Extent of Aortic Coverage and Incidence of Spinal Cord Ischemia After Thoracic Endovascular Aneurysm Repair

Extent of Aortic Coverage and Incidence of Spinal Cord Ischemia After Thoracic Endovascular Aneurysm Repair Robert J. Feezor, MD, Tomas D. Martin, MD, Philip J. Hess Jr, MD, Michael J. Daniels, ScD, Thomas M. Beaver, MD, Charles T. Klodell, MD, and W. Anthony Lee, MD Divisions of Vascular Surgery and Endovascular Therapy, and Thoracic and Cardiovascular Surgery, Department of Surgery, and Division of Biostatistics, Department of Epidemiology and Biostatistics, University of Florida, Gainesville, Florida Background. Risk factors for spinal cord ischemia (SCI) after thoracic endovascular aneurysm repair (TEVAR) remain unclear. Aortic coverage was examined as a risk factor for SCI using quantitative three-dimensional computed tomography angiography (CTA) analysis. Methods. The medical records, radiographic imaging studies, and a prospectively maintained database of all TEVAR procedures performed during a 7-year period were retrospectively reviewed. Preoperative anatomic dimensions and postoperative graft path lengths were measured from CTAs using curved planar and orthogonal multiplanar reformations along centerline paths. SCI was defined as transient or permanent lower extremity neurologic deficit without associated intracerebral hemispheric events. Results. Of 326 TEVAR cases, 241 patients (74%) had satisfactory imaging. Thirty-three (10%) had SCI. These patients were older (72.7 10.6 vs 64.7 15.8 years, p 0.005) and had longer intraoperative procedure times (137 65 vs 113 68 minutes, p 0.05). Despite similar total lengths of native thoracic aorta (295.0 36.3 vs 283.1 39.8 mm, p 0.17), patients with permanent SCI had a greater absolute (260.5 40.9 vs 195.8 81.6 mm, p 0.002) and proportionate (88.8% 12.1% vs 67.6% 24.0%, p 0.001) length of aortic coverage. The average length of uncovered aorta proximal to the celiac artery in patients with SCI was 17.3 21.8 mm vs 63.1 62.9 mm in patients without SCI (p 0.0006). Neither the patency of the hypogastric arteries nor left subclavian artery was associated with SCI. Conclusions. The extent and distal location (relative to the celiac artery) of aortic coverage were associated with an increased risk of SCI. Prophylactic measures for spinal cord protection should be considered in patients whose thoracic aortas require extensive coverage. (Ann Thorac Surg 2008;86:1809 14) 2008 by The Society of Thoracic Surgeons Spinal cord ischemia (SCI) is a devastating complication after surgical or endovascular repair (TEVAR) of the thoracic aorta. The results from the W. L. Gore TAG (Flagstaff, AZ) pivotal trial reported a 30-day incidence of SCI of 3% [1], which was significantly lower than that reported with open surgical repair. Risk factors for SCI after TEVAR are multifactorial and have been previously reported to include length of aortic coverage [2], prior abdominal aortic aneurysm (AAA) repair [3], hypotension [4], iliac artery injury [5], renal failure [6], and left subclavian artery coverage [6]. Although the putative mechanism of loss of direct intercostal perfusion in SCI appears intuitive, occurrence of symptoms are inconsistent and seemingly unpredictable. In this study we examined the role of thoracic aortic coverage by the endograft in the development of SCI Accepted for publication Sept 4, 2008. Presented at the Forty-fourth Annual Meeting of The Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 28 30, 2008. Address correspondence to Dr Lee, Division of Vascular Surgery and Endovascular Therapy, 1600 SW Archer Rd, Ste NG-45, PO Box 100286, Gainesville, FL 32610-0286; e-mail: anthony.lee@surgery.ufl.edu. using quantitative analysis of preoperative and postoperative computed tomography angiography (CTA) data sets. Material and Methods The medical records, radiographic imaging studies, and a prospectively maintained database of all thoracic endovascular procedures performed at a single tertiarycare medical center between September 2000 and May 2008 were retrospectively reviewed. CTA of the chest, abdomen, and pelvis was performed using a timedbolus, intravenous contrast enhanced technique acquired at 2-mm collimation. The data set was reconstructed and postprocessed using the Aquarius Workstation (TeraRecon, San Mateo, CA). Anatomic dimensions and endograft path lengths were measured from three-dimensional (3D) reconstructions using curved planar and orthogonal multiplanar reformation along centerline paths. The first postoperative CTA, which was typically performed either before discharge or at 1-month, was compared with the preoperative CTA. 2008 by The Society of Thoracic Surgeons 0003-4975/08/$34.00 Published by Elsevier Inc doi:10.1016/j.athoracsur.2008.09.022

1810 FEEZOR ET AL Ann Thorac Surg SPINAL CORD ISCHEMIA AFTER TEVAR 2008;86:1809 14 Table 1. The Incidence of Any and Permanent Spinal Cord Ischemia Based on Aortic Pathology Aortic Pathology No. No SCI, No. (%) Any SCI, No. (%) p Value a Perm SCI, No. (%) p Value a TAA 164 145 (88) 19 (12) 0.46 5 (3) 0.29 Dissection 80 70 (88) 10 (13) 0.40 7 (9) 0.05 Ulcer 43 39 (91) 4 (9) 1.00 2 (5) 1.00 Transection 21 21 (100) 0 (0) 0.15 0 (0) 0.61 Other 18 18 (100) 0 (0) 0.23 0 (0) 1.00 a Values for p are calculated for the incidence of SCI for each pathology relative to the aggregate of other patients. Perm permanent; SCI spinal cord ischemia; TAA thoracic aortic aneurysm. SCI was defined as any new lower extremity motor or sensory deficit, or both, in the absence of any documented intracerebral hemispheric events. A patient who was fully ambulatory preoperatively must have been able to bear his or her own weight without assistance to be considered neurologically intact. SCI was considered transient (vs permanent) when a clear deficit was documented and then fully resolved at the time of discharge. When a patient s symptoms had improved but his or her functional status was not completely restored to preoperative levels, the complication was considered permanent. Spinal drainage was not performed prophylactically in most patients. Patients were admitted postoperatively to the cardiac intensive care unit, where neurologic exams were performed hourly. Upon detection of symptoms, the blood pressure was elevated to a systolic pressure of more than 160 mm Hg (mean arterial pressure of 100 mm Hg) with vasopressors or fluids, or both, and if it had not been performed preoperatively, a spinal drainage catheter was promptly ( 2 hours of symptoms) inserted by a cardiac anesthesiologist. The catheter was placed 10 cm above the level of the heart and adjusted higher or lower depending on therapeutic effect and amount of spinal fluid drainage. Drainage was limited to less than 15 ml/h or 350 ml/24 h to avoid potential complications of subdural hematoma or cerebral herniation. The catheter was left to drain for 72 hours. If therapeutic effect was achieved, the catheter was clamped for another 24 hours in case symptoms returned, and then it was removed. Continuous data were analyzed using a two-tailed t test and categoric variables using the Fisher exact test, with p 0.05 considered statistically significant. Univariate and multivariate logistic regression models were constructed using a set of 20 potential predictors: age, sex, American Society of Anesthesiologists (ASA) classification, urgency of the procedure, total duration of procedure, fluoroscopy time, contrast volume, preoperative spinal drainage, endograft type, anesthetic technique, blood loss, use of an iliac conduit, history of AAA repair, aortic pathology, total thoracic aortic length (from left common carotid artery to celiac artery), length of total aortic coverage, length of proximal uncovered aorta, length of distal uncovered aorta, left subclavian artery (L SCA) perfusion, and hypogastric artery patency. Odds ratio (OR) estimates were reported with 95% confidence intervals (CIs). This study was approved by the Institutional Review Board with waiver of informed consent. Results Between September 2000 and May 2008, 326 TEVARs were performed. The mean age of the patients was 65.5 15.5 years, and 222 (68%) were men. Comorbidities included hypertension (69%), coronary artery disease (49%), tobacco use (42%), chronic obstructive pulmonary disease (20%), renal insufficiency (16%), cerebrovascular occlusive disease (13%), diabetes mellitus (12%), and peripheral vascular occlusive disease (9%). Postoperative complications occurred in 121 patients (37.1%) comprising 57 neurologic (17%), 26 pulmonary (8%), 21 renal (6%), 20 hemorrhagic (6%), 17 ischemic (5%), 13 cardiac (4%), 8 wound (2%), and 7 gastrointestinal (2%) complications. Overall median length of stay was 5 days (range, 1 to 79 days) and 30-day or in-hospital mortality was 7.4% (24 of 326). Kaplan-Meier estimates of late mortality were 81%, 74%, and 66% at 6, 12, and 24 months, with a median survival of 42.3 months. SCI occurred in 33 patients, (10%) of SCI, and 14 (4%) were permanent. The distribution of aortic pathologies treated and the incidence of SCI in each category are compiled in Table 1. Univariate analyses of preoperative and intraoperative risk factors in the development of any SCI and the subset that had permanent SCI are summarized in Table 2. Any (temporary or permanent) SCI was associated with age (72.7 10.6 vs 64.7 15.8 years, p 0.005), procedure time (137 65 vs 113 68 minutes, p 0.05), fluoroscopy time exceeding 35 minutes (27% vs 13%, p 0.04), and general anesthesia (82% vs 64%, p 0.05). Variables not associated with SCI included gender, ASA classification, urgency of procedure, the device implanted, blood loss, the use of an iliac conduit, prior AAA repair, and the pathology being treated. Of interest was that there was no difference between prophylactic and expectant placement of a spinal drain in the development of SCI. In the subset of 14 of 326 patients (4%) who had permanent SCI, procedure time exceeding 140 minutes (50% vs 22%, p 0.03), fluoroscopy time (31.4 17.4 vs 23.3 14.0 minutes, p 0.04), general anesthesia (93% vs 65%, p 0.04), blood loss exceeding 350 ml (43% vs 18%, p 0.03), and aortic dissection (50% vs 22%, p 0.03) were significant risk factors.

Ann Thorac Surg FEEZOR ET AL 2008;86:1809 14 SPINAL CORD ISCHEMIA AFTER TEVAR 1811 Table 2. Univariate Analyses of Clinical Variables in the Development of Any and Permanent Spinal Cord Ischemia Variable No SCI Any SCI p Value Transient or No SCI Perm SCI p Value Patients, No. (%) 293 (90) 33 (10)... 312 14... Age, mean SD, years 64.7 15.8 72.7 10.6 0.005 65 16 73 9 0.06 Male, No. (%) 195 (67) 27 (82) 0.08 211 (68) 11 (79) 0.56 ASA IV, No. (%) 187 (64) 26 (79) 0.12 197 (63) 12 (86) 0.10 Emergency, No. (%) 46 (16) 8 (24) 0.22 49 (16) 5 (36) 0.06 Procedure time, min Mean SD 113 68 137 65 0.05 113 67 164 95 0.007 140, No. (%) 64 (22) 13 (39) 0.03 70 (22) 7 (50) 0.03 Fluoroscopy time, min Mean SD 23 14 28 15 0.07 23 14 31 17 0.04 35, No. (%) 38 (13) 9 (27) 0.04 42 (14) 5 (36) 0.04 Contrast, mean SD, ml 133 50 141 50 0.38 133 49 159 66 0.06 Prophy spinal drain, No. (%) 79 (27) 8 (24) 0.99 85 (27) 2 (14) 0.37 TAG, No. (%) 226 (77) 26 (79) 0.99 239 (77) 13 (93) 0.20 GETA, No. (%) 188 (64) 27 (82) 0.05 202 (65) 13 (93) 0.04 Estimated blood loss, ml Mean SD 313 362 324 180 0.86 310 351 400 234 0.34 350 ml, No. (%) 55 (19) 8 (24) 0.49 57 (18) 6 (43) 0.03 Iliac conduit, No. (%) 53 (18) 7 (21) 0.64 55 (18) 5 (36) 0.15 AAA repair, No. (%) 51 (17) 6 (18) 0.99 47 (17) 1 (7) 0.48 Adequate imaging, No. (%) 218 (74) 23 (70) 0.54 232 (74) 9 (64) 0.37 Aortic length, mean SD, mm a 283 40 295 36 0.17 284 40 290 42 0.66 Aortic coverage Total, mm 196 82 261 41 0.0001 199 81 273 47 0.007 Relative, % 68 24 89 12 0.0001 69 24 94 7 0.002 Uncovered distance from L CCA Total, mean SD, mm 26 38 24 24 0.8 26 38 9 12 0.18 Relative, % 9 14 8 8 0.68 9 13 3 4 0.17 Uncovered distance from celiac Total, mean SD, mm 63 63 17 22 0.0001 61 62 8 8 0.01 Relative, % 24 25 6 7 0.0001 23 24 3 3 0.01 L SCA perfusion, No (%) b 174 (80) 19 (83) 0.99 185 (80) 6 (67) 0.39 Patent hypogastric artery 0, No. (%) 4 (2) 0 (0) 0.99 4 (2) 0 (0) 1.00 1, No. (%) 16 (8) 3 (14) 0.39 18 (8) 1 (13) 0.50 2, No. (%) 188 (90) 18 (86) 0.45 199 (90) 7 (88) 0.58 a Left common carotid artery to celiac artery. b Includes those cases with either uncovered or revascularized left subclavian artery. AAA abdominal aortic aneurysm; ASA American Society of Anesthesiology; GETA general endotracheal anesthesia; L CCA left common carotid artery; L SCA left subclavian artery; Perm permanent; Prophy prophylactic; TAG TAG endograft (W. L. Gore and Associates, Flagstaff, AZ). Quantitative 3D-CTA Analysis Satisfactory preoperative and postoperative CT angiograms were available in 241 patients (74%), 23 of whom had SCI (9%). The reasons for exclusion of the remaining 85 patients are listed in Table 3. Select baseline characteristics of those with and without adequate imaging were compared (Table 4) to ascertain that the former subset was representative of the overall cohort. The only significant difference was a higher proportion of traumatic aortic transections among those with adequate imaging (8% vs 1%, p 0.02). More importantly, the incidences of any (10% vs 12%, p 0.54) and permanent (4% vs 6%, p 0.37) SCI were similar between those who did and did not have adequate imaging. On centerline analysis, the preoperative length of the thoracic aorta (distal margin of left common carotid artery to the proximal margin of the celiac artery) was similar between SCI and no-sci groups (295.0 36.3 mm vs 283.1 39.8 mm, p 0.17). However, the absolute length of aortic coverage (260.5 40.9 mm vs 195.8 81.6 mm, p 0.001) and the fractional length of coverage, calculated as length of covered aorta/total aortic length (88.8% 12.1% vs 67.6% 24.0%, p 0.001), were both significantly greater in patients with SCI. This held true for the subset of those with permanent SCI compared with those without SCI (272.9 46.9 mm vs 199.2 80.7 mm, p 0.007), but not significantly compared with those with only temporary SCI (272.9 46.9 mm vs 252.5 36.1 mm, p 0.17).

1812 FEEZOR ET AL Ann Thorac Surg SPINAL CORD ISCHEMIA AFTER TEVAR 2008;86:1809 14 Table 3. Reasons for Exclusion of the 85 Patients Who Did Not Undergo Three-Dimensional Quantitative Analysis Reason SCI was strongly associated with the distal extent of thoracic aortic coverage. The mean length of uncovered aorta proximal to the celiac artery was 17.3 21.8 mm in patients with SCI compared with 63.1 62.9 mm in those without SCI (p 0.0001). When expressed as a fraction of the total aortic length, SCI patients had relatively less uncovered aorta distally (5.7% 7.0% vs 23.8% 24.6%, p 0.0001; Fig 1A and B). This difference was also seen between those who had transient and permanent SCI (22.4 25.6 mm vs 8.4 8.3 mm, p 0.06). On the other hand, the extent of proximal coverage as measured by the distance from the left common carotid artery to the proximal covered edge of the endograft did not differ between SCI and no-sci patients (absolute 23.7 24.4 mm vs 25.8 38.4 mm, p 0.80, fractional 7.9 % 8.2% vs 9.1% 13.7%, p 0.68). A multivariate logistic regression model showed the absolute length of total aortic coverage and the length of distal uncovered aorta were both independently associated with a higher incidence of (temporary/permanent) SCI (Table 5). Specifically, for every 2 cm of additional thoracic aortic coverage, the risk of SCI increased by 30% (95% confidence interval [CI], 1.1 to 1.5; p 0.0006). Conversely, every 2 cm of uncovered distal thoracic aorta was associated with a 40% decrease in the risk of SCI (95% CI, 0.42 to 0.87; p 0.006). Other independent risk factors for SCI included age (OR, 1.6; 95% CI, 1.1 to 2.2; p 0.006) and the use of general anesthesia (OR, 2.5; 95% CI, 1.0 to 6.3; p 0.05). Comment No. (%) a Adequate imaging 241 (74) No post-op imaging 35 (11) Inadequate post-op CT imaging b 16 (5) Abdominal or aortic arch debranching 34 (10) a Percentages are given for the total group of 326 patients. b Criteria for inadequate imaging included one or more of the following: noncontrast scans, poor arterial opacification, motion artifact and/or incomplete thoracic aortic coverage, and/or acquisition at more than 3-mm collimation. CT computed tomography imaging. Historically, the risk of SCI after TEVAR has been reported to be less than 10% and less than that typically associated with open repair (14%) [7]. The W. L. Gore TAG (W. L. Gore & Associates, Flagstaff, AZ) pivotal trial reported a 2.9% incidence of SCI among 139 patients who had repair of descending thoracic aneurysms [1]. Although the overall incidence of any SCI in our study was higher than what had been previously published, the subset of those who had permanent deficit was 4%, which is similar to other reports. Furthermore, we had included all forms of paraparesis as well as complete paraplegia in our definition of SCI. In a study of 153 Table 4. Comparison of Patients Who Had Adequate and Inadequate Imaging Variable a Adequate Imaging (n 241) Inadequate Imaging (n 85) p Value Any SCI 23 (10) 10 (12) 0.54 Permanent SCI 9 (4) 5 (6) 0.37 Age, years 64.5 16.4 68.2 12.6 0.06 Male 165 (68) 57 (67) 0.89 Pathology TAA 103 (43) 45 (53) 0.13 Ulcer 36 (15) 7 (8) 0.14 Dissection 59 (24) 18 (21) 0.66 Transection 20 (8) 1 (1) 0.02 Other 23 (10) 14 (14) 0.11 Emergency 43 (18) 11 (13) 0.40 GETA 153 (63) 62 (73) 0.14 a Categoric data are presented as number (%), and continuous data as mean standard deviation. GETA general endotracheal anesthesia; SCI spinal cord ischemia; TAA descending thoracic aortic aneurysm. patients who underwent TEVAR for a variety of aortic pathologies, the incidence of any symptoms of SCI was 5.2%, but of permanent SCI was 3.9% [8]. On univariate Table 5. Multivariate Logistic Regression Analysis of Variables That Influenced the Development of any Spinal Cord Ischemia Variable OR (95% CI) p Value Age (every 10 years) 1.6 (1.1 2.2) 0.006 Male 2.3 (0.90 5.7) 0.08 ASA class IV 2.3 (0.95 5.4) 0.06 Emergency 1.7 (0.73 4.0) 0.22 Procedure time (every 60 min) 1.3 (0.98 1.6) 0.07 Fluoroscopy time (every 10 min) 1.2 (0.98 1.5) 0.07 Contrast (every 10 ml) 1.0 (0.96 1.1) 0.38 Prophylactic spinal drainage 1.2 (0.50 2.7) 0.74 TAG 1.1 (0.46 2.6) 0.83 General endotracheal anesthesia 2.5 (1.0 6.3) 0.05 Estimated blood loss (every 50 ml) 1.0 (0.96 1.1) 0.86 Iliac conduit 1.2 (0.50 3.0) 0.66 AAA repair 1.6 (0.61 4.4) 0.33 Aortic length (every 20 mm) a 1.2 (0.93 1.4) 0.17 Aortic coverage (every 20 mm) 1.3 (1.1 1.5) 0.0004 Uncovered distance From L CCA (every 25 mm) 0.99 (0.87 1.1) 0.81 From celiac (every 20 mm) 0.61 (0.42 0.87) 0.006 L SCA perfusion b 1.2 (0.39 3.7) 0.75 Patent hypogastric artery 0.84 (0.28 2.5) 0.75 a Left common carotid artery to celiac artery. b Includes those cases with either uncovered or revascularized left subclavian artery. AAA abdominal aortic aneurysm; ASA American Society of Anesthesiologists; L CCA left common carotid artery; L SCA left subclavian artery; TAG TAG endograft (W. L. Gore and Associates, Flagstaff, AZ).

Ann Thorac Surg FEEZOR ET AL 2008;86:1809 14 SPINAL CORD ISCHEMIA AFTER TEVAR 1813 Fig 1. (A) Fractional coverage of the aorta in patients with spinal cord ischemia (SCI). (B) Fractional coverage of the aorta in patients without any SCI. The lengths of coverage have been normalized from the distal margin of the left common carotid artery to the proximal margin of the celiac artery. analysis, the study showed that aneurysmal disease (p 0.073), an iliac conduit (p 0.004), and occluded hypogastric artery (p 0.042) were significant risk factors. Variables that were not associated with SCI included emergency procedures, prior abdominal aortic operation, blood loss, general anesthesia, intraoperative hypotension, and left subclavian coverage [8]. Our current study examined the risk of SCI as a function of thoracic aortic coverage. We found that the total length of aortic coverage was greater in patients with SCI, with a mean difference of approximately 6.5 cm or 20% of the thoracic aorta. Furthermore, not only the absolute length but also the distal extent of coverage was strongly associated with SCI. Mechanistically, this secondary observation would be anatomically consistent given the distal origin of the Artery of Adamkiewicz (arteria magna), which arises from T11 to L3 levels. The exact mechanism of SCI after thoracic aortic repair remains unclear and is clearly multifactorial. Spinal cord perfusion is a net function of highly variable and differential contributions from the intercostals [9] and their principle collateral vessels, namely the lumbar, vertebral, and hypogastric arteries [10], which can develop compensatory changes in chronic aortic diseases or after surgical aortic replacement. It stands to reason that any systemic conditions that result in hypoperfusion of these vessels, especially intercostal arteries, will also increase the chances of SCI [11]. Although an association between left subclavian artery coverage and SCI had been previously suggested [6], neither our study nor the one by Khoynezhad and colleagues [8] found such a correlation. Despite its apparent anatomic basis, the actual contribution to overall spinal cord perfusion by one or both proximal branches of the anterior spinal artery is difficult to determine, and we do not believe that this alone justifies prophylactic left subclavian artery revascularization. Currently, the main indications for preoperative subclavian artery bypass are a dominant left vertebral artery with a diminutive right vertebral artery or a patent left internal mammary artery

1814 FEEZOR ET AL Ann Thorac Surg SPINAL CORD ISCHEMIA AFTER TEVAR 2008;86:1809 14 graft to the left anterior descending coronary artery, or both. To this end, CTA imaging of the intracranial circulation is routinely performed as part of preoperative imaging. The incidence of symptomatic left arm claudication is extremely small, but in those rare instances revascularization may be performed electively in the postoperative period. The association between prior AAA repair and SCI has also been inconsistent among published reports. The results in our study (2% vs 5%, p 0.70) were similar to the results of the TAG pivotal trial (4.7% vs 2.1%, p NS), which did not find any difference in the rates of SCI between those with and without prior AAA repair [1]. A history of abdominal aortic replacement is likely a surrogate marker for decreased spinal cord perfusion as it relates to the lumbar arteries. Similar to the anterior spinal artery, the contribution of this or any other single blood supply to the development of clinically significant SCI cannot be easily determined. An important weakness of our study is the lack of adequate postoperative imaging data in 85 of the 326 patients (26%). In 34 of these excluded patients, they involved abdominal or aortic arch debranching procedures, and the extent of endograft coverage was outside the proximal or distal limits, or both, of our quantitative analysis. Of the remaining 51 patients, 35 (11%) had no postoperative imaging and 16 (5%) had inadequate imaging as a result of early death or lost follow-up because of transfer to another facility. It should be noted, however, that both the rates of any SCI and permanent SCI were similar between those with and without adequate imaging at 10% vs 12% (p 0.54) and 4% vs 6% (p 0.37), respectively. In conclusion, using quantitative 3D analysis of CT angiograms, our study showed a significant association with the extent of aortic coverage and the development of SCI. The need for sufficient proximal and distal aortic fixation to achieve a successful short and long-term repair must be weighed against the increased risk of spinal cord ischemia, especially for distal thoracic pathologies. Therefore, in cases which require greater than 200 mm of thoracic aortic coverage or distal coverage within 20 mm of the celiac artery, prophylactic measures for spinal cord protection should be considered. 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;41:1 9. 2. Gravereaux EC, Faries PL, Burks JA, et al. Risk of spinal cord ischemia after endograft repair of thoracic aortic aneurysms. J Vasc Surg 2001;34:997 1003. 3. Baril DT, Carroccio A, Ellozy SH, et al. Endovascular thoracic aortic repair and previous or concomitant abdominal aortic repair: is the increased risk of spinal cord ischemia real? Ann Vasc Surg 2006;20:188 94. 4. Weigang E, Hartert M, Siegenthaler MP, et al. Perioperative management to improve neurologic outcome in thoracic or thoracoabdominal aortic stent-grafting. Ann Thorac Surg 2006;82:1679 87. 5. Cheung AT, Pochettino A, McGarvey ML, et al. Strategies to manage paraplegia risk after endovascular stent repair of descending thoracic aortic aneurysms. Ann Thorac Surg 2005;80:1280 8. 6. Buth J, Harris PL, Hobo R, et al. Neurologic complications associated with endovascular repair of thoracic aortic pathology: Incidence and risk factors. A study from the European Collaborators on Stent/Graft Techniques for Aortic Aneurysm Repair (EUROSTAR) Registry. J Vasc Surg 2007; 46:1103 11. 7. Bavaria JE, Appoo JJ, Makaroun MS, et al. Endovascular stent grafting versus open surgical repair of descending thoracic aortic aneurysms in low-risk patients: a multicenter comparative trial. J Thorac Cardiovasc Surg 2007;133:369 77. 8. Khoynezhad A, Donayre CE, Bui H, et al. Risk factors of neurologic deficit after thoracic aortic endografting. Ann Thorac Surg 2007;83:S882 9. 9. Lazorthes G, Gouaze A. [Supply routes of arterial vascularization of the spinal cord. Applications to the study of vascular myelopathies]. Bull Acad Natl Med 1970;154:34 41. 10. Strauch JT, Spielvogel D, Lauten A, et al. Importance of extrasegmental vessels for spinal cord blood supply in a chronic porcine model. Eur J Cardiothorac Surg 2003;24: 817 24. 11. Griepp RB, Griepp EB. Spinal cord perfusion and protection during descending thoracic and thoracoabdominal aortic surgery: the collateral network concept. Ann Thorac Surg 2007;83:S865 9. DISCUSSION DR WILLIAM L. HOLMAN (Birmingham, AL): That is an interesting study. It gives me some hope that this terrible complication can be minimized. The question I had is the duration of these measures, and whether they are prophylactic or not. Let s say you are placing an aortic stent with some periprocedural measure of neurologic function in place, and then things start to go bad. Presume that you drain CSF [cerebrospinal fluid], increase the blood pressure, and do other things with improvement of neurological function. How long must you maintain these special conditions and how will you know when it s safe to restore normal physiology without having spinal ischemia? DR FEEZOR: Our typical course is to leave the spinal drain in place at a level of 10 cm of water for 24 hours. If the neurological events stabilize or improve, then we clamp the spinal drain for 24 additional hours, with ongoing neurologic monitoring, then remove the spinal drain if the patient remains asymptomatic. As far as the blood pressure is concerned, generally we pharmacologically raise the systolic blood pressure to 160 to 180 mm Hg for 2 to 4 days. DR ROBERT S. D. HIGGINS (Chicago, IL): Do you have any other insights about how you manage those dissection patients now with this information in hand? DR FEEZOR: Endovascular treatment of aortic dissection is evolving. I think that when we anticipate greater lengths of coverage, we are more apt to put in spinal drains prophylactically. A little bit depends on the chronicity of dissection. Complicated acute dissections with malperfusion or rupture tend to have worse outcomes than chronic dissections.