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Ann Thorac Surg 1996;61:1389-1393
© 1996 The Society of Thoracic Surgeons


Original Articles: Cardiovascular

Surgical Treatment of Systemic Atheroembolism From the Thoracic Aorta

Robert M. Bojar, MD, Douglas D. Payne, MD, Richard E. Murphy, PA, Steven L. Schwartz, MD, John R. Belden, MD, Louis R. Caplan, MD, Hassan Rastegar, MD

Divisions of Cardiothoracic Surgery, Cardiology, and Neurology, New England Medical Center, Boston, Massachusetts

Accepted for publication January 19, 1996.


    Abstract
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 Footnotes
 Abstract
 Introduction
 Case Reports
 Comment
 References
 
Background. Surgical procedures performed exclusively for atheroembolic events arising from the thoracic aorta rarely have been reported. Presented here are 2 patients who underwent successful operation for these problems.

Methods. The clinical presentation, diagnostic evaluation, and surgical approach to 2 patients with different embolic sources in the thoracic aorta are presented. One patient had experienced three strokes and was noted by multiplane transesophageal echocardiography to have protruding atheromas with ulcerations in the transverse arch and origin of the brachiocephalic vessels. The transverse arch was replaced using hypothermic circulatory arrest with individual reimplantation of the brachiocephalic vessels. The second patient presented with ``blue toe'' syndrome from mobile atheromas in the mid-descending thoracic aorta defined by transesophageal echocardiography. A localized debridement was performed using simple aortic cross-clamping.

Results. Both patients had uneventful postoperative courses and had no further atheroembolic events.

Conclusions. When standard diagnostic modalities do not delineate an embolic source for either stroke or peripheral embolization, transesophageal echocardiography is recommended as an excellent means of identifying atheromas in the thoracic aorta that could be the source for emboli. Once these lesions are identified, a surgical procedure should be performed to prevent further embolization.


    Introduction
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 Abstract
 Introduction
 Case Reports
 Comment
 References
 
Aortic atheroembolism can produce a variety of devastating complications, ranging from stroke to visceral or peripheral ischemia. During open heart operations, cardiac surgeons have become increasingly cognizant of the risk of embolic stroke from aortic atheroma and commonly use echocardiographic imaging to identify plaques in the ascending aorta or transverse arch. In fact, several groups have suggested performing endarterectomy or aortic resection under deep hypothermic circulatory arrest along with the planned cardiac procedure if severe atheromatous disease is discovered [13].

Spontaneous atheroembolic events from the thoracic aorta, on the other hand, are relatively uncommon causes of stroke and peripheral embolization. If the clinical findings and computerized tomographic (CT) scanning or magnetic resonance imaging of the brain suggest an embolic mechanism, extracranial and transcranial ultrasound studies and transthoracic echocardiography will identify the embolic source in most patients. If an embolic origin cannot be identified, biplane or multiplane transesophageal echocardiography (TEE) is helpful in detecting atherosclerosis in the ascending aorta or arch [48]. A surgical procedure to prevent future embolization should then be considered.

It is generally believed that peripheral embolization (``blue toe'' syndrome) originates from aortoiliac or infrainguinal atherosclerotic disease, but one should be aware of other potential sources, such as atherosclerotic plaques in the thoracic aorta [9]. In cases of blue toe syndrome, CT scanning of both the thoracic and abdominal aorta can identify thrombus and plaque better than aortography, while obviating the risk of catheter-induced embolization from an invasive procedure. When thoracic aortic disease is noted, TEE provides excellent images of protruding atheromas that may be the source of embolization.

We present herein the case reports of 2 patients, 1 of whom had recurrent strokes and the other blue toe syndrome, both of whom underwent successful repair of atherosclerotic lesions of the thoracic aorta that were the source of embolization.


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Patient 1
In a 61-year-old woman with a long-standing history of hypertension and hypercholesterolemia, the sudden onset of right hemiparesis and aphasia developed in June 1994. A magnetic resonance imaging scan showed a left parietotemporal infarct and a magnetic resonance angiogram suggested occlusion of the distal left middle cerebral artery. She recovered with slight right arm and hand weakness. Nearly 1 year later, she noted a left upper quadrant visual field deficit and a new right occipital lobe infarct was seen on CT scan. She was treated with heparin and warfarin anticoagulation. One week later, short-term memory loss and transient blindness developed with lower quadrant field deficits in both eyes, resulting from posterior cerebral artery embolism. Extracranial ultrasound showed less than 20% narrowing of the right internal carotid artery and 20% to 40% narrowing of the left carotid. Duplex and transcranial Doppler studies of the posterior circulation were normal. An electrocardiogram showed normal sinus rhythm at a rate of 52/minute. A TEE showed normal ventricular function with no intracardiac thrombus, valvular heart disease, or intracardiac shunt. It did demonstrate, however, broad-based atheromas of the transverse arch at the base of the brachiocephalic vessels and along the lesser curve of the distal arch with mobile elements (Fig 1Go).



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Fig 1. . Transesophageal echocardiogram of patient 1 demonstrating protruding atheromas with mobile elements (arrows) in the transverse arch.

 
The patient subsequently underwent a median sternotomy. Intraoperative epiaortic echocardiography confirmed the presence of atheromatous disease in the arch but showed the ascending aorta to be free of disease. Cardiopulmonary bypass was established with femoral arterial cannulation and bicaval venous drainage and the patient was cooled to 18°C. Circulatory arrest was initiated and retrograde superior vena cava perfusion was maintained at a rate of approximately 250 mL/min during the arrest period. A longitudinal aortotomy was made across the transverse arch. Several shallow ulcerations on both sides of the transverse arch were filled with soft, old thrombus. These ulcerations extended approximately 0.5 cm into the origins of all three of the brachiocephalic vessels (Fig 2AGo).



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Fig 2. . (A) Diagram of the atherosclerotic involvement of the arch and brachiocephalic vessels in patient 1. The dotted lines indicate the resection margin. The insert shows more detail of the ulcerated areas. (B) A graft has been placed from the distal ascending aorta to the proximal descending aorta, with individual reimplantation of the brachiocephalic vessels.

 
A localized debridement was contemplated, but was not considered feasible because of the presence of ulcerated plaques in the proximal arch vessels. Resection of the entire segment of diseased aorta was performed, including the transverse arch and the proximal portion of the arch vessels. A 20-mm Hemashield graft (Meadox Medicals, Inc, Oakland, NJ) was sewn to the proximal descending aorta with a running 4-0 polypropylene suture (Fig 2BGo). The three arch vessels were individually reimplanted into the graft using running 4-0 polypropylene sutures. Bypass flow was reinstituted after a 60-minute period of circulatory arrest. The proximal anastomosis was then performed to the distal ascending aorta. The patient was rewarmed to 37°C and bypass was uneventfully terminated.

The patient's recovery was characterized by recurrent atrial fibrillation and transient swallowing difficulties. She was discharged to a rehabilitation facility on the eleventh postoperative day. She had no further embolic events and noted improvement in her preoperative neurologic deficits at 6-month follow-up.

Patient 2
Acute onset of left leg pain and heaviness developed in a 69-year-old woman with untreated moderate hypertension and a 60-pack-year smoking history. A femoral arteriogram demonstrated occlusion of the left anterior tibial artery and she was treated with urokinase and subsequently with warfarin. Over the next 2 weeks, she experienced bilateral foot pain with mottling and discoloration of several toes of both feet. Pulse examination revealed bilateral femoral bruits and 1+ distal pulses bilaterally. A CT scan showed significant atheromatous disease extending from the proximal descending thoracic aorta down to the abdominal aorta. A TEE showed a large plaque with mobile atheroma in the mid-thoracic aorta and no evidence of an intracardiac source. This was considered to be the most likely source of embolization and therefore, an abdominal aortogram was not performed.

A left posterolateral thoracotomy was performed through the fifth intercostal space and the left lung was deflated. The aorta had a normal external appearance. An epicardial echocardiographic probe was used to identify the area of the atherosclerotic plaque and mobile atheroma (Fig 3Go). The aorta was cross-clamped proximal and distal to the diseased area, and a longitudinal incision was made. A localized debridement of the diseased area was performed. The aorta was closed with running 4-0 polypropylene and the chest closed in routine fashion. The patient made an uneventful recovery and was discharged from the hospital on the sixth postoperative day. At 6-month follow-up, the patient reported continued improvement with no further embolic episodes.



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Fig 3. . Transesophageal (left) and epiaortic (right) echocardiograms of patient 2 showing the mobile atheroma (arrows) in the mid-descending aorta. Epiaortic imaging identified the exact location of the atheromas to guide the site of aortic clamping.

 

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Embolization of plaque from the ascending aorta or transverse arch has been recognized recently as the most frequent cause of stroke after open heart operations. The identification of atherosclerotic plaque in these locations, usually by transesophageal or epiaortic two-dimensional echocardiography, may allow for modification of standard methods of cannulation, aortic clamping, and construction of both proximal and distal anastomoses to minimize the risk of stroke. Some surgeons have suggested endarterectomy or aortic resection under deep hypothermic circulatory arrest along with the planned open heart procedure to reduce the risk of stroke [13].

The role of spontaneous embolization of atheromatous plaque from the aorta in the generation of neurologic events has also received more attention. Recent studies using TEE have shown a high incidence of atherosclerotic disease in the ascending aorta and arch in patients with an ischemic stroke. Karalis and associates [4] noted intraaortic atherosclerotic debris in 7% of all patients undergoing TEE at their institution and noted that 31% of these patients had an embolic event within 1 month of the study. Amarenco and associates [5] noted an odds ratio of 9.1 for stroke in patients with atherosclerotic plaques in the arch 4 mm or more in thickness. They also demonstrated a 61% prevalence of ulcerated plaques in the arch among autopsy patients with no known cause of cerebral infarction [6].

It should be kept in mind, however, that atherosclerosis of the ascending aorta and arch is a marker of diffuse atherosclerotic disease and is commonly associated with carotid or peripheral vascular disease [10]. Therefore, a thorough search for other more common sites of embolization is required to ensure that the appropriate treatment is given. However, if evaluation of a patient after an embolic stroke does not yield firm evidence of a carotid or cardiac source, an echocardiographic evaluation should be considered to exclude aortic atheromata. Although TEE provides superior imaging of the ascending and descending aorta, imaging of the arch is commonly suboptimal because of interposition of the left main bronchus. The transthoracic suprasternal window may provide better images of the arch, although image quality may not be ideal, especially in elderly patients, because of the variable window and the use of a lower frequency (2.5 to 3.5 MHz) transducer with less resolution.

The development of an embolic stroke when protruding atheromatous plaque is identified in the ascending aorta or arch should prompt consideration of a surgical procedure. Neither antiplatelet agents nor warfarin has been shown to be effective in preventing further embolization from aortic plaque. Although protruding mobile atheromas or severely ulcerated plaques are associated with an increased risk of embolic brain infarction [46], surgical therapy cannot be recommended routinely for the asymptomatic patient because the risks inherent in such complex surgical procedures may outweigh the benefits. In contrast, an aggressive approach may be warranted if severe ascending aortic and arch disease is encountered during a planned cardiac operation [13].

The operative approach to patients with ascending aortic and arch disease should use well-established techniques for operation on the aortic arch. These include femoral artery cannulation, bicaval venous cannulation, and deep hypothermic circulatory arrest. Retrograde superior vena cava perfusion should also be considered because it has been demonstrated to minimize neurologic morbidity during periods of circulatory arrest [11]. It may also flush air and atherosclerotic debris from the head vessels [12]. We perform this by clamping the aortic line, unclamping a bridge between the arterial and venous lines, and perfusing the superior vena cava catheter with cold blood at a rate of 250 mL/min, maintaining a central venous pressure less than 15 to 20 mm Hg.

Although localized endarterectomy can be performed for focal atheroma [13], more extensive disease may require resection and grafting. Hemashield grafts are helpful to minimize bleeding. Aprotinin can also be used to reduce bleeding during operations using deep hypothermic circulatory arrest, although there are reports of severe neurologic morbidity and renal dysfunction, probably from microvascular platelet–fibrin thrombosis [14]. Alternative protocols to full-dose aprotinin should be considered to avert these sequelae. These may include low-dose aprotinin without infusion during the period of circulatory arrest, dosing only after reinstitution of cardiopulmonary bypass, or additional heparin before the period of circulatory arrest to ensure adequate anticoagulation. One potential concern with femoral artery perfusion is the risk of retrograde brain embolization if there is diffuse atherosclerotic disease in the descending thoracic aorta as well as in the arch.

The vast majority of atheroembolism to the lower extremities (blue toes) arises from the abdominal aorta or distal vascular bed. Keen and associates [9] noted that 85% of lower extremity embolization arose from aortoiliac occlusive or aneurysmal disease in patients who had not previously undergone abdominal grafting, whereas the remainder arose from infrainguinal sites. In contrast, Karmody and associates [15] found that 74% arose from infrainguinal sites. Because of the safety of CT scanning and its sensitivity in identifying atheromatous disease and plaque, evaluation of both the thoracic and abdominal aorta by CT scanning should probably be performed as the initial diagnostic test to exclude isolated or concomitant thoracic aortic disease.

When CT scanning suggests significant pathology in the thoracic aorta, TEE should also be performed because it not only provides superior images of protruding and mobile atheromas, but also obviates the necessity for an invasive aortogram [4]. The location and characteristics of the atheromas identified by TEE can provide insight into their embolic potential and can guide the operative procedure. For example, Tunick and associates [8] noted that protruding atheromas in the arch and descending aorta had an odds ratio of 4.3 in predicting embolic events. They noted that 33% of patients with protruding atheromas suffered embolic events to sites including the brain, visceral vessels, and lower extremities. Karalis and associates [4] noted embolization in 73% of patients with pedunculated and highly mobile atheromas, but in only 12% when the atheroma was layered and immobile.

There are several considerations in the operative management of atheromatous involvement of the descending thoracic aorta. The external appearance of the diseased thoracic aorta may be normal because the pathology is primarily within the vessel wall with protrusion into the lumen. An intraoperative epiaortic echocardiographic probe is superior to TEE and CT scanning in identifying the exact location and extent of the atheromatous segment. It can also assess the degree of atherosclerosis immediately proximal and distal to this segment. These images are helpful in defining the extent of aorta that must be excluded between cross-clamps and may help with the decision to perform a localized debridement/endarterectomy or interposition grafting. Consequently, depending on the extent of resection and the degree of atherosclerosis, the surgeon can decide between the ``clamp and run'' technique or use of left atrial–femoral bypass.

If clamping of the aorta is not feasible because of extensive disease, partial cardiopulmonary bypass and deep hypothermic circulatory arrest can be used for descending thoracic aortic resection [16, 17]. Venous drainage can be established from a catheter inserted through the femoral vein up to the right atrium, and can be supplemented by pulmonary artery drainage [18]. Arterial inflow is usually through the femoral artery. After the proximal anastomosis is completed, the arterial cannula is inserted into the graft to resume cardiopulmonary bypass. This not only minimizes the duration of circulatory arrest, but also reduces the risk of retrograde embolization of abdominal aortic atheroma.

These 2 patients represent two different manifestations of atheroembolic disease from the thoracic aorta and their surgical management. It is suggested that TEE is a valuable diagnostic modality in the evaluation of stroke when no other obvious embolic sources can be identified. Transesophageal echocardiography is also an excellent means of supplementing CT scanning or magnetic resonance imaging in the evaluation of descending thoracic aortic disease that may be the source of distal embolization. Standard, although complex, surgical approaches should be considered in patients who have had brain or distal embolization to prevent further events. Although an aggressive approach to the severely atherosclerotic ascending aorta or arch may be warranted when encountered during a planned cardiac surgical procedure, it cannot be recommended at this time for the asymptomatic patient in whom atheromatous disease of high embolic potential is identified during diagnostic evaluations. Further investigation is warranted into the relative risk of medical versus surgical intervention for these patients.


    Footnotes
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 Footnotes
 Abstract
 Introduction
 Case Reports
 Comment
 References
 
Address reprint requests to Dr Bojar, Division of Cardiothoracic Surgery, New England Medical Center, Box 266, 750 Washington St, Boston MA 02111.


    References
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 Footnotes
 Abstract
 Introduction
 Case Reports
 Comment
 References
 

  1. Wareing TH, Davila-Roman VG, Barzilai B, et al. Management of the severely atherosclerotic ascending aorta during cardiac operations. A strategy for detection and treatment. J Thorac Cardiovasc Surg 1992;103:453–62.[Abstract]
  2. Blauth CI, Cosgrove DM, Webb BW, et al. Atheroembolism from the ascending aorta. An emerging problem in cardiac surgery. J Thorac Cardiovasc Surg 1992;103:1104–12.[Abstract]
  3. Ribakove GH, Katz ES, Galloway AC, et al. Surgical implications of transesophageal echocardiography to grade the atheromatous aortic arch. Ann Thorac Surg 1992;53:758–63.
  4. Karalis DG, Chandrasekaran K, Victor MG, Ross JJ, Mintz GS. Recognition and embolic potential of intraaortic atherosclerotic debris. J Am Coll Cardiol 1991;17:73–8.[Abstract]
  5. Amarenco P, Cohen A, Tzourio C, et al. Atherosclerotic disease of the aortic arch and risk of ischemic stroke. N Engl J Med 1994;331:1474–9.[Abstract/Free Full Text]
  6. Amarenco P, Duyckaerts C, Tzourio C, Jenin D, Bousser MG, Hauw JJ. The prevalence of ulcerated plaques in the aortic arch in patients with stroke. N Engl J Med 1992;326:221–5.[Abstract]
  7. Rubin DC, Plotnick GD, Hawke MW. Intraaortic debris as a potential source of embolic stroke. Am J Cardiol 1992;69: 819–20.[Medline]
  8. Tunick PA, Rosenzweig BP, Katz ES, Freedberg RS, Perez JL, Kronzon I. High risk for vascular events in patients with protruding aortic atheromas: a prospective study. J Am Coll Cardiol 1994;23:1085–90.[Abstract]
  9. Keen RR, McCarthy WJ, Shireman PK, et al. Surgical management of atheroembolization. J Vasc Surg 1995;21:773–81.[Medline]
  10. Nihoyannopoulos P, Joshi J, Athanasopoulos G, Oakley CM. Detection of atherosclerotic lesions in the aorta by transesophageal echocardiography. Am J Cardiol 1993;71: 1208–12.[Medline]
  11. Deeb GM, Jenkins E, Bolling SF, et al. Retrograde cerebral perfusion during hypothermic circulatory arrest reduces neurologic morbidity. J Thorac Cardiovasc Surg 1995;109:259–68.[Abstract/Free Full Text]
  12. Yerglioglu ME, Wolfe D, Mezrow CK, et al. The effect of retrograde cerebral perfusion after particulate embolization to the brain. J Thorac Cardiovasc Surg 1995;110:1470–85.[Abstract/Free Full Text]
  13. Swanson SJ, Cohn LH. Excision of focal aortic arch atheroma using deep hypothermic circulatory arrest. Ann Thorac Surg 1995;60:457–8.[Abstract/Free Full Text]
  14. Sundt TM, Kouchoukos NT, Saffitz JE, Murphy SG, Wareing TH, Stahl DJ. Renal dysfunction and intravascular coagulation with aprotinin and hypothermic circulatory arrest. Ann Thorac Surg 1993;55:1418–24.[Abstract]
  15. Karmody AM, Powers SR, Monaco VJ, Leather RPl. ``Blue-toe'' syndrome. An indication for limb salvage surgery. Arch Surg 1976;111:1263–8.[Abstract/Free Full Text]
  16. Szentpetery S, Crisler C, Grinnan GLB. Deep hypothermic arrest and left thoracotomy for repair of difficult thoracic aneurysms. Ann Thorac Surg 1993;55:830–3.[Abstract]
  17. Kouchoukos NT, Daily BB, Rokkas CK, Murphy SF, Bauer S, Abboud N. Hypothermic bypass and circulatory arrest for operations on the descending thoracic and thoracoabdominal aorta. Ann Thorac Surg 1995;60:67–77.[Abstract/Free Full Text]
  18. Kouchoukos NT, Wareing TH, Izumoto H, Klausing W, Abboud N. Elective hypothermia, cardiopulmonary bypass, and circulatory arrest for spinal cord protection during operations on the thoracoabdominal aorta. J Thorac Cardiovasc Surg 1990;99:659–64.[Abstract]



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