study demonstrated mild calcified plaque in the right anterior carotid bulb and proximal internal carotid artery, no atherosclerotic plaque in the left internal carotid artery, and anterograde flow in the vertebral arteries bilaterally. Transesophageal echocardiogram (TEE) revealed two protuberant aortic atheromas, one in the aortic arch and one in the very proximal descending aorta (Fig 1).
Nine months later, a third cerebral event occurred, despite continued treatment with aspirin and Coumadin (crystalline warfarin sodium; DuPont Pharmaceuticals, Wilmington, DE). Examination at that time was notable for dysarthria, left sensorimotor deficits, and extensor plantar responses bilaterally. Transesophageal echocardiogram again demonstrated the same two pedunculated atheromas in the aortic arch region, and they now appeared larger than previously. No intracardiac source for thromboembolization was identified.
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Fig 1. Transesophageal echocardiogram showing (A) the mobile atheroma in the aortic arch, and (B) the mobile atheroma in the very proximal descending aorta.
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The patient was transferred to Yale for consideration of aortic arch resection. Cerebral magnetic resonance imaging diffusion study revealed multiple 3-mm to 4-mm subacute infarctions in the right striatum, left internal capsule posterior limb, and left corona radiata (Fig 2).
Several smaller subacute infarctions were seen in the centrum semiovale bilaterally, posterior left cingulate gyrus and corpus callosum, and pons. Magnetic resonance angiogram of the anterior and posterior intracranial circulations was negative for atherosclerotic disease. Neck magnetic resonance imaging revealed an anomalous origin of the left common carotid artery from the innominate artery ("bovine arch"), a 9-mm thickening of a focal portion of the wall of the aortic arch (Fig 3),
and no intrinsic stenotic or atheromatous disease of the carotid or vertebral arteries. Transcranial ultrasound demonstrated 15 cerebral microembolic events in the left internal carotid artery distributed over a period of 30 minutes of monitoring. A persantine thallium scan was negative for cardiac ischemia. Cardiac catheterization was avoided for fear of causing embolization by passing catheters into the ascending aorta.
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Fig 2. Magnetic resonance imaging scan of the brain showing the various acute and subacute infarcts (arrows) accumulated by the time of transfer to our institution, after a total of three acute stroke events over a 10-month period.
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Fig 3. Magnetic resonance angiogram showing thickening (9 mm) of a focal segment of the wall of the ascending aorta (arrow).
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The patient was taken to the operating room. After sternotomy, the "bovine" aortic arch was confirmed, with an innominate and a left carotid artery originating as a single trunk from the aortic arch. The aorta was completely soft and free of palpable arteriosclerosis. The patient was placed on cardiopulmonary bypass with an arterial cannula in the midascending aorta (to avoid the area of mobile atheroma) and standard right atrial cannulation. Under deep hypothermic circulatory arrest at 18°C, the aorta was opened. Both atheromas were visualized, one located just at the base of the innominate artery and the other just beyond the subclavian artery. The arch lesion was perfectly situated to shed emboli into the common origin of the innominate and left carotid arteries, thus accounting for emboli to right and left sides of the brain. Pink, friable, but formed mobile atheromatous material was removed from each lesion, revealing an ulcer at the base of each atheroma. All other areas of the aorta were entirely normal in appearance. The descending ulcer, of less importance in terms of embolic consequences, was imbricated by two pledgeted mattress sutures placed from within the aortic lumen. The area of the aortic arch with the ulcerated atheromatous lesion was excised and replaced with a triangular segment cut from a Dacron (DuPont, Wilmington, DE) tube graft. This replaced segment was situated just below the innominate artery coursing to the right and left carotid arteries. The patient was rewarmed and weaned from cardiopulmonary bypass without difficulty. The patient did well postoperatively and suffered no surgical complications.
Histologic examination (Fig 4)
of the resection specimen revealed an intima that was markedly thickened by hypocellular material, atheroma, and no overlying thrombus. Focal destruction of the elastic layer beneath the atheroma was evident. Cholesterol clefts and occasional spindle-shaped nuclei were present within a hypocellular matrix. The features were all typical of an atheromatous plaque of no specific etiology.
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Fig 4. Histologic specimen of aortic arch lesion, revealing atheroma, not thrombus. Marked intimal (I) thickening by atheromatous material is evident. (M = media; A = adventitia.) (Hematoxylin and eosin; x10). Inset (left) shows focal destruction of the elastic fibers within the media and proliferation of thin-walled vessels into the atheroma. (Elastic van Gieson; x40.) Inset (right) gives high-power view of indicated area, revealing cholesterol clefts (C) and hypocellular amorphous material with occasional nuclei. (Hematoxylin and eosin; x200.)
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The patient did well postoperatively, with no additional cerebral events over the 1 year since operation. She walks independently and shows no obvious defects in mentation. No anticoagulation agents were used at any time postoperatively. Transcranial ultrasound done 4 months after the operation was normal, with no embolic signals detected.
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Comment
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Emboli, including those from the aortic arch, are becoming increasingly recognized as causes of cerebral ischemic events [1–6]. In the present case, the microembolic signals detected on transcranial ultrasound clearly indicated active embolization as a possible cause of the recurrent ischemic events. The simultaneous bilateral hemisphere and posterior fossa infarctions detected by diffusion magnetic resonance imaging pointed to a cardiac or aortic source for the emboli. Serial TEE examinations excluded a cardiac source and revealed the enlarging protuberant aortic atheromas. The rapid occurrence of repeated cerebral events in this case is typical, as the annual incidence of infarction from mobile aortic plaques has been estimated at 32% [2]. The postoperative cessation of neurologic events, and the absence of microemboli on repeat transcranial ultrasound, verified the aortoembolic etiology.
The anomalous origin of the left common carotid artery from the innominate artery resulted in exposure of both the right and left sides of the brain to embolic material.
We believe that the aortic arch is a frequent and still underrecognized source of cerebral emboli, and that arch lesions are similar to carotid atheromas in impact but are simply located more proximally in the arterial tree, proximal to the cerebral vasculature proper. The importance of aortic lesions is slowly becoming better appreciated, as TEE examinations have begun to be used increasingly in the evaluation of cerebral symptoms. The French cooperative study found a high incidence of ischemic infarctions associated with ascending or arch atheromatous plaque detected on TEE [6]. Fully 60% of patients over 60 years of age who had arch atheroma thicker than 4 mm by TEE had ischemic brain events.
Despite studies that suggest warfarin may help in these patients [2], there are frequent cases of treatment failure, as in our case.
In the French cooperative study, anticoagulation therapy was not effective in preventing recurrent events. Recurrence on anticoagulation therapy was 11.9 per 100 patient-years for plaque wall thickness equal to or exceeding 4 mm, 3.5 per 100 patient-years for plaque wall thickness 1 mm to 3.9 mm, and 2.8 per 100 patient-years for plaque wall thickness less than 1 mm.
In patients with cerebral events from aortic arch atheromas, we believe that surgical correction is an important therapeutic option, especially as certain atheromas may not be thrombotic in nature and therefore may not respond to standard medical therapy with anticoagulation agents. Surgical correction of these lesions will likely assume greater importance in the future, as these lesions and their consequences are identified more frequently.
The demonstrated safety of aortic arch replacement under deep hypothermic circulatory arrest [7] indicates that operations for aortic arch atheromas can be carried out at acceptable perioperative risk, with a reliable expectation for good recovery. We believe that aortic arch replacement for atheromatous disease producing cerebral symptoms may be an important area for collaboration between neurologists and cardiothoracic surgeons in the future.
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References
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Hier D., Foulkes M., Swiontoniowski M., et al. Stroke recurrence within 2 years after ischemic infarction. Stroke 1991;22:155-161.[Abstract/Free Full Text]
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Abstract
Introduction
