Endovascular stent-graft treatment of penetrating aortic ulcer

Peripheral Vascular Disease

Endovascular stent-graft treatment of penetrating aortic ulcer: Results over a median follow-up of 27 months Holger Eggebrecht, MD,a Ulf Herold, MD,b and Axel Schmermund MDaAlexander Y. Lind MDaOliver Kuhnt MDa Stefan Martini MDaHilmar Ku ¨ hl MDcPeter Kienbaum MDdJu ¨ rgen Peters MDdHeinz Jakob MDb Raimund Erbel MDaDietrich Baumgart, MDa Essen, Germany

Background Penetrating aortic ulcer (PAU) is increasingly acknowledged as a pathological variant of classic falselumen aortic dissection with a high incidence of bleeding complications and rupture in up to 40% of patients. The objective of this study was to investigate the results of endovascular stent-graft placement for the treatment of patients with PAUs. Methods

Between July 1999 and December 2004, endovascular stent-graft repair of PAU was performed in 22 patients (69.1 F 7.8 years, 16 men), 3 (14%) of whom had contained aortic rupture. Stent-graft placement was performed in the cardiac catheterization laboratory with the patient under general anesthesia, using a surgical access.

Results Procedural success was achieved in all but 1 patient (technical success rate 96%). Postoperatively, 1 (5%) patient had minor stroke with transient amentia. There were no other inhospital complications or deaths. During a median follow-up of 27 (range 1-62) months, 1 patient underwent adjunctive stent-graft placement for type I endoleak. Three patients died unrelated to the aortic disease late during follow-up. Overall survival rates were 100% at 30 days, 100% at 1 year, 82.5% F 11.3% at 2 years, and 61.9% F 20.0% at 5 years. Conclusions Endovascular stent-graft treatment is an effective treatment for patients with PAU and is associated with low procedural morbidity. Both acute and midterm mortality of this novel treatment concept appear to be favorable compared with the natural course of the disease. (Am Heart J 2006;151:530- 6.) Although first described in 1934,1 penetrating atherosclerotic ulcer (class 4 aortic dissection according to Svensson et al2) of the aorta has only recently been acknowledged as a distinct pathological variant of classic false-lumen aortic dissection.3 Owing to improved vascular imaging techniques, penetrating aortic ulcer (PAU) is increasingly encountered in patients with acute aortic syndromes.4,5 Penetrating aortic ulcers are caused by rupture of an aortic atherosclerotic plaque through the internal elastic lamina into the media and may be complicated by intramural hematoma (IMH) formation due to erosion of vasa vasorum, development of (pseudo)aneurysm, or From the Departments of a Cardiology, bCardio-thoracic Surgery, cDiagnostic and Interventional Radiology, and dAnesthesiology and Intensive Care Medicine, WestGerman Heart Center Essen, University of Duisburg–Essen, Essen, Germany. This study was supported by a research grant from the University Duisburg–Essen, Essen, Germany (IFORES 10+2) (Dr Eggebrecht). Submitted March 18, 2005; accepted May 9, 2005. Reprint requests: Holger Eggebrecht, MD, Department of Cardiology, University of Duisburg–Essen, Hufelandstrage 55, 45122 Essen, Germany. E-mail: [email protected] 0002-8703/$ - see front matter n 2006, Mosby, Inc. All rights reserved. doi:10.1016/j.ahj.2005.05.020

aortic rupture.6 Recent studies revealed the malignant nature of PAU.5,7 It has been suggested that the presence of PAU in combination with IMH is particularly ominous. The risk for aortic rupture during initial hospital admission may be higher in patients presenting with PAU compared with that in patients with classic aortic dissection.8 Even after initial medical stabilization, the propensity of PAU toward development of aneurysm or pseudoaneurysm during long-term follow-up may result in late aortic rupture and require early or late operation.9,10 Therefore, a more aggressive therapeutic approach (ie, early surgical graft replacement of the aorta) is now advocated in symptomatic patients, particularly in those with unrelenting pain, increasing pleural effusion, or with a large or expanding PAU.7,11 Over recent years, endovascular stent-graft placement is emerging as a less invasive alternative to open surgery for patients with thoracic aortic disease.12,13 Endovascular repair may also be promising in patients with PAU, particularly as these patients are usually elderly with a variety of comorbidities, thus portending an inherently increased surgical risk.14,15 So far, however, only short-term results of endovascular repair in patients with PAU have been reported. In the light of

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Table I. Patient characteristics

Table II. Lesion characteristics All patients (n = 22)

Age (y) Sex (male-female) Body mass index (kg/m2) ASA classification Candidates for open repair Estimated risk for surgery (logistic Euro-SCORE)* Hypertension COPD Impaired renal function CAD Initial presentation with acute aortic syndrome Interval between onset and procedure (d)*

69.1 F 7.8 (48-86) 16:6 25.3 F 3.2 (20-33) 3.1 F 0.4 (3-5) 12 (55) 16.04 (6.67-68.14) 22 1 9 12 14 36

(100) (5) (41) (55) (64) (0-112)

Values are presented as mean F SD (range) or n (%) unless otherwise noted. ASA, American Society of Anesthesiologists; COPD, chronic obstructive pulmonary disease; CAD, coronary artery disease. *Median (range).

our encouraging initial results with stent-graft placement in 10 patients with PAU,16 we have expanded the use of endovascular stent-graft placement to now 22 patients. The present study details our experience over a period of 5 years.

All patients (n = 22) Location of the ulcer Distal arch Descending thoracic aorta Thoracoabdominal aorta Infrarenal aorta Concomitant pseudoaneurysm Contained aortic rupture Presence of IMH Increasing ulcer size Multiple ulcers Max ulcer depth (mm) Max ulcer diameter (mm) Max aortic diameter (mm)

3 (14) 13 (59) 4 (18) 2 (9) 12 (55) 3 (14) 13 (59) 10 (46) 6 (27) 14 F 8 (5-36) 17 F 8 (6-34) 41 F 12 (19-66)

Values are presented as mean F SD (range) or n (%).

stent-grafts) for the individual patient. Tailored stent-graft devices were shorter (60-90 mm) than the conventional stentgraft devices (100-200 mm) and were used in very focal lesion to just cover the lesion, but not otherwise bhealthyQ parts of the aorta. In general, the endoprostheses were sized 4-mm larger than measurements taken from contrast-enhanced CT scans to ensure secure anchoring of the endoprostheses.

Stent-graft procedure

Methods Patient population Between July 1999 and December 2004, 89 patients (70 men, average age 65 F 13 years) underwent endovascular aortic stentgraft placement at our institution. Of these, 22 (25%) patients had PAU. Penetrating aortic ulcer was defined as z1 focal, contrast material–filled, craterlike outpouchings of the endoluminal border of the aortic wall with or without concomitant IMH formation. Written informed consent for vascular access and stent-graft placement was obtained from every patient.

Preinterventional imaging All hemodynamically stable patients routinely underwent a preinterventional vascular staging that included the use of contrast-enhanced computed tomography (CT) or magnetic resonance imaging, transesophageal echocardiography (TEE), and aortography as well as coronary angiography. In patients with hemodynamic compromise, diagnosis and localization of PAU were confirmed using standard criteria by TEE and/or CT, immediately before urgent stent-graft placement.

Stent-graft prosthesis In 18 (86%) patients, self-expandable endoprostheses with circumferential nitinol stent springs arranged in a zigzag formation sandwiched between thin layers of a polyester graft membrane (Talent; Medtronic Vascular, Santa Rosa, CA) were used. In the remaining patients, self-expanding nitinol stents with expanded polytetrafluoroethylene graft material (GoreTAG; WL Gore Inc, Flagstaff, AZ) were used. The size of the delivery system and introducer sheath, respectively, ranged between 20F and 24F. The stent-grafts were available in standard configurations (n = 20 stent-grafts) or tailored (n = 3

Stent-graft placement was performed in the cardiac catheterization laboratory by a team of cardiologists, cardiothoracic surgeons, and anesthesiologists. All patients were under general anesthesia receiving mechanical ventilation. The operative field was prepared under sterile conditions. Ceftriaxone (2 g intravenous) was administered before the procedure. Direct surgical access through the aorta was necessary in a single (5%) patient because of insufficient luminal diameters of both femoral arteries; in all other patients, the femoral artery was used for access after surgical exposure. After exposition of the femoral artery and insertion of a standard 6F arterial sheath, 5000 IU of heparin was administered. A biplane angiogram was obtained using a graduated 6F pigtail catheter with metallic markers to determine the optimal stent-graft landing zones and its relation to side branches (ie, left subclavian artery). The stent-graft delivery system was advanced over an ultrastiff 0.035-in guidewire (Meier Back-Up; Boston Scientific, Natick, MA). The stent-grafts were positioned into the thoracic aorta under fluoroscopic guidance. Additional guidance by TEE or intravascular ultrasound was used in 15 (71%) and 9 (43%) patients, respectively. Before the stentgraft was deployed, systolic blood pressure was lowered to approximately 65 mm Hg using intravenous sodium nitroprusside to prevent inadvertent downstream displacement of the stent-graft during delivery. Immediate procedure success was evaluated using biplane angiography and TEE. No additional heparin or antiplatelet medications were administered after completion of the procedure.

Follow-up All patients were subjected to a strict follow-up protocol. Clinical examination and imaging of the aorta by contrastenhanced CT or magnetic resonance imaging and TEE were

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Figure 1

Contrast-enhanced CT scan showing 2 adjacent PAUs of the distal descending thoracic aorta (A and B) in a patient presenting with acute aortic syndrome. C to F, Rapid progression of the ulcers during short-term follow-up. G and H, Result 4 months after successful stent-graft treatment with complete resolution of the ulcers.

performed before discharge; after 3, 6, and 12 months; and then annually. A chest x-ray was performed at every follow-up visit to exclude mechanical stent failure (fracture) or dislocation.

Definitions and statistical analysis Patient’s clinical health status was evaluated according to the classification of the American Society of Anesthesiologists.17 For each patient, the logistic European System for Cardiac Operative Risk Evaluation (Euro-SCORE) was used to predict the individual mortality risk for conventional surgery.18 For the Euro-SCORE, the predicted mortality of surgery (in percent) was calculated by adding the weights assigned to each risk factor, as previously described. Procedural success was defined by technically successful deployment of the endoprosthesis at the intended target location. Primary success was defined as complete exclusion of the PAU without additional intervention.15 Secondary success was defined as complete PAU exclusion after any type of secondary intervention. Major adverse vascular events (MAVE) were defined comprehensively as a composite end point including (1) any early or late aortic-related or sudden unexplained death (without autopsy), (2) procedure-related or aorta-related major complications (eg, stroke, paraplegia), or (3) need for aortic reinterventions (ie, adjunctive stent-graft placement or surgery).19 Endoleaks were categorized as previously proposed (type I, insufficient sealing of the proximal or distal part of the stent-graft; type II, retrograde flow from collateral branches; type III, endoleak due to fabric tears, stent-graft defects, or modular disconnection; type IV, porosity of the stent-graft membrane).20

All statistical analyses were performed using the SPSS software package (version 11.0; SPSS, Chicago, IL). Continuous variables are presented as mean F 1 SD (range) or median (range), and categorical variables are presented using frequencies and percentages. The Kaplan-Meier nonparametric method was used to generate estimates of survival and freedom from MAVE. The Kaplan-Meier curves of patients with PAU were compared using the log-rank test to according Kaplan-Meier curves of 38 patients who underwent stent-graft placement for classic false-lumen aortic dissection at our institution during the study period, as was recently published.21

Results Patient demographics Baseline characteristics of our patients are given in Table I. There were 16 male and 6 female patients with an age of 69.1 F 7.8 (48-86) years. Of the 22 patients, 14 (64%) initially presented with acute aortic syndrome. Of these, 3 (14%) patients had contained aortic rupture and were treated immediately. The remaining 11 (50%) patients presenting with acute aortic syndrome were stabilized medically at first, but 10 showed clinical or radiological evidence of disease progression during short-term follow-up, and thus underwent urgent stentgraft placement within 12 to 66 days after onset of symptoms (Table II, Figure 1). The indication for stentgraft placement in the 8 of the 22 patients presenting

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Table III. Procedural data

Table IV. Postoperative morbidity and mortality All patients (n = 22)

Technical success Surgical access Femoral artery Aorta Stent-grafts per patient* N1 stent-graft used Stent-graft diameter (mm)* Stent-graft length (mm)* Procedure length (min) Fluoroscopy time (min) Contrast media (mL) Concomitant coronary stent placement Intraoperative use of TEE Intraoperative use of IVUS

21 (96) 20 1 1 2 34 130 137 F 61 9.6 F 5.4 242 F 140 3 15 9

(95) (5) (1-3) (10) (24-46) (60-200) (50-276) (2-23) (84-526) (14) (71) (43)

Values are presented as mean F SD (range) or n (%) unless otherwise noted. IVUS, intravascular ultrasound. *Median (range).

without acute symptoms was the presence of enlarging saccular (pseudo)aneurysms (bgiant ulcersQ).

Early outcomes Procedural success was obtained in all but 1 (96%) patient (Table III). No surgical conversions were necessary. Concomitant percutaneous coronary interventions were successfully performed in 3 patients. One stent-graft was implanted in 19 (90%) patients, 2 stent-grafts were implanted in 1 (5%) patient, and 3 stent-grafts in another (5%) patient. Overall, 1.1 F 0.5 stent-grafts with a median length of 130 mm were implanted during the index procedure. Complete ulcer sealing was achieved in 20 of 21 patients, yielding a primary success rate of 91%. A mild distal type I endoleak was detected immediately in a single patient and required successful implantation of a second stentgraft 4 weeks after the initial procedure (secondary success rate 96%). All but 1 patient were extubated on the day of the stent-graft procedure. The median length of stay in the intensive care unit was 2 (0-29) days (Table IV). The median inhospital stay was 12 (4-38) days. There was 1 (5%) procedure-related inhospital complication: a 70-year-old patient had a minor stroke with transient mental disorientation but no motoric or sensible deficit. He recovered completely after 2 days without sequelae. There were no deaths within the 30-day period. Late outcomes The median follow-up period was 27 (1-62) months. Eight patients had a follow-up of N30 months, and 3 patients had N60 months. In 1 patient with infrarenal PAU, progression of previously documented bilateral renal artery stenoses and subsequent renal failure prompted surgical revascularization 12 months after the

All stented patients (n = 21) ICU stay (d) Hospital stay (d) Early endoleak Conversion to open repair Paraplegia Stroke 30-day mortality

2 (0-29) 12 (4-38) 1 (5) 0 0 1 (5) 0

Values are presented as median (range) or n (%). ICU, intensive care unit.

stent-graft procedure. During surgery of the renal arteries, the intact stent-graft in the infrarenal aorta was surgically explanted and the diseased aortic segment was replaced with a Dacron graft owing to the surgeons’ decision. There were no other major complications or aorticrelated deaths during follow-up. Nevertheless, there were 3 late deaths but unrelated to the aortic disease: a female patient died 18 months after the procedure because of severe congestive heart failure, a male patient died after 21 months because of thyroid cancer, and another patient died at home 54 months after the procedure. The overall survival rates were 100% at 30 days, 100% at 1 year, 82.5% F 11.3% at 2 years, and 61.9% F 20.0% at 5 years (Figure 2). The corresponding freedom from MAVE rates were 95.2% F 4.7% at 30 days, 89.3% F 7.2% at 1 year, 78.1% F 12.2% at 2 years, and remained at 78.1% F 12.2% at 5 years (Figure 3). Comparison with patients who underwent stent-graft placement for classic false-lumen aortic dissection showed no difference with respect to overall survival (Figure 2). There was a nonsignificant trend ( P = .0768) toward a better freedom from MAVE in patients with PAU, which was primarily related to less reinterventions in these patients as compared with those in dissection patients (Figure 3).

Imaging follow-up In 18 patients with a follow-up of N6 months, all stentgrafts were patent without evidence of migration, twisting, or fracture. Ten (56%) patients showed radiological evidence of ulcer regression with complete thrombosis and shrinkage. In 7 (39%) patients, complete resolution with apparent incorporation of the ulcer into the aortic wall was observed (Figure 4). A single asymptomatic patient showed evidence of disease progression developing a new PAU proximal to the previously stented aortic segment and is scheduled for elective endovascular repair.

Discussion The present study indicates that endovascular stentgraft repair of PAU can be achieved with high technical success rates and low morbidity and mortality. Moreover,

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Figure 2

Figure 3

Kaplan-Meier estimate of overall survival (all-cause mortality) in comparison to patients with classic false-lumen aortic dissection.21 AD indicates patients with classic false-lumen aortic dissection.

Kaplan-Meier estimate of freedom from MAVE in comparison to patients with classic false-lumen aortic dissection.21

our results suggest that the promising short-term results are sustained during extended follow-up with respect to both clinical and morphologic outcome. During a median follow-up period of 27 months, no deaths related to aortic disease were encountered. The MAVE-free survival at 5 years was 78.1% F 12.2%. Rather, different degrees of disease regression up to complete PAU resolution were observed in all but a single patient, without evidence of late dilatation of the diseased aortic segment. The prevalence of PAU among symptomatic patients with suspected acute aortic syndromes is estimated as 2.3% to 7.6%4,5; however, the actual incidence of PAU is unknown. Symptoms of PAU may be very similar to those of acute classic false-lumen aortic dissection (eg, sudden onset of severe chest or back pain), and patients cannot be distinguished reliably based on clinical presentation alone. Unlike classic aortic dissection, PAUs are usually focal lesions limited to a short segment of the aorta. Conceptually, such localized lesions appear to be ideal anatomic targets for stentgraft treatment.15 In the present study, complete exclusion of the PAU without need for additional interventions (ie, primary success) was achieved in 91%. In 90% of our patients, a single stent-graft was sufficient to exclude the lesion and only occasionally a second or third stent-graft had to be placed. This is very similar to the results by Demers et al15 reporting a

primary success rate of 92%. In their series, N1 stentgraft was required in 4 of 26 treated patients. The localized nature of PAU may be favorable with respect to the risk for procedure-related paraplegia.11 Although the incidence of neurologic complications is low (1%-3%) compared with conventional surgery (up to 21%), stroke and paraplegia in particular remain the most dreaded complications of endovascular repair.22,23 At present, it is not completely understood which effect of endovascular repair results in the development of paraplegia. However, coverage of numerous potentially critical intercostal arteries by the stent-graft is commonly believed to evoke an increased risk for paraplegia.24 In particular, simultaneous abdominal and thoracic aortic repair, with loss of lumbar and intercostals arteries, appears to pose an increased risk for spinal cord damage caused by insufficient collateral circulation.23,25 In the present study, no case of paraplegia or paraparesis was observed after stent-graft placement. So far, however, 3 cases of paraplegia (1 transient, 2 permanent) have been reported in 70 patients undergoing endovascular repair of PAU, which warrants further research.11 We encountered 1 case of procedure-related minor stroke with transient neurologic deficit. It is commonly believed that periprocedural stroke occurs because of manipulation of the relatively rigid guidewire or stentgraft delivery system within the aortic arch. This may be

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Figure 4

A, Multiplanar reconstruction of contrast-enhanced CT showing a PAU with large pseudoaneurysm formation (giant ulcer) and secondary IMH (asterisk) of the mid-descending thoracic aorta (arrow). B, Immediate postinterventional result showing complete exclusion and thrombosis of the ulcer with residual IMH. C, CT 4 months after successful stent-graft placement showing complete resolution of both PAU and IMH.

of particular concern in patients with PAU because these are usually elderly patients with advanced atherosclerosis. Further technical developments and miniaturization of the relatively rigid stent-graft devices will hopefully help to decrease the risk for periprocedural stroke. The localized nature of PAU may further be favorable with respect to reinterventions. In this regard, only a single patient required adjunctive stent-graft placement for mild type I endoleak, which was already present at conclusion of the initial procedure but did not resolve spontaneously. As a consequence of less reinterventions as compared with patients with classic dissection, there was a trend toward a better MAVE-free survival in patients with PAU. Several studies revealed the malignant nature of PAU.3,5,7,8 Coady et al8 showed that the risk for aortic rupture in patients with symptomatic PAU was higher than in patients with classic aortic dissection (40% vs 4% for Stanford type B dissections). At present, rupture cannot be reliably predicted in patients presenting with PAU. Presence of pain at admission may indicate an ongoing pathological process with a higher probability of life-threatening complications.26 In addition, the diameter of the involved aortic segment may be an important predictor of rupture.8 However, aortic rupture may still occur in patients with normal-sized aortas.4 Unrelenting pain and/or interval increase in pleural effusion have recently been identified as predictors of disease progression.5 Ganaha et al5 also reported that the size and depth of the ulcer are important predictors of disease progression. Therefore, a more aggressive treatment approach (ie, surgical graft replacement) is now advocated in symptomatic high-risk patients.7,11 Surgery of the descending thoracic aorta is, however,

still associated with high morbidity and mortality despite remarkable improvements in surgical and anesthesiologic techniques.27 Patients with PAU are usually elderly with a variety of comorbidities and thus have an inherently increased surgical risk. Accordingly, the predicted mortality risk for open surgery in our patients ranged between 7% and 68% (median 16%). Cho et al10 recently showed that patients with PAU may also be managed conservatively with reasonable safety, even in the acute setting. Surgical repair, in their retrospective analysis, was associated with an excess in early mortality of 21% compared with 4% with medical treatment. Therefore, the authors advocated a more expectant approach in the management of patients with PAU. However, progressive dilation of the diseased aortic segment resulting in late development of saccular aneurysms was observed in 48% of the medically treated patients, which may require late operation.9,10 In this regard, sealing of PAU by the stent-graft decreases wall stress and thus provides stabilization of the diseased aortic segment,16 although it cannot be considered bcurativeQ as in the sense of surgical replacement.15 However, our results suggest that endovascular stentgraft repair may preserve aortic integrity and thus prevent aortic rupture or aneurysm formation in the long-term course but can also be used successfully in emergency situations for contained aortic rupture, as performed in 3 of our patients. The indication for treatment in asymptomatic patients is more complex. At present, these patients are usually managed medically with reasonable safety. However, close surveillance including repeat imaging is mandatory to detect any signs of disease progression as early as possible. This is of particular importance because, in our

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experience, clinical or radiological signs of disease progression were found, even during short-term followup, in almost all our patients who initially presented with acute aortic syndrome. All of our patients had complications of PAU or were considered at high risk for complications; endovascular stent-graft placement was thus performed in lieu of surgical repair.

Limitations Our study is limited by the relatively small number of patients treated. However, the overall incidence of PAU is low. In the present study, we reported our experience with a median follow-up of 27 months. Long-term followup studies in larger patient numbers are necessary to assess the durability and effectiveness of endovascular repair. Furthermore, we presented the imaging follow-up of only 18 of 21 successfully treated patients, which may introduce selection bias. However, we believe that a sufficient follow-up time interval is crucial to evaluate morphologic changes of the aorta after stent-graft placement, and thus, only patients with imaging followup of N 6 months were included. It is an inherent limitation of our approach that the natural course of the disease in our patients remains unknown. All patients were considered to be at high risk for complications and therefore underwent stent-graft placement. However, we cannot rule out that our patients would have done well with medical treatment alone. Clinical implications Our follow-up results over a median of 27 months indicate that endovascular stent-graft treatment of patients with PAU using second-generation stent-graft prostheses is effective and is associated with low operative morbidity and mortality, even in patients with aortic rupture. The localized nature of PAU appears to represent an ideal anatomic target for stent-grafting.

References 1. Shennan T. Dissecting aneurysms. Medical Research Council, special report series no 193. London: HSMO; 1934. 2. Svensson LG, Labib SB, Eisenhauer AC, et al. Intimal tear without hematoma: an important variant of aortic dissection that can elude current imaging techniques. Circulation 1999;99:1331 - 6. 3. Stanson AW, Kazmier FJ, Hollier LH, et al. Penetrating atherosclerotic ulcers of the thoracic aorta: natural history and clinicopathologic correlations. Ann Vasc Surg 1986;1:15 - 23. 4. Vilacosta I, San Roman JA, Aragoncillo P, et al. Penetrating atherosclerotic aortic ulcer: documentation by transesophageal echocardiography. J Am Coll Cardiol 1998;32:83 - 9. 5. Ganaha F, Miller DC, Sugimoto K, et al. Prognosis of aortic intramural hematoma with and without penetrating atherosclerotic ulcer: a clinical and radiological analysis. Circulation 2002;106:342 - 8. 6. Erbel R, Alfonso F, Boileau C, et al. Diagnosis and management of aortic dissection. Eur Heart J 2001;22:1642 - 81.

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7. Tittle SL, Lynch RJ, Cole PE, et al. Midterm follow-up of penetrating ulcer and intramural hematoma of the aorta. J Thorac Cardiovasc Surg 2002;123:1051 - 9. 8. Coady MA, Rizzo JA, Hammond GL, et al. Penetrating ulcer of the thoracic aorta: what is it? How do we recognize it? How do we manage it? J Vasc Surg 1998;27:1006 - 15. 9. Harris JA, Bis KG, Glover JL, et al. Penetrating atherosclerotic ulcers of the aorta. J Vasc Surg 1994;19:90 - 8. 10. Cho KR, Stanson AW, Potter DD, et al. Penetrating atherosclerotic ulcer of the descending thoracic aorta and arch. J Thorac Cardiovasc Surg 2004;127:1393 - 9. 11. Eggebrecht H, Baumgart D, Schmermund A, et al. Penetrating atherosclerotic ulcer of the aorta: treatment by endovascular stentgraft placement. Curr Opin Cardiol 2003;18:431 - 5. 12. Dake MD, Miller DC, Semba CP, et al. Transluminal placement of endovascular stent-grafts for the treatment of descending thoracic aortic aneurysms. N Engl J Med 1994;331:1729 - 34. 13. Nienaber CA, Fattori R, Lund G, et al. Nonsurgical reconstruction of thoracic aortic dissection by stent-graft placement. N Engl J Med 1999;340:1539 - 45. 14. Murgo S, Dussaussois L, Golzarian J, et al. Penetrating atherosclerotic ulcer of the descending thoracic aorta: treatment by endovascular stent-graft. Cardiovasc Intervent Radiol 1998;21: 454 - 8. 15. Demers P, Miller DC, Mitchell RS, et al. Stent-graft repair of penetrating atherosclerotic ulcers in the descending thoracic aorta: mid-term results. Ann Thorac Surg 2004;77:81 - 6. 16. Eggebrecht H, Baumgart D, Schmermund A, et al. Endovascular stent-graft repair for penetrating atherosclerotic ulcer of the descending aorta. Am J Cardiol 2003;91:1150 - 3. 17. Schneider AJ. Assessment of risk factors and surgical outcome. Surg Clin North Am 1983;63:1113 - 26. 18. www.euroscore.org. 19. Nienaber CA, Zanetti S, Barbieri B, et al. Investigation of stent-grafts in patients with type B aortic dissection: design of the INSTEAD trial — a prospective, multicenter, European randomized trial. Am Heart J 2005;149:592 - 9. 20. Chaikof EL, Blankensteijn JD, Harris PL, et al. Reporting standards for endovascular aortic aneurysm repair. J Vasc Surg 2002;35:1048 - 60. 21. Eggebrecht H, Herold U, Kuhnt O, et al. Endovascular stent-graft treatment of aortic dissection: determinants of post-interventional outcome. Eur Heart J 2005;26:489 - 97. 22. Dake MD. Endovascular stent-graft management of thoracic aortic diseases. Eur J Radiol 2001;39:42 - 9. 23. Tiesenhausen K, Amann W, Koch G, et al. Cerebrospinal fluid drainage to reverse paraplegia after endovascular thoracic aortic aneurysm repair. J Endovasc Ther 2000;7:132 - 5. 24. Fattori R, Napoli G, Lovato L, et al. Descending thoracic aortic diseases: stent-graft repair. Radiology 2003;229:176 - 83. 25. Mitchell RS, Miller DC, Dake MD, et al. Thoracic aortic aneurysm repair with an endovascular stent graft: the bfirst generationQ. Ann Thorac Surg 1999;67:1971 - 4. 26. Troxler M, Mavor AI, Homer-Vanniasinkam S. Penetrating atherosclerotic ulcers of the aorta. Br J Surg 2001;88:1169 - 77. 27. Kouchoukos NT, Masetti P, Rokkas CK, et al. Hypothermic cardiopulmonary bypass and circulatory arrest for operations on the descending thoracic and thoracoabdominal aorta. Ann Thorac Surg 2002;74:S1885 - 7.