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Ann Thorac Surg 2008;85:987-992. doi:10.1016/j.athoracsur.2007.10.079
© 2008 The Society of Thoracic Surgeons
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Original Articles: Cardiovascular

Endovascular Repair for Penetrating Atherosclerotic Ulcers of the Descending Thoracic Aorta: Early and Mid-Term Results

Luca Botta, MDa, Katia Buttazzi, MDb, Vincenzo Russo, MDb, Mario Parlapiano, MDa, Valentina Gostoli, MDb, Roberto Di Bartolomeo, MDa, Rossella Fattori, MDb,*

a Cardiac Surgery, Cardiothoracovascular Department, University of Bologna, S. Orsola-Malpighi Hospital, Bologna, Italy
b Cardiovascular Radiology Unit, Cardiothoracovascular Department, University of Bologna, S. Orsola-Malpighi Hospital, Bologna, Italy

Accepted for publication October 24, 2007.

* Address correspondence to Dr Fattori, Cardiothoracovascular Department (Pad 21), University Hospital S. Orsola-Malpighi, Via Massarenti 9, Bologna, 40138, Italy (Email: rossella.fattori{at}unibo.it).


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 References
 
Background: Penetrating atherosclerotic ulcer is an acute aortic syndrome with a high incidence of complications and rupture. Until now, no generally accepted therapeutic regimen has been established because the natural history of penetrating atherosclerotic ulcers is extremely variable. We investigated the technical feasibility and the early and mid-term results of endovascular stent graft treatment in a consecutive series of patients who had penetrating ulcers.

Methods: From July 1997 to December 2006, 19 patients (14 men and 5 women) with a mean age of 71.8 ± 7.2 years were treated for penetrating ulcers. Seven patients presented with an acute and symptomatic penetrating atherosclerotic ulcer, and in 12 patients, the ulcerative process was chronic. Clinical and imaging follow-up was performed in all patients using computed tomography or magnetic resonance imaging.

Results: Technical success (insertion and deployment of the stent graft) was achieved in 18 of 19 cases. Neither paraplegia nor other perioperative complications occurred. Two patients treated under emergency conditions in whom the aortic syndrome was recognized after the acute onset died in the hospital (11.1%) of multiorgan failure. Follow-up has been completed in all patients, with a median time of 22 months (range, 3 to 108 months). Endoleaks occurred in 3 patients: 1 had surgical repair (5.6%), 1 leak sealed spontaneously, and 1 sealed after a second endovascular procedure. Late death occurred in 4 patients from non-aortic causes.

Conclusions: Endovascular stent graft repair is a low-invasive, attractive, and rational treatment option in aortic ulcers that provides satisfactory perioperative and mid-term results.


   Introduction
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 Abstract
 Introduction
Material and Methods
 Results
 Comment
 References
 
Penetrating atherosclerotic ulcers (PAUs) develop in patients with advanced atherosclerosis. The lesion is initially asymptomatic and confined to the intimal layer. Progression towards a deep atherosclerotic ulcer that penetrates through the elastic lamina and into the media may occur, leading to a complete rupture of the adventitial wall [1, 2]. Penetrating atherosclerotic ulcers have only recently been acknowledged among acute aortic syndromes as a distinct pathologic variant of classic aortic dissection [3, 4]. Recent studies have revealed the evolutive nature of symptomatic PAUs [3–6]. Penetrating atherosclerotic ulcers can be complicated by intramural hematoma, with a propensity towards development of a saccular aneurysm or pseudoaneurysm and a risk of aortic rupture.

Limited information is available about the natural history of PAUs or their therapeutic regimen. However, there is a general consensus about the high risk of disease progression in patients with recurrent thoracic pain, whereas asymptomatic ulcers may be managed conservatively [7–9]. In recent years, endovascular stent graft repair has been emerging as a less-invasive alternative to open surgical repair for patients with thoracic aortic disease [10, 11]. Endovascular repair may be promising in patients with PAU because these patients often present a variety of comorbidities, thus portending an increased surgical risk. This study analyzed the procedural feasibility, early and mid-term results, and clinical outcome of patients treated for PAUs during a 9-year period.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 References
 
Patients
This retrospective study was approved by the local Ethics Committee, and all involved patients provided a signed informed consent. From July 1997 to December 2006, 198 patients (160 men and 38 women; mean age, 57.2 ± 16.1 years), affected by thoracic aortic diseases underwent endovascular stent graft treatment. Of these, PAUs were present in 19 patients (9.6%), consisting of 14 men and 5 women with a mean age of 71.8 ± 7.2 years (range, 55 to 83 years). Penetrating atherosclerotic ulcer was defined as one or more focal, contrast material-filled outpouchings of the endoluminal border of the aortic wall, with or without intramural hemorrhage or limited parietal flap (Fig 1). The patients were at a mean American Society of Anesthesiologists (ASA) class of 3.6 ± 0.8. The mean diameters of the pseudoaneurysm, proximal neck, and distal neck were 55.1 ± 11.6, 31.9 ± 4.8, and 30.2 ± 4.9 mm, respectively. Monolateral or bilateral hemothorax was present in 4 patients. Previous cardiac or aortic operations, or both, were reported in 6 patients (31.6 %), consisting of three aortobisiliac grafts, two Bentall operations, and one isolated coronary artery bypass grafting. Renal insufficiency was found in 7 (36.8 %) patients and chronic obstructive pulmonary disease in 13 (68.4 %). Other patient characteristics and procedural data are summarized in Table 1.


Figure 1
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  		Fig 1. (A) Contrast-enhanced computed tomography scan reconstruction shows 3 simultaneous penetrating atherosclerotic ulcers (white arrows) of the descending thoracic aorta in a patient presenting with acute aortic syndrome. (B) Complete resolution of the ulcers is detected 3 months after endovascular repair.

 

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  		Table 1 Patient Characteristics and Procedural Data
 
Indications for Intervention
Seven patients were admitted under emergency conditions, with hemodynamic instability and imaging findings of an impending rupture. Signs of impending rupture were considered recurrent thoracic pain associated with periaortic hematoma, hemorrhagic pleural effusion, contrast media extravasation outside the adventitial wall, and rapid growth rate of the pseudoaneurysm. These patients underwent emergency procedures.

A chronic PAU was occasionally identified on computed tomography (CT) scan in the remaining 12 patients. In the initial follow-up, these patients were managed medically with β-blockers or vasodilators, or both, statins, and a yearly imaging study. Indications for treatment were aortic diameter exceeding 55 mm in 9 patients, an increase in diameter exceeding 10 mm/year in 4 patients after 1, 2, 3, and 4 years from first CT scan detection, and repeated thoracic pain during follow-up in 3 patients after 8 months, 1, and 2 years. Our algorithm with indications for intervention is shown in Figures 2 and 3. Go


Figure 2
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  		Fig 2. This algorithm shows the decision-making process for acute penetrating atherosclerotic ulcers (PAUs). Hemodynamic instability refers to uncontrolled blood pressure. The PAU is frequently associated with severe back/chest pain on admission or unrelenting pain.

 

Figure 3
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  		Fig 3. This algorithm shows the decision-making process for chronic penetrating atherosclerotic ulcers (PAUs).

 
Preoperative Examination and Location
All hemodynamically stable patients underwent routine examination of the heart, lung, liver, and kidney functions as well as contrast-enhanced CT, magnetic resonance imaging (MRI), angiography, or a combination. Hemodynamically compromised patients underwent CT just before emergency or urgent endovascular repair. Anatomic conditions allowing endovascular treatment were no aortic wall alteration (thrombus, severe atherosclerosis, intramural hemorrhage), a diameter of 42 mm or smaller at the proximal and distal necks, and diameter of the femoral or iliac arteries of 8 mm or larger. Length of landing zones exceeded 15 mm in all but 1 patient (<5 mm), who required a preventive subclavian–carotid bypass. The landing zone was involved with intramural hematoma only in this case. Preoperative imaging techniques showed PAUs were in the proximal third of the descending aorta in 18 patients, in the mid-third in 6, and in the distal third in 1 patient. No ulcers were detected in the distal arch or at the thoracoabdominal transition (Table 1). A single ulcer was observed in 13 patients (68.4%), and multiple outpouchings of the endoluminal border of the aortic wall were detected in 6 patients (31.6%).

Stent Graft and Interventional Procedure
Patients underwent general anesthesia and received mechanical ventilation. Blood pressure was monitored by right radial artery cannulation. Ceftriaxone (2 g intravenously) was administered before the procedure. Cerebrospinal fluid drainage was never used in this series of patients. The common femoral or the external iliac artery, or the iliac graft in patients previously operated on, were used for access after surgical exposure. Heparin (2500 IU) was generally administered, with the exception of patients who had active bleeding into the pleural and or mediastinal space. Angiography and transesophageal echocardiography (TEE) were used to identify the lesion, landing zones, and their relationship with the side branches. Thoracic stent grafts (Talent in 15 patients and Valiant in 3 patients, Medtronic, Santa Rosa, CA) were loaded on an extra-stiff guidewire and delivered under fluoroscopic and TEE control with induced hypotension (systolic pressure <70 mm Hg) to prevent the inadvertent downstream displacement of the stent graft during delivery. Because lowering blood pressure appears to be associated with a risk of delayed paralysis, the induced hypotension was maintained only for few seconds during the deployment of the device.

The proximal end of endografts was always an uncovered stent (free-flow end). On the basis of CT/MRI measurement, over-sizing of 10% to 15% was applied in the choice of stent graft diameter. Postprocedural angiography and TEE control were performed to reveal the final result.

Follow-Up Imaging
All patients underwent a strict follow-up protocol. Clinical examination, CT scan, or MRI controls were performed at discharge, at 1, 3, 6, and 12 months after treatment, and every 12 months thereafter. Follow-up was 100% complete.

Statistical Analysis
Incidence rates of events are reported by giving the number of patients experiencing the event followed by the corresponding percentage. Continuous data are reported as the mean ± standard deviation or median and the range of values. A paired-samples t test was used to compare mean preoperative and follow-up aortic diameters. The Kaplan-Meier actuarial method was used to generate survival estimates and is reported with 95% confidence limits. All statistical analyses were performed using the SPSS 14.0 software package (SPSS Inc, Chicago, IL).


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 References
 
Four patients underwent an emergency endovascular procedure at a mean time of 33.5 ± 14.9 hours from the acute onset of symptoms because of unstable imaging findings (periaortic hematoma and hemorrhagic pleural effusion) and a precarious hemodynamic condition (hemorrhagic shock in 2 patients). Three acute patients showed clinical or radiologic evidence of disease progression (increasing pleural effusion or periaortic hematoma, or both) during their in-hospital stay and underwent urgent stent graft repair within 3 to 8 days after the onset of symptoms.

Stent graft implantation was technically successful in 18 patients (94.7%). Blood loss was limited to less than 200 to 300 mL in all cases. Technical failure owing to the inadequate caliber of the femoral and iliac arteries occurred in 1 patient. Thirteen patients each received 1 stent graft, 3 patients each received 2 stent grafts, and 2 patients each received 3 stent grafts. Mean length of aortic coverage was 140.9 ± 35.9 mm. The entire thoracic aorta (from the left subclavian to celiac artery) was never covered. Only 1 patient required coverage of the aorta from T-6 to the celiac artery. Intraoperative mortality was 0%.

One patient required left subclavian artery (LSA) coverage due to an inadequate proximal landing zone. A subclavian–carotid bypass with proximal ligation of the LSA was preventively performed on this patient 1 week before the endovascular procedure. Postoperatively, 13 of 18 patients (72.2 %) were transferred to the intensive care unit (ICU). Median intubation time was 6 hours (range, 0 to 312 hours). Median lengths of stay were 18 hours (range, 12 to 312 hours) in the ICU and 6 days (range, 2 to 16 days) in the hospital. Only 2 patients received blood cell transfusions. Blood pressure was carefully controlled in all patients (systolic blood pressure <110 mm Hg).

Two patients treated under emergency conditions, who had been admitted in hemorrhagic shock with loss of consciousness and anuria, died in hospital (11.1%) of multiorgan failure despite successful procedures. In both patients, a bilateral hemothorax (>1000 mL) was drained after stent graft deployment. These patients were transferred from a tertiary hospital at 30 and 36 hours from the acute onset of symptoms because the PAU had not been identified at the initial evaluation.

None of the surviving patients had paraplegia or other perioperative complications. An early type II endoleak was detected in 1 patient, who underwent surgical repair 3 months later. In-hospital results are summarized in Table 2. Two patients showed late endoleaks. One sealed spontaneously during follow-up (type II endoleak), and adjunctive endovascular treatment with insertion of a graft extension allowed resolution of the type I endoleak in the other patient.


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  		Table 2 In-Hospital Results
 
The median follow-up period was 22 months (range, 3 to 108 months). A reduction of the mean diameters of the aortic segments involved was observed in all but 1 patient at the last follow-up compared with preoperative mean values: 51.7 ± 11.6 mm vs 55.1 ± 11.6 mm (p = 0.014). Neither stent-related deaths nor complications were detected at follow-up. Nevertheless, four late deaths, caused by respiratory failure and pancreatic cancer in 1 patient each, and cardiac arrest in 2 patients, occurred 3, 36, 32, and 40 months after endovascular repair. The overall survival rates were 88.9% at 30 days, 83.3% at 1 year, 72.2% at 3 years, and 66.7% at 5 years (Fig 4). Actuarial freedom from endoleaks was 94.1% at 1 month, 88.2% at 3 months, and 81.4% at 12, 24, and 60 months (Fig 5).


Figure 4
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  		Fig 4. Kaplan-Meyer estimate of overall survival (all-cause mortality). The line represents the product-limit estimate curve and the circles signify censored observations.

 

Figure 5
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  		Fig 5. Freedom from any type of endoleak.

 

   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
References
 
Epidemiology and Natural History of Penetrating Atherosclerotic Ulcers
First recognized by Shennan in 1934 [12], PAUs were further characterized by Stanson and colleagues [13] in 1986 and by Coady and colleagues [2] in 1998. The actual incidence of PAUs is still unknown, although the prevalence among symptomatic patients with suspected acute aortic syndrome is estimated as 2.3% to 7.6% [3–5]. Controversies exist about the natural history of PAUs. Harris and colleagues [14] reported that PAU progression is slow, with a low prevalence of acute rupture or other life-threatening complications, whereas many authors [4–6, 13, 15–17] report a more negative prognosis with respect to classic aortic dissection, with a high incidence of complications and rupture in up to 40% of symptomatic patients [6].

Predictors of Ulcer Progression
Recurrent and refractory pain may indicate an ongoing process and is considered to be one of the most important variables in determining the appropriateness of surgical intervention. In addition, a rapid diameter increase of the aortic ulcer as well as unrelenting pain or an interval increase in pleural effusion, or both, and periaortic hematoma have been identified as predictors of disease progression [5, 7, 18].

Imaging Findings
The limited longitudinal extension of the aortic lesion may result in difficult detection, even with advanced imaging techniques, if no adequate CT multiformat reconstructions are performed. A rapid recognition of the disease can be of paramount importance in addressing the appropriate therapeutic choices. In the imaging evaluation before endovascular repair, particular attention should also be paid to vascular access, considering the diffuse atherosclerotic vascular disease of these patients, which can compromise the possibility of stent graft insertion and deployment.

Therapeutic Options
Currently, no generally accepted therapeutic regimen has been established. Asymptomatic patients may be managed medically with reasonable safety although a strict follow-up is mandatory to detect early signs of disease progression [1, 4]. In a population of patients with PAUs initially managed with medical therapy, Cho and colleagues [9] reported one-third required surgical repair during follow-up for the progression of PAUs to aneurysms, dissections, or perforations. Several authors suggest a more aggressive treatment approach, especially in symptomatic patients [2, 5, 15–17, 19].

Despite improvements in surgical techniques and postoperative care, conventional operative repair of the descending thoracic aorta for penetrating ulcers is still associated with high morbidity and mortality rates [5, 6, 14, 20, 21]. Patients with PAUs are usually elderly, with a variety of comorbidities that result in an increased surgical risk. Unlike classic aortic dissection, a PAU is usually a focal, localized lesion representing an ideal anatomic target for self-expandable stent graft [4, 8, 22]. Endovascular repair seems to be a promising option showing lower morbidity and mortality rates with respect to open surgical repair [8, 18, 22].

Complete exclusion of the PAU was achieved with a single stent graft in 72.2% of our patients. However, even if a PAU is usually a localized lesion, the aortic wall is often affected by a diffuse atherosclerotic process, which increases the risk of endoleaks. Endoleak occurred in 3 of 16 patients (18%) of our series during follow-up, one of them probably related to a diseased aortic wall at the neck site. Two patients who were admitted to the hospital under emergency conditions with free exsanguination into the periaortic and the pleural spaces died of multiorgan failure despite successful endovascular treatment. In these patients, both admitted from a tertiary hospital, the diagnosis of a PAU had been determined more than 24 hours after the onset of symptoms, resulting in hemorrhagic shock and multiorgan damage. The relative rarity of this disease, the difficult detection of PAUs even with advanced imaging techniques, and the lack of precise guidelines about management of this entity may result in diagnostic delay that negatively influences the outcome.

Spinal Cord Protection
Spinal cord protection remains a concern for endovascular repair of the descending thoracic aorta. The lack of aortic cross-clamping, the minimal intraoperative blood loss, fewer hemodynamic and fluid shift changes (both resulting in less hypotension), and the tolerance for higher blood pressure (absence of surgical sutures) can reduce the risk of spinal cord ischemia with respect to surgical repair. Paraplegia after endovascular repair has been reported with a low incidence (1% to 5%) and seems to be associated with a long aortic coverage, especially in patients previously operated on for an abdominal aortic aneurysm [23]. In this series, we never covered the entire thoracic aorta, even in the 2 patients who received 3 endografts. Only 1 patient had the stent graft positioned from T6 to L2. In every patient, we limited the period of induced hypotension just to the deployment of the device, avoiding abrupt intraoperative and perioperative hemodynamic changes.

Despite the absence of cerebrospinal fluid drainage, no paraplegia or paraparesis was observed in our series. However, we believe that intraoperative selective cerebrospinal fluid drainage may be helpful in reducing the incidence of paraplegia in patients who require a total aortic coverage or when coverage involves high-risk segments of the thoracic aorta (below T6), especially in case of previous surgical procedures on the abdominal aorta or in the presence of femoroiliac disease.

Conclusions
Endovascular repair in penetrating aortic ulcers is a less-invasive, attractive, and rational treatment option with low perioperative and mid-term morbidity and mortality rates, even in high-risk, symptomatic patients treated under emergency conditions. Mid-term results show a substantial durability of the procedure despite the diffuse aortic wall involvement.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 

  1. Hayashi H, Matsuoka Y, Sakamoto I, et al. Penetrating atherosclerotic ulcer of the aorta: imaging features and disease concept Radiographics 2000;20:995-1005.[Abstract/Free Full Text]
  2. Coady MA, Rizzo JA, Hammond GL, Pierce JG, Kopf GS, Elefteriades JA. Penetrating ulcer of the thoracic aorta: what is it? How do we recognize it? How do we manage it? J Vasc Surg 1998;27:1006-1015.[Medline]
  3. Vilacosta I, San Roman JA, Aragoncillo P, et al. Penetrating atherosclerotic aortic ulcer: documentation by transesophageal echocardiography J Am Coll Cardiol 1998;32:83-89.[Abstract/Free Full Text]
  4. Eggebrecht H, Herold U, Schmermund A, et al. Endovascular stent-graft treatment of penetrating aortic ulcer: Results over a median follow-up of 27 months Am Heart J 2006;151:530-536.[Medline]
  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;106:342-348.[Abstract/Free Full Text]
  6. 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;123:1051-1059.[Abstract/Free Full Text]
  7. Troxler M, Mavor AI, Homer-Vanniasinkam S. Penetrating atherosclerotic ulcers of the aorta Br J Surg 2001;88:1169-1177.[Medline]
  8. Brinster DR, Wheatley 3rd GH, Williams J, Ramaiah VG, Diethrich EB, Rodriguez-Lopez JA. Are penetrating ulcers best treated using an endovascular approach? Ann Thorac Surg 2006;82:1688-1691.[Abstract/Free Full Text]
  9. Cho KR, Stanson AW, Potter DD, Cherry KJ, Schaff HV, Sundt 3rd TM. Penetrating atherosclerotic ulcer of the descending thoracic aorta and arch J Thorac Cardiovasc Surg 2004;127:1393-1401.[Abstract/Free Full Text]
  10. Fattori R, Napoli G, Lovato L, et al. Descending thoracic aortic diseases: stent-graft repair Radiology 2003;229:176-183.[Abstract/Free Full Text]
  11. Nienaber CA, Fattori R, Lund G, et al. Nonsurgical reconstruction of thoracic aortic dissection by stent-graft placement N Engl J Med 1999;340:1539-1545.[Abstract/Free Full Text]
  12. Shennan T. Dissecting aneurysms. Medical Research Council, Special Report Series, No. 193. 1934.
  13. Stanson AW, Kazmier FJ, Hollier LH, et al. Penetrating atherosclerotic ulcers of the thoracic aorta: natural history and clinicopathological correlations Ann Vasc Surg 1986;1:15-23.[Medline]
  14. Harris JA, Bis KG, Glover JL, Bendick PJ, Shetty A, Brown OW. Penetrating atherosclerotic ulcers of the aorta J Vasc Surg 1994;19:90-99.[Medline]
  15. Cooke JP, Kazmier FJ, Orszulak TA. The penetrating aortic ulcer: pathologic manifestations, diagnosis, and management Mayo Clin Proc 1988;63:718-725.[Medline]
  16. Welch TJ, Stanson AW, Sheedy 2nd PF, Johnson CM, McKusick MA. Radiologic evaluation of penetrating aortic atherosclerotic ulcer Radiographics 1990;10:675-685.[Abstract]
  17. Benitez RM, Gurbel PA, Chong H. Penetrating atherosclerotic ulcer of the aortic arch resulting in extensive and fatal dissection Am Heart J 1995;129:821-823.[Medline]
  18. Eggebrecht H, Baumgart D, Schmermund A, et al. Penetrating atherosclerotic ulcer of the aorta: treatment by endovascular stent-graft placement Curr Opin Cardiol 2003;18:431-435.[Medline]
  19. Nienaber CA, Sievers HH. Intramural hematoma in acute aortic syndrome Circulation 2002;106:284-285.[Free Full Text]
  20. Kouchoukos NT, Masetti P, Rokkas CK, Murphy SF. Hypothermic cardiopulmonary bypass and circulatory arrest for operations on the descending thoracic and thoracoabdominal aorta Ann Thorac Surg 2002;74:S1885-S1887.[Abstract/Free Full Text]
  21. Svensson LG, Crawford ES. Aortic dissection and aortic aneurysm surgery: clinical observations, experimental investigations, and statistical analyses; II Curr Probl Surg 1992;29:915-1007.
  22. Demers P, Miller DC, Mitchell RS, Kee ST, Chagonjian L, Dake, MD. Stent-graft repair of penetrating atherosclerotic ulcers in the descending thoracic aorta: midterm results Ann Thor Surg 2004;77:81-86.[Abstract/Free Full Text]
  23. 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;132:332-339.[Abstract/Free Full Text]

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