Risk Factors for Perioperative Stroke After Thoracic Endovascular Aortic Repair

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1 Risk Factors for Perioperative Stroke After Thoracic Endovascular Aortic Repair Jacob T. Gutsche, MD, Albert T. Cheung, MD, Michael L. McGarvey, MD, William G. Moser, RN, Wilson Szeto, MD, Jeffrey P. Carpenter, MD, Ronald M. Fairman, MD, Alberto Pochettino, MD, and Joseph E. Bavaria, MD Departments of Anesthesiology and Critical Care, Neurology, and Surgery, University of Pennsylvania, Philadelphia, Pennsylvania Backgound. Stroke has emerged as an important complication of thoracic endovascular aortic repair (TEVAR). Identifying risk factors for stroke is important to define the risks of this procedure. Methods. All neurologic complications were analyzed in a prospective database of patients in thoracic aortic stent graft trials from 1999 to Serial neurological examination was performed. Stroke was defined as any new onset focal neurologic deficit. Results. The TEVAR was performed on 171 patients; 52 had lesions requiring coverage of the proximal descending thoracic aorta (extent A), 50 requiring coverage of the distal descending aorta (extent B), and 69 requiring coverage of the entire descending thoracic aorta (extent C). The incidence of stroke was 5.8%. Eighty-nine percent (8 of 9) of strokes occurred within 24 hours of operation. Stroke was associated with a 33% in-hospital mortality rate. Risk factors identified for stroke included prior stroke (odds ratio [OR] 9.4, confidence interval [CI] 2.3 to 38.1, p 0.002) and extent A or C coverage (OR 5.5, CI , p 0.001). The stroke rate in patients with both prior stroke and extent A or C coverage was 27.7%. Severe atheromatous disease involving the aortic arch by computed tomographic scan was strongly associated with perioperative stroke (OR 14.8, CI 1.7 to 675.6, p ). Transesophageal echocardiography demonstrated mobile atheroma in two patients with stroke. Conclusions. Stroke after TEVAR was associated with a high mortality. The TEVAR of the proximal descending aorta (extent A or C) in patients with a history of stroke had the highest perioperative stroke rate. These risk factors, together with high grade aortic atheroma of the aortic arch, predicted a high probability for cerebral embolization and can be used to identify patients at high risk for stroke as a consequence of TEVAR. (Ann Thorac Surg 2007;84: ) 2007 by The Society of Thoracic Surgeons Accepted for publication April 24, Presented at the Forty-third Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 29 31, Address correspondence to Dr Gutsche, Department of Anesthesiology and Critical Care, Dulles 6, Hospital of University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104; gutschej@uphs.upenn. edu. In 2005, the findings of the multicenter Gore TAG study [1] led to U.S. Food and Drug Administration approval for endovascular repair of thoracic aortic aneurysms (TEVAR). This technique provides an additional therapeutic option for patients with thoracic aortic aneurysm. Stroke was recognized as a complication in the Gore TAG study and has also been noted as an important complication in an analysis of the combined EuroSTAR and United Kingdom Thoracic Endograft registries [1, 2]. In relative terms, stroke complicating TEVAR was more common than spinal cord ischemia in the Gore TAG study. The Gore TAG trial reported a stroke rate of 3.5% with an associated mortality of 20%, which was comparable to the composite average stroke rate of 3.9% reported in other large contemporary studies (Table 1). The mechanisms contributing to acute ischemic stroke and the timing of stroke in relation to the procedure in patients undergoing TEVAR is not well understood because this procedure is still relatively new. Many patients undergoing TEVAR in published studies to date were elderly, had occlusive vascular disease, and had multiple risk factors for stroke. Because of the limited clinical experience with TEVAR, and the high mortality rate associated with perioperative stroke, an effort to understand the etiology and mechanisms for stroke in this setting is justified. The risk of stroke in patients undergoing TEVAR was not surprising because atherosclerotic disease of the thoracic aorta is a recognized risk factor for stroke after cardiac operations [3]. In addition, higher grade atheroma of the thoracic aorta predicts a higher risk of stroke after heart surgery [4]. In the setting of heart surgery, perioperative stroke is believed to be caused by disruption of vulnerable atheromas in the ascending aorta or aortic arch leading to cerebral embolization. As with cardiac operations, TEVAR may also cause cerebral embolization in patients with a vulnerable atheroma of the aortic arch or proximal descending thoracic aorta. The potential for atheroembolism as a consequence of wire Drs McGarvey and Bavaria disclose that they have financial relationship with W. L. Gore, Inc by The Society of Thoracic Surgeons /07/$32.00 Published by Elsevier Inc doi: /j.athoracsur

2 1196 GUTSCHE ET AL Ann Thorac Surg PERIOPERATIVE STROKE AFTER TEVAR 2007;84: Table 1. Stroke Incidence in the Contemporary Series of Thoracic Endovascular Aortic Repair Study Year No. and catheter-based interventions of the thoracic aorta was demonstrated in 50% of patients undergoing percutaneous coronary revascularization procedures [5]. The purpose of this study was to identify risk factors for stroke associated with TEVAR. The hypothesis was that stroke during TEVAR is caused by atheroembolism from instrumentation of the aortic arch in patients with severe atheromatous disease. Understanding the risk factors for stroke will help explain pathophysiologic mechanisms for perioperative stroke, improve risk stratification, and enable the development of new algorithms or refinement of existing endovascular techniques to prevent or decrease the incidence of stroke complicating TEVAR. Patients and Methods Stroke Incidence Gore TAG [1] (3.5%) Eurostar and UK Registries [2] (2.3%) Talent Thoracic Retrospective (3.7%) Registry [15] Arizona Heart Institute [16] (4.5%) McGill University [17] (7.1%) UCLA [18] (5.5%) University of Michigan [19] (8.2%) Total 1, (3.9%) All consecutive patients presenting for repair of the descending thoracic aorta by endovascular stent graft from April 1, 1999 to March 30, 2006 were prospectively entered into a clinical database. Inclusion criteria for stent repair were patients with saccular aneurysm of any size, fusiform aneurysm diameter greater than 5.0 cm or greater than two times the adjacent aorta, and contained rupture of the descending thoracic aorta. In a small number of cases TEVAR was performed for contained rupture of the descending thoracic aorta or type B aortic dissection. All protocols and procedures associated with the procedure were approved by the Food and Drug Administration and the Institutional Review Board with written informed consent. Patients Table 2. Modified Computed Tomography Grading Scale for Aortic Atheroma Grade Grade I (normal) Grade II Grade III Grade IV Description Smooth and continuous aortic intimal surface Intimal thickening 3 to 5 mm Atheroma protruding 5 mm into aortic lumen Atheroma protruding 5 mm into aortic lumen and ulcerated or pedunculated T should be added as a separate descriptor for presence of mural thrombus. Table 3. Patient Demographics and Comorbidities Demographics and Comorbidities No. % Age years Gender: Male 99 (58%) Female 72 (42%) Preoperative comorbidity: Hypertension 154 (90%) Tobacco use 130 (76%) Dyslipidemia 85 (50%) Coronary artery disease 74 (43%) COPD 71 (42%) Atrial fibrillation 38 (22%) Stroke/TIA 34 (20%) Prior cardiac operation 33 (19%) Prior open AAA or TAAA repair 30 (18%) Diabetes mellitus 29 (17%) Renal insufficiency a 28 (16%) a Renal insufficiency creatinine concentration 1.5 mg/dl. AAA abdominal aortic aneurysm; COPD chronic obstructive pulmonary disease; TAAA thoracoabdominal aortic aneurysm; TIA transient ischemic attack. were analyzed for preoperative comorbidities and intervention-associated risks that would predispose patients to stroke. The Gore endoprosthesis (W.L. Gore, Inc, Newark, DE) was delivered through a 20 to 24 French sheath and expanded with a trilobed balloon that did not occlude flow in the aorta. The Talent thoracic stent graft (Medtronic, Inc, Minneapolis, MN) was delivered using a 24 to 25 French system and also expanded with a balloon. All procedures were performed using standard endovascular techniques with fluoroscopy. Transfemoral access was usually attained by a groin cutdown. In some patients, a small retroperitoneal incision was performed to gain access to the common iliac artery. Angiographic access was through the contralateral femoral artery or brachial artery. The minimum amount of aorta was covered to exclude the aneurysm with an adequate seal. The extent of endovascular stent coverage of the descending thoracic aorta was classified into three groups: extent A was coverage from the origin of the left subclavian artery to the sixth thoracic vertebral level; extent B was coverage from the sixth thoracic vertebral level to the diaphragm; and extent C was coverage of the entire descending thoracic aorta from the left subclavian artery to the diaphragm [6]. A carotid-to-left subclavian bypass or left subclavian transposition into the left carotid artery was performed prior to TEVAR for all cases involving stent coverage of the left subclavian artery [7]. By protocol, all patients had general anesthesia with inhalation anesthetics maintained at less than or equal to 0.5 minimum alveolar concentration for intraoperative somatosensory evoked potential (SSEP) monitoring. Intraoperative SSEP monitoring and lumbar cerebrospinal fluid drainage were used in patients at increased risk for

3 Ann Thorac Surg GUTSCHE ET AL 2007;84: PERIOPERATIVE STROKE AFTER TEVAR 1197 Table 4. Characteristics of Patients With Stroke Patient No. Age Gender Device Extent a Sign of Stroke Type of Stroke 1 67 F Talent A Left sided hemiparesis Right MCA stroke 2 71 M Gore C Diagnosed by intraop SSEP Left MCA stroke 3 80 M Gore C Patient did not recover consciousness Multiembolic stroke after procedure 4 78 F Talent A Change in mental status Bilateral occipital lobe 5 58 F Gore A Right sided hemiparesis Right internal capsule, right basal ganglia, and left thalamus 6 90 F Gore C Patient did not recover consciousness after procedure Bilateral cerebellar, right PCA, and right MCA 7 75 F Talent C Left sided hemiparesis Right MCA 8 66 M Talent A Right sided hemiparesis Left parietal, left internal capsule, and left posterior inferior cerebellar artery 9 74 F Talent C Left sided hemiparesis Right MCA a Extent of endovascular stent coverage of the descending thoracic aorta. A left subclavian artery to T6; B T6 to diaphragm; C left subclavian artery to diaphragm; AAA abdominal aortic aneurysm; MCA middle cerebral artery; PCA posterior cerebral artery. spinal cord ischemia. Patients were considered at high risk for spinal cord ischemia when presenting with a history of a prior thoracic aortic aneurysm repair, abdominal aortic aneurysm repair, or an extent B or C coverage of the thoracic aorta was planned [8]. Arterial pressure was monitored with an intraarterial catheter, and the mean arterial pressure (MAP) was maintained at 75 to 85 mm Hg during general anesthesia. If spinal cord ischemia was detected, MAP was augmented with vasopressor therapy in combination with lumbar cerebrospinal fluid drainage [8]. Neurophysiologic monitoring consisted of continuous 12 channel, 11 electrode electroencephalogram (EEG) and upper and lower extremity SSEP using the montages recommended by the American Clinical Neurophysiology Society [9]. Lower extremity SSEPs were recorded from the popliteal fossa, lumbar spine, cervical spine, and scalp to localize injury to the peripheral nerve, spinal cord, or brain [9]. Postoperative MAP was maintained at 85 mm Hg or at a MAP at which intraoperative SSEP signals were intact using vasopressors or vasodilators. Postoperative neurologic assessments were performed as per protocol on an hourly basis in the intensive care unit to detect neurologic deficits until the patient was able to report symptoms of weakness or numbness. The purpose of this protocol was to detect signs or symptoms of spinal cord ischemia. Strength in each lower extremity proximal and distal muscle groups was assessed and compared with the upper extremity motor strength. The Table 5. Prior Stroke and Risk of Stroke Complication Prior Stroke No Prior Stroke Stroke 5 a 4 No stroke Total (n 171) a Prior stroke and perioperative stroke, p presence or absence of a sensory deficit was recorded. If a neurologic deficit was detected, a full neurologic examination was performed emergently by a neurologist dedicated to the study. Subsequent neurologic examinations were performed serially and during any periods of improvement or decline in neurologic function. Special attention was directed toward diagnosing spinal cord ischemia to distinguish from brain ischemia or peripheral nerve injury as etiologies. Stroke was defined a priori as any new onset focal neurologic deficit and confirmed by computed tomography (CT) or magnetic resonance Fig 1. The relationship between descending thoracic aortic aneurysm extent and perioperative stroke after thoracic endovascular aortic repair. The upper panel presents examples of the extent coverage (A, B, or C) of the descending thoracic aortic aneurysm. The lower panel presents the number of strokes associated with each extent aneurysm. *All of the strokes occurred in patients with extent A or C coverage of the descending thoracic aorta (p 0.001). (Adapted from Estrera AL, Rubenstein FS, Miller CC III, Huynh TT, Letsou GV, Safi HJ. Descending thoracic aortic aneurysm: surgical approach and treatment using the adjuncts cerebrospinal fluid drainage and distal aortic perfusion. ATS 2001;72: Copyright 2001, with permission from Elsevier.)

4 1198 GUTSCHE ET AL Ann Thorac Surg PERIOPERATIVE STROKE AFTER TEVAR 2007;84: imaging, together with a full neurological examination by a neurologist. Therapy for stroke included maintenance of MAP greater than 85 mm Hg and maintenance of normoglycemia. The severity of atheromatous disease was assessed by preoperative CT scans of the chest. The severity of atheromatous disease was graded using a modified scale of I to IV based on a previously described transesophageal echocardiography (TEE) grade for atheromatous disease [3] (Table 2). In addition, a small number of patients had TEE performed during TEVAR. Intraoperative TEE examinations were assessed for severity of atheromatous disease using a grading scale devised by Katz and colleagues [3] which has been shown to correlate with stroke risk [3]. Statistical Analysis All analyses were performed using STATA 8 (STATA Corp, College Station, TX). Demographic data were analyzed using one-way analysis of variance, the Mann- Whitney U test, and the Fisher exact test (2-tailed) for continuous, ordinal, and proportional data, respectively. Risk factors for stroke were determined using logistic regression analysis. Due to the sparsity of outcome (stroke) univariate analysis was performed and then bivariate analysis to determine the presence of confounding variables. Results A total of 171 patients had endovascular stent graft repair of the descending thoracic aorta from April 1, 1999 to March 30, One-hundred-sixty patients had stent graft of the aorta for repair of aneurysm and 11 patients had stent graft placed for type B dissection. The mean age was 73 years, with 72 (42%) females. Sixty-five patients had Talent (Medtronic) endovascular grafts, 17 patients had Zenith TX2 (Cook, Bloomington, MN) endovascular grafts, and 90 had Gore TAG (W.L. Gore) endoprosthetic grafts. Preoperative comorbidities are listed in Table 3. Stroke occurred in 9 of 171 patients (5.8%). All strokes were classified as embolic based on imaging characteristics (Table 4). None of the strokes were hemorrhagic. Two patients suffered from stroke in the right cerebral circulation, two patients had strokes in the left cerebral circulation, and five patients had bilateral strokes. Perioperative stroke was diagnosed within 24 hours after TEVAR in eight of nine patients. In the remaining patient, stroke was diagnosed on postoperative day number 5. The patient experienced an acute mental status change associated with respiratory failure on postoperative day number 5, which prompted a full medical and neurologic evaluation. A multiembolic stroke was diagnosed by CT scan and a transesophageal echo revealed a large mobile atheroma in the aortic arch. Stroke was associated with 33% in-hospital mortality (three of nine patients). In comparison, patients who did not stroke had an in-hospital mortality rate of 6.5% (10 of Table 6. Thoracic Endovascular Aortic Repair and Perioperative Stroke Risk Outcome Extent A Extent B Extent C Prior stroke and periop stroke 3 (60%) 0 (0%) 2 (15%) (n 5) Prior stroke and no periop stroke (n 19) Subtotal (n 24) No prior stroke and periop 1 (2%) 0 (0%) 3 (5%) stroke (n 4) No prior stroke and no periop stroke (n 143) Subtotal (n 147) ). The total overall in-hospital mortality for patients undergoing TEVAR was 8.2% (13 of 171). Using logistic regression analysis, the only comorbidity associated with perioperative stroke was a history of prior stroke (OR 9.4, CI , p 0.002) (Table 5). Four of the nine patients with stroke had extent A coverage of the aorta (Fig 1). Five of the nine patients with stroke had extent C coverage of the aorta. Forty-six patients with extent A or extent C coverage of the aorta also had coverage of the left subclavian artery, and 29 of these patients had carotid-to-subclavian bypass performed. Neither coverage of the left subclavian nor carotid-tosubclavian bypass was found to be an independent risk factor for stroke. Combining a history of prior stroke with extent A coverage resulted in a 60% stroke incidence (three of five patients; Table 6) Combining a history of stroke with extent C coverage resulted in a stroke incidence of 15% (2 of 13 patients). Combining either extent A or C coverage with a history of prior stroke resulted in a perioperative stroke incidence of 27.7% (5 of 18 patients). Preoperative CT scan of the aorta was analyzed in 117 of 171 patients. Grade IV atheromatous disease was present in 7 of 8 perioperative stroke patients and 35 of 109 patients without perioperative stroke. A CT grade IV atheroma was strongly associated with stroke (OR 14.8, CI 1.7 to 675.6, p ). Intraoperative EEG and SSEP monitoring was performed in 43 of 171 patients. The SSEP monitoring detected intraoperative stroke in one patient (patient No. 2 in Table 4). This patient had sudden loss of cortical SSEP amplitude from the right arm during the operation that persisted throughout the operation. The patient awoke with right arm weakness, and a stroke in the left middle cerebral artery distribution was confirmed by postoperative head CT scan. Intraoperative TEE was performed on two of seven patients who had intraoperative strokes. Analysis of the intraoperative TEE studies in those two patients showed grade V atheromatous disease characterized by protruding atheroma greater than 5 millimeters with mobile elements within the distal aortic arch.

5 Ann Thorac Surg GUTSCHE ET AL 2007;84: PERIOPERATIVE STROKE AFTER TEVAR 1199 Comment Stroke was identified as an important and relatively frequent complication of TEVAR with reported frequencies in individual clinical series that ranged from 2.3% to 8.2% (Table 1). In addition, stroke was associated with a high mortality rate in this patient population. Analysis of patients suffering stroke after TEVAR in our series support the importance of this complication. The neurologic examination and the pattern of brain infarction after perioperative stroke during TEVAR were consistent with cerebral embolization as the primary mechanism. The timing of perioperative stroke was consistent also with atheroembolism. The observation of acute ischemic stroke caused by atheroembolism during operation detected by intraoperative SSEP monitoring in one patient in the series added further support for the hypothesis that patients undergoing TEVAR are at risk for atheroembolic events. Instrumentation of the aortic arch in patients with severe atheromatous disease may not result in immediate atheroembolism but may disrupt vulnerable plaques, with subsequent development of superimposed thrombi that may embolize at a later time in the postoperative period [10]. This was the presumed mechanism for the delayed stroke that occurred on postoperative day number 5 in patient number 4 [Table 4]. The risk factors for stroke were identified as history of preoperative stroke, CT grade IV atheroma ( 5 mm) in the aortic arch or proximal descending aorta, and extent A or C coverage. These risk factors were significant predictors for perioperative stroke despite the small sample size. These risk factors for perioperative stroke further confirmed that cerebral atheroembolism was the mechanism of perioperative stroke in TEVAR. History of prior stroke, especially embolic stroke, indicated the presence of vulnerable atheroma in the thoracic aorta with an increased likelihood of dislodgement and subsequent cerebral embolism in response to wire or catheter instrumentation. Atheroma grade by CT scan also identified patients with severe atherosclerotic disease of the aortic arch and proximal descending thoracic aorta at risk for dislodgement and atheroembolism in response to instrumentation. The observation that only patients undergoing extent A or C coverage involving the distal aortic arch or proximal descending thoracic aorta had perioperative strokes suggested wire or catheter instrumentation of the aortic arch or proximal descending aorta was a necessary additional factor leading to cerebral atheroembolism and stroke in patients with vulnerable atheroma. These findings were consistent also with the existing experience in cardiac operations, indicating that severe atheromatous disease of the aorta combined with surgical manipulation of the aorta are important risk factors for perioperative stroke [11 13]. Grading the severity of atherosclerotic disease in the aortic arch and proximal descending aorta by chest CT scan was studied based on initial observations that cerebral atheroembolism was the most likely explanation for perioperative stroke after TEVAR. The ability to detect and quantify the severity of atheromatous disease in the aortic arch and proximal descending thoracic aorta with CT scan was feasible because most patients had high resolution CT imaging studies in preparation for TEVAR. Because there was no established score to grade the severity of atherosclerotic disease using CT imaging, a grading scale was developed based on established criteria used in transesophageal echocardiography (Table 2) [3]. One small published study [14] reported that CT imaging for detection of aortic atheroma in comparison with TEE had a sensitivity of 87% and a specificity of 82%. A CT grade IV atheromatous disease of the aortic arch or proximal descending thoracic aorta identified perioperative stroke with a sensitivity of 87.5%, but with a specificity of only 67.9%. One possible explanation for the low specificity of CT imaging of aortic atheroma to identify perioperative stroke patients was that CT images did not provide information on the stability of the atheroma because the technique cannot detect mobile elements within the atheroma. For this reason, although CT atheroma grade provided information about the atherosclerotic burden within the aorta, CT imaging could not discriminate within the group of high risk patients with grade IV disease; which individual patients would actually stroke in response to catheter or wire manipulations of the aorta. Prior studies using TEE have found that the presence of mobile atheroma was a strong predictor of vulnerability for atheroembolism [13, 15]. In our series, two patients who suffered perioperative stroke after TEVAR had mobile atheroma of the distal aortic arch and proximal descending aorta detected by intraoperative TEE. A potential limitation of the study was the small sample size and the findings will need to be validated in a larger clinical experience. In addition, not all patients had preoperative CT imaging studies that were satisfactory for grading of atheromatous disease and only a few patients had TEE studies. For this reason, the sensitivity and specificity of TEE for identifying mobile atheroma in this patient population and its ability to predict perioperative stroke after TEVAR could not be estimated. The sample size may have limited the statistical power to detect other patient characteristics or comorbidities that were significant predictors for perioperative stroke. Finally, subclinical strokes that were not manifested by focal neurologic deficits on a standard neurologic examination may have been missed. Similarly, postoperative brain imaging to detect the appearance of new brain infarctions was not performed in all patients and it was possible that the incidence of perioperative stroke after TEVAR may have been underestimated. Despite the limitations of the prospective observational study, the findings provided important information for guiding clinical decision making in patients undergoing TEVAR. For example, considering the morbidity associated with perioperative stroke, the risk of TEVAR requiring extent A or C coverage in patients with prior stroke, or mobile atheroma in the aortic arch or proximal descending thoracic aorta may require alternative surgical strategies. The TEE or CT characterization and localization of a vulnerable atheroma in the thoracic

6 1200 GUTSCHE ET AL Ann Thorac Surg PERIOPERATIVE STROKE AFTER TEVAR 2007;84: aorta may provide a useful guide to limit wire or catheter manipulations within the aorta to decrease the risk of cerebral embolism. It may be possible to refine endovascular techniques by developing safer catheters, by employing an umbrella to catch atheroembolic debris, or even combining endovascular stenting with supraaortic rerouting of the aortic arch branch vessels to increase the safety of TEVAR in patients at high risk for perioperative stroke. References 1. Makaroun MS, Dillavou ED, Kee ST, et al. Endovascular treatment of thoracic aortic aneurysms: results of the phase II multicenter trial of the GORE TAG thoracic endoprosthesis. J Vasc Surg 2005;41: Leurs LJ, Bell R, Degrieck Y, Thomas S, Hobo R, Lundbom J. Endovascular treatment of thoracic aortic diseases: combined experience from the EUROSTAR and United Kingdom Thoracic Endograft registries. 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J Thorac Cardiovasc Surg 1995;109: van der Linden J, Hadjinikolaou L, Bergman P, Lindblom D. Postoperative stroke in cardiac surgery is related to the location and extent of atherosclerotic disease in the ascending aorta. J Am Coll Cardiol 2001;38: Tenenbaum A, Garniek A, Shemesh J, et al. Dual-helical CT for detecting aortic atheromas as a source of stroke: comparison with transesophageal echocardiography. Radiology 1998;208: Fattori R, Nienaber CA, Rousseau H, et al. Results of endovascular repair of the thoracic aorta with the Talent thoracic stent graft: the Talent Thoracic Retrospective Registry. J Thorac Cardiovasc Surg 2006;132: Wheatley GH III, Gurbuz AT, Rodriguez-Lopez JA, et al. Midterm outcome in 158 consecutive Gore TAG thoracic endoprostheses: single center experience. Ann Thorac Surg 2006;81: Iyer VS, Mackenzie KS, Tse LW, et al. Early outcomes after elective and emergent endovascular repair of the thoracic aorta. J Vasc Surg 2006;43: Khoynezhad A, Donayre C, Bui H, Kopchok G, White R. Risk factors of neurological deficits following thoracic endografting. New York: Aortic Surgery Symposium; Patel HJ, Williams DM, Upchurch GR Jr, et al. Long-term results from a 12-year experience with endovascular therapy for thoracic aortic disease. Ann Thorac Surg 2006;82: DISCUSSION DR GRAYSON H. WHEATLEY (Phoenix, AZ): I have two questions. First, was there a difference of stroke rate by device that you have? I see [in] your study that multiple devices were used. Obviously the numbers are low, but did you see any differences in stroke rate by device? Second, is there a way do you think of standardizing the manipulation of the wires and device if you have a high risk patient? So, for example, make sure that you minimize the manipulation but do it in a very standardized way so that you have less manipulation and less potential for stroke in these patients? DR GUTSCHE: The answer to the first question is we did not find any association of stroke with any particular device. We actually analyzed that. Secondly, minimizing manipulation in the aortic arch, that may be a better question for Dr Bavaria, because manipulation with the wires, there is a certain amount that has to be done if you are going to place a stent. DR JOSEPH E. BAVARIA (Philadelphia, PA): The take-home message from our group is that if you have the combination of a preoperative stroke plus grade IV mobile atheromatous disease then you better have a very, very good indication for your operation. That is the first piece of important information from our data. We have actually changed our practices a little bit in that regard. As you saw, eight of the nine strokes had mobile atheromatous disease. The other issue is that, and this is a technical issue for Grayson s question, if we find that we have mobile atheromatous disease or some sort of higher stroke risk issues at the arch and the anatomy will allow us to avoid the arch and land the stent graft at the proximal landing zone below no man s land, if we can do that and the anatomy allows us to do that, then we will not place our wires past the left subclavian artery. This is another technical change we have made since we have had this data in our hands in an attempt to reduce stroke in high risk arch anatomy.