Short and midterm results with minimally invasive endovascular repair of acute and chronic thoracic aortic pathology

Article Outline

• Abstract
• Patients and methods
  • Procedural details and devices
  • Follow-up
• Results
  • Patient demographics
  • Early mortality
  • Early complications
  • Follow-up
  • Late mortality
  • Nonfatal late complications
• Discussion
• Author contributions
• Acknowledgment
• References
• Copyright

Objectives

Endovascular management of both acute and chronic thoracic aortic pathology has emerged as an alternative to open surgery. We reviewed our single center experience with endovascular devices for the treatment of thoracic aortic pathology.

Methods

Between April 2000 and October 2007, 116 thoracic aortic stent grafts were placed to treat a variety of acute or chronic thoracic aortic lesions. Thirty-five percent of the cases were performed emergently. Sixty-five percent of the patients were male; the average age was 63.9 years (range 20-93 years). Indications for treatment were chronic degenerative aneurysms (n = 70), traumatic aortic disruption (n = 20), complicated dissection, intramural hematoma, or penetrating aortic ulcer (n = 14), pseudoaneurysm (n = 10), and Diverticulum of Kommerell (n = 2). Arch vessel revascularization (n = 32) or mesenteric debranching (n = 7) was performed in select cases. Devices used were industry-approved thoracic aortic devices (n = 80), aortic cuff extenders (n = 19), or custom made by the surgeon (n = 17).

Results

The 30-day death, stroke and paraplegia/paresis rates were 5.2%, 8.6%, and 2.6%, respectively. Arterial access complications requiring immediate operative repair occurred at a rate of 11.2% (n = 13). The endoleak rate requiring repeat intervention was 6.9% (n = 8). The delayed graft infection rate was 5.2% (n = 6), with four of these cases resulting in death. The mean follow-up is 15 months (range 1-78 months). Computed tomography angiograms were performed at 1, 6, and 12 months following the index procedure, and yearly thereafter.

Conclusions

Endovascular therapy for acute and chronic thoracic aortic pathology is a viable alternative to open surgery with comparable operative morbidity and mortality. Midterm results suggest that endografts are durable, but require more secondary interventions and imaging surveillance than open reconstruction.

The traditional operative approach to the treatment of thoracic disease remains a highly morbid, and often mortal, procedure for elderly patients with pre-existing illnesses. Advances in endovascular technology used in the treatment of abdominal aortic aneurysms have been applied to thoracic aortic pathologies. Thoracic endovascular repair is now a viable alternative to open thoracic aortic reconstruction.¹, ², ³, ⁴ From the early use of custom-made stent grafts in 1994, through the development of industry-designed and FDA-approved thoracic aortic endografts, a number of significant advances have been made.¹ Despite this technical revolution there remains significant risk associated with minimally invasive treatment of the thoracic aorta. Current reports in literature describe morbidity and mortality rates ranging from 2% to 28%.², ³, ⁴, ⁵ Furthermore, reports suggest that secondary interventions are frequently required for patients treated with these devices.⁶, ⁷, ⁸ We sought to review the early and midterm results from our single center with the use of custom-made, as well as industry-designed, endovascular devices for the treatment of acute or chronic thoracic aortic pathology.

Back to Article Outline

Patients and methods 

A retrospective review was conducted of all thoracic endovascular aortic repairs (TEVAR) performed between April 2000 and October 2007. There were a total of 116 primary TEVAR procedures performed on 115 patients at Northwestern Memorial Hospital and the Lakeside and Jesse Brown Veteran Administration Medical Centers. Data collection was performed according to approved Institutional Review Board protocols. A total of 28 of the thoracic aortic aneurysm patients were enrolled in a clinical trial involving the use of industry devices for the endovascular treatment of thoracic aortic aneurysms.

Indications for treatment included asymptomatic degenerative thoracic aneurysms (DTA), aortic dissections with chronic aneurysmal change ≥5.5 cm or thoracic aneurysm rupture (n = 70; 60.3%); traumatic aortic disruption (n = 20; 17.2%); anastomotic pseudoaneurysm (n = 10; 8.6%); acute complicated dissection (n = 6; 5.2%), penetrating aortic ulcer (n = 4; 3.4%), intramural hematoma (n = 4; 3.4%), and Diverticulum of Kommerell (n = 2; 1.7%) (Table I). Emergency procedures were defined as those performed within 24 hours of patient presentation to the institution.

Table I. Thoracic aortic pathology treated and devices implanted

Thoracic aortic pathology	Thoracic device (n = 80)	Aortic cuff extender (n = 19)	Custom (n = 17)
Degenerative aortic aneurysm
Elective	48	1	10
Rupture	9	1	1
Aortic dissection, complicated	5	0	1
Traumatic injury	6	14	0
Pseudoaneurysm	7	0	3
Intramural hematoma	1	2	1
Penetrating aortic ulcer	2	1	1
Diverticulum of Kommerell	2	0	0

All patients underwent computed tomography angiogram (CTA) with or without preoperative digital subtraction angiography to assess the suitability of the thoracic aorta for endovascular treatment. Proximal and distal landing zones of at least 2 cm were required for suitable fixation of the endograft. Arch or mesenteric artery revascularization procedures were performed ahead of time or during the index procedure in 41 (35.3%) cases to allow for adequate proximal or distal fixation when indicated and time permitted.

Procedural details and devices 

All procedures were performed in an operating suite equipped with a fixed fluoroscopic unit (Philips V5000, Nederland, BV). A total of 110 cases were performed under general anesthesia, four patients had monitored anesthesia care (MAC) and two patients had spinal anesthesia. Prophylactic spinal drains were placed in 19 patients (16.4%). Indications for drains included previous aortic surgery with compromise to lumbar or pelvic arterial flow and need for multiple endovascular devices with anticipation of extensive thoracic intercostal artery coverage. Drains were placed prior to induction of anesthesia unless patient hemodynamic instability required postoperative insertion. All patients were administered preoperative antibiotics. All patients received either a first generation cephalosporin or clindamycin in the event of a documented penicillin or cephalosporin allergy. Devices used included industry-designed thoracic aortic endografts (n = 80) [GORE TAG, W. L. Gore & Associates, Flagstaff, Ariz (n = 74); COOK TX2, Cook, Inc, Bloomington, Ind (n = 4); Medtronic Talent, Medtronic/AVE, Santa Rosa, Calif (n = 2)], endovascular aortic proximal extension cuffs (n = 19) [Excluder, W. L. Gore & Associates, Flagstaff, Ariz (n = 18); AneuRx, Medtronic/AVE, Santa Rosa, Calif (n = 1)], or custom-made stent grafts (n = 17) constructed of 5 cm long stents (Gianturco Z-stents; Cook, Inc, Bloomington, Ind) covered with ironed woven polyester fabric (Cooley Veri Soft, Boston Scientific Corp, Oakland, NJ) delivered via a 22F delivery system. Further details of the custom-made graft construction and delivery have been previously reported.⁹ Aortic arterial access was obtained via percutaneous (n = 45; 38.8%) or cut-down femoral arterial approach (n = 54; 46.6%), direct iliac access (n = 4; 3.4%) or iliac arterial conduit (n = 8; 6.9%), direct aortic access (n = 4; 3.4%) or via the aortic arch (n = 1; 0.9%). The choice of arterial access for each patient was made based on surgeon preference taking into account patient anatomy and the presence of previous groin operative intervention. All patients underwent aortic arch and thoracic aortic angiography before and after TEVAR to ensure satisfactory placement of the device and to evaluate for endoleaks.

Follow-up 

In the immediate postoperative period, all patients were evaluated by the operating surgeon for any complications. If any neurological deficit was suspected, a neurologist was consulted to evaluate the patient. Major stroke was defined as any central neurologic deficit that persisted beyond 24 hours. Acute renal failure was defined as any increase in the creatinine level to greater than 3.0 mg/dL with or without the need for dialysis. Respiratory failure is defined as any patient with postoperative pneumonia, prolonged intubation beyond the fifth postoperative day, or any patient requiring tracheostomy. All patients underwent a clinical exam and a computed tomography angiogram (CTA) at 1 month, 6 months, 1 year, and yearly thereafter to evaluate for endoleaks, graft migration, regression or growth of the aneurysm sac, and other late adverse events.

Back to Article Outline

Results 

Patient demographics 

A total of 115 patients underwent 116 primary thoracic aortic endovascular procedures by surgeons. The disease entity and type of device used to treat each is detailed in Table I. Thirty-five percent of the procedures were considered emergent. The average age of the patient cohort was 63.9 years old (± 15.9 years, range 20-93 years old). Sixty-five percent of the patients were male. Of the total patients treated, 85% were American Society of Anesthesiologists (ASA) class ≥ 3 and nearly 13% of the patients were ≥ 80 years old. Baseline characteristics are listed in Table II.

Table II. Demographics

ASA, American Society of Anesthesiologists; CABG, coronary artery bypass graft; PTCA, percutaneous transluminal coronary angioplasty; COPD, chronic obstructive pulmonary disease; CVA, cerebrovascular accident.

Subclavian transposition was performed in 28 patients (24.1%) and a carotid to subclavian bypass was performed in two patients (1.7%) with prior left internal mammary artery coronary revascularization. The subclavian artery was covered without revascularization in a total of seven cases. Total arch debranching was performed in two patients (1.7%) and hybrid elephant trunk procedures were utilized in two patients (1.7%). Mesenteric arterial revascularization was utilized in seven patients (6.1%). Of the mesenteric procedures, two patients underwent celiac bypass alone while five patients underwent multivisceral revascularization. One patient had celiac artery coverage without prior revascularization.

Early mortality 

The 30-day mortality rate was 5.2% (n = 6) for all primary and secondary endograft procedures (Table III). Four of six deaths followed emergent operations. As such, the 30-day mortality for emergency procedures was 9.8%. One patient treated for a ruptured thoracic aneurysm died from multisystem organ failure after a massive retroperitoneal bleed. One patient died from sepsis after treatment of a leaking mycotic pseudoaneurysm. One patient succumbed from multisystem organ failure after polytrauma and repair of an acute aortic disruption. A final patient died from unknown causes after being discharged to an extended care facility after repair of a ruptured thoracic aortic aneurysm. This final patient presented with aortic rupture and concomitant acute cholecystitis; a cholecystostomy tube was placed for drainage, however, the potential for endograft infection and rupture cannot be excluded since no postmortem examination was performed.

Table III. Thirty-day major adverse events

The remaining two deaths occurred following elective cases. One patient died from a massive stroke on postoperative day 3. The other patient, who underwent a total hip replacement several days after the endograft procedure, died from respiratory failure after being discharged to an extended care facility.

Early complications 

Arterial access injuries occurred in 13 cases (11.2%) (cut-down approach [n = 8], percutaneous approach [n = 3], iliac conduit [n = 2]). In general, arterial injuries were identified and repaired during the time of the initial procedure with either placement of iliac stents (n = 7), or reconstruction of the iliac or femoral artery (n = 4). The remaining two patients with access site complications returned to the operating room for a thromboembolectomy of the lower extremity. One of these patients recovered without sequelae, while the other patient, who had suffered from polytrauma, developed further limb ischemia, compartment syndrome, and eventual limb loss. One other patient suffered limb loss in this series. This patient developed heparin induced thrombocytopenia and diffuse arterial thrombosis, eventually requiring bilateral below knee amputations. Three patients developed significant access site hematomas in the days after TEVAR, one required operative decompression.

Neurological complications, consisting of stroke or spinal cord ischemia occurred in 11.2% of the patients treated with both primary and secondary interventions (Table III). Major stroke and paraplegia or paresis rates were 8.6% (n = 10) and 2.6% (n = 3), respectively.

Strokes occurred in the middle cerebral artery distribution in five patients, in the posterior circulation in two patients, and in a multifocal distribution in three patients. One of the strokes occurred during a repeat intervention to treat a proximal endoleak.

Complete paralysis from spinal cord ischemia occurred in two patients without recovery, while one patient experienced paresis and urinary incontinence. One patient who suffered paralysis had a spinal drain placed electively prior to TEVAR because of a history of ruptured abdominal aortic aneurysm (AAA) repair. She was neurologically intact until she experienced a period of bradycardia and hypotension on postoperative day 2; despite vasopressor induced hypertension and continual spinal drainage, she did not recover neurologic function. The second patient, who suffered paralysis, was treated emergently for aneurysm rupture and had a spinal drain placed immediately after surgery; the patient experienced a prolonged period of hypotension in the perioperative period from a retroperitoneal bleed. As mentioned earlier, this patient developed multisystem organ failure and died within 2 weeks of the endograft placement. The one case of paresis occurred on the fourth postoperative day and a spinal drain was not placed; this patient had a history of aortobifemoral bypass for treatment of AAA.

The left common carotid artery was inadvertently covered in one case and was treated with a retrograde carotid stent at the time of the initial procedure. Another patient was noted to have a left common carotid artery dissection during the procedure which also required stent placement. Neither patient suffered short or long-term sequelae. One patient with intentional coverage of the subclavian developed vertebral steal syndrome and underwent a late subclavian transposition without complication.

Eight patients (6.9%) suffered from respiratory failure requiring prolonged intubation or tracheostomy. The primary reason for prolonged intubation was pneumonia in four patients. Failure to wean oxygen occurred in two patients with severe chronic pulmonary obstructive disease. One patient suffered a traumatic intubation requiring a tracheostomy and one patient had hemoptysis and required reintubation in the immediate postoperative period.

One instance of device collapse occurred in a young trauma patient with aortic transection. The collapse was asymptomatic and was detected on the first postoperative day. This complication was treated satisfactorily by placing four infrarenal aortic extension cuffs within the thoracic device.

Three patients experienced acute postoperative renal failure. Two of them recovered renal function without the need for dialysis. Early nonfatal adverse events are listed in Table IV.

Table IV. Procedural adverse events

Follow-up 

Mean follow-up with imaging of the graft was 15 months (±15 months, range 1-78 months). There were eight patients who were lost to follow-up after their 1 month CTA, five of these were trauma patients treated for acute aortic transection.

Late mortality 

A total of 21 patients died after the 30-day perioperative period (Fig. 1). Causes of death included coronary artery disease or heart failure (n = 6), rupture or sepsis from an infected graft (n = 4), sepsis from other causes (n = 3), respiratory failure (n = 3), pneumonia with endocarditis (n = 1), perforated duodenal ulcer following ascending arch repair (n = 1), rupture awaiting reintervention (n = 1), aspiration (n = 1), and unknown causes (n = 1).

• 
  • View Large Image
  • Download to PowerPoint

• Fig. 1. 

  Survival of patients who underwent endovascular thoracic aortic repair.

Mortality due to graft infection is detailed in Table V. The overall delayed infection rate, including two patients who are still alive, was 5.2% (n = 6). The four deaths occurred within days to weeks after graft infection was detected either from rupture or sepsis. Of the six grafts that developed infectious complications, four were placed under emergent conditions. One patient who died presented with an acute symptomatic intramural hematoma. This patient was receiving chemotherapy and was neutropenic at the time of endograft placement; the specific source of the endograft infection remains unknown. Another graft infection occurred in a patient who initially presented emergently with a penetrating aortic ulcer and acute aneurysmal degeneration; in retrospect, this may have been mycotic on presentation. One dialysis dependent patient developed pyuria 2 days following endograft implantation. The same organisms were identified in the blood at the time of aortic infection and subsequent death. A fourth patient who died from graft infection a year after implantation had been found down and uroseptic in her home just prior to admission. This graft infection was proven at autopsy.

Table V. Delayed endograft infections

EL, Elective; EM, emergent; MSSA, methicillin sensitive staphylococcus aureus; PAU, penetrating aortic ulcer; ESRD, end stage renal disease; UTI, urinary tract infection.

The two surviving patients developed type I endoleaks with subsequent aneurysm sac enlargement. One remains under observation and one was successfully explanted. The first, also a chronic hemodialysis patient, developed pneumonia after a post-TEVAR aortic valve repair. The pneumonia persisted for several months despite aggressive antibiotic therapy. On routine graft surveillance following resolution of the pneumonia, gas was seen around the implanted graft. Perigraft fluid samples and pulmonary washings revealed no bacterial or fungal isolate. This patient was deemed too high risk for an explant procedure and is currently receiving antibiotic therapy. The final patient, who is described in more detail below, underwent emergent endograft placement for a ruptured infected pseudoaneurysm. Following removal of the subsequently infected endograft, the patient underwent a complete aortic replacement and is recovering.

Nonfatal late complications 

Nine patients developed type I or type III endoleaks (7.8%). Of the nine patients, four were originally treated with custom-made stent grafts (Table VI). The average time to appearance of endoleak was 10.2 months. Seven patients underwent repeat operative intervention while one patient with a distal type I leak, died from aneurysm rupture in the hospital prior to planned operative intervention. Two patients, who developed proximal type I endoleaks from disease progression and arch dilatation, underwent ascending arch repair with the distal aspect of the arch graft sewn directly to the endograft. As briefly mentioned above, another patient, who originally underwent emergent endograft placement for a mycotic pseudoaneurysm, had an additional stent graft placed for a proximal endoleak with immediate satisfactory results. However, at 1 year following the original endograft procedure and 2 months following the secondary procedure, the patient was found to have overt graft infection with sac enlargement and recurrence of the type I leak. This patient underwent device explantation and aortic reconstruction with an antibiotic soaked graft. Four patients underwent additional graft insertion with satisfactory treatment of the endoleak (proximal type I [n = 2]; distal type I [n = 1]; type III [n = 1]). One patient was found to have a small distal type I endoleak at the conclusion of the procedure for treatment of a ruptured aneurysm. Subsequent imaging and clinical follow-up revealed the asymptomatic, persistent endoleak without sac enlargement. Additionally, the patient was found to have metastatic breast cancer and therefore further treatment of the endoleak has not been pursued. Nine additional patients (7.8%) were found to have type II endoleaks on surveillance imaging. None have resulted in sac enlargement and therefore have not been treated. Only 3 (33%) of these patients with type II leaks have persisted beyond 1 year.

Table VI. Endoleaks requiring operative intervention

EL, Elective; EM, emergent; SCA, subclavian artery; IMH, intramural hematoma.

Three additional patients underwent operative intervention for progression of their aortic disease in the absence of an endoleak. One patient underwent an aortic arch repair simultaneous with coronary bypass grafting procedure for aneurysmal degeneration of the ascending arch at seven months. Another patient who was initially treated for a symptomatic subacute type B dissection was noted to have developed an asymptomatic retrograde type A dissection on a 6-month surveillance CTA. This likely resulted from aortic penetration by the endoprosthesis. This patient underwent a conversion to a hybrid procedure with aortic arch replacement. A third patient, originally treated for an acute complicated dissection, developed aneurysmal degeneration of the visceral segment with rupture and underwent emergent open reconstruction and replacement of the aorta from the endograft to the aortic bifurcation.

Back to Article Outline

Discussion 

The natural history of untreated major thoracic aortic pathology is a strong impetus for patients to consider operative repair, even if they are severely compromised or elderly. Several large series report significant morbidity following traditional open approaches to thoracic aortic reconstruction, especially when performed under emergent circumstances.¹⁰, ¹¹ The use of endovascular devices for the treatment of thoracic aortic aneurysms, as well as other off-label indications such as traumatic aortic disruptions and dissection, have been shown to result in decreased rates of mortality, renal failure, and paralysis in both small series and large trials.², ³, ⁴, ⁶, ⁷, ¹² This new technology, has provided higher risk patients, originally denied treatment via conventional operative repair, the opportunity to be treated with satisfactory results. Data from this series would support continued use of TEVAR in a high risk group, however, our data suggest that the incidence of significant complications remains high in this patient population. Our results are consistent with other reports with similar risk patients noting a combined stroke, death, and paralysis/paresis rate of 16.4%.⁴, ⁵, ¹³ We identified a periprocedural mortality rate of 5.2%, which compares favorably with the periprocedural mortality rate in some conventional surgical series.¹¹, ¹⁴ The combined rate of stroke, death, and paralysis/paresis for emergent procedures in our series was 22%. In comparison, large series of open repair quote mortality rates as high as 26%.¹⁴, ¹⁵ Our midterm results with the endovascular treatment of thoracic aortic pathology reflect the relative high-risk patient population that we have treated at our institution. The life table analysis (Fig) indicates that a significant portion of the patients died within 1 year of their index procedure; the causes of which are not related to their endograft procedure. This reflects the complex medical problems that these patients possess and their inability to tolerate open surgical repair. These results reinforce the severity of illness in patients with thoracic aortic pathology and also bring forth the question of who will reap the most benefit from a minimally invasive method of treatment of aortic disease.

The durability and effectiveness of minimally invasive treatment of the thoracic aorta warrants discussion and continued imaging surveillance of these devices remains paramount.⁷, ¹⁶, ¹⁷ In our series, the rate of type I or III endoleaks was significant at 6.9%. Many of the leaks were early type, none required immediate conversion to open repair, and most followed treatment with custom-made devices. Industry-manufactured devices seem to perform more favorably, provided they are used in the appropriate setting. Excluding devices placed for traumatic aortic injury (which would not be expected to leak), the type I and type III endoleak rate for industry-manufactured devices and custom-made devices in this series was 6.25% and 23.5%, respectively. In midterm reports endoleak rates as high as 24% have been reported for custom-made grafts.⁸, ¹⁶, ¹⁷, ²⁰ The GORE TAG investigators report an incidence of any endoleak at 2 years to be 9%; of these only three patients required endovascular revision.² The Talent thoracic registry, which included 457 patients treated for various thoracic aortic pathology, reports a persistent primary endoleak rate of 9.6% with type I endoleak being the most common and the most important risk factor for late rupture.⁴ Other series of patients treated with industry-designed thoracic stent grafts have reported rates of endoleaks ranging between 6% and 20 %, type I being the most common.³, ⁷, ⁸, ¹², ¹⁸ Early type I leaks, defined as those identified on completion angiography or on a ≤1 month CT scan, should be expected to resolve spontaneously. As such, a period of observation is not unreasonable. However, early leaks that persist beyond 6 months should be treated. Type I leaks that develop late (after 6 months) rarely resolve spontaneously and should be considered for open or endovascular treatment.

Patients with concomitant ascending arch disease may require even more strict surveillance. Two of our patients developed type I endoleaks, with sac expansion, as a result of progression of arch pathology. Demers et al did not report graft migration in their series, but instead proposed inadequate fixation as the contributing factor to the development of type I endoleaks.¹⁹ They suggest that continued aortic aneurysmal degeneration changes the morphology of the landing zones thus making late endoleaks possible. This would appear to be a plausible mechanism for late failure in our series as well. These patients require intervention, usually with open arch reconstruction incorporating the endograft into the distal anastomosis, as these leaks would not be expected to resolve spontaneously and most are adjacent to the great vessels.

In patients with traumatic aortic disruption, the rate of endoleak was 0%. Trauma patients generally have a healthy, normal caliber, aorta with an acute tear and without aneurysmal pathology. Endoleaks would not be expected to occur in these patients and, therefore, should probably not be included in the context of early or late complications of TEVAR for this subgroup. In fact, all patients treated with aortic extender cuffs for this indication in this series did not experience any device related complications during follow-up. The primary concern for endograft placement in a healthy but acutely transected aorta is the possibility of device collapse.²¹, ²² In these young, hyperdynamic patients, when grafts are oversized relative to the aorta, there is a risk for device collapse and distal malperfusion. We did observe this complication in one patient with aortic transection who was treated with a GORE TAG device. Nevertheless, we noted a very low incidence of device related complications in the endovascular treatment of traumatic thoracic aortic injury. Current literature reflects the decreased morbidity and mortality with endograft placement for the treatment of polytrauma patients with thoracic aortic injury, as well as a low rate of repeat intervention for device related complications making it a preferred alternative to open surgical repair.³, ²³

Delayed endograft infection and subsequent type I endoleak from presumed aortic wall degeneration was a cause for both early and late aneurysm-related deaths in our series. Patients in our series, who developed graft infection within 6 weeks of device implantation, may have had a primary aortic infection that was not recognized at the time of initial presentation. The patients that presented with delayed graft infection likely had seeding of their graft from remote infections that occurred after or around the time of the index procedure. What is evident from our experience is that graft placement in the setting of primary aortic or active remote infection may result in a high incidence of endograft infection and subsequent rupture and death. Since there are few reports of endografts placed for thoracic aortic infections or fistulas and fewer reports of delayed thoracic aortic graft infection, the natural history of endovascular repair in the setting of infection is relatively unknown.²⁴, ²⁵ The treatment of a known thoracic aortic infection with an endograft should be undertaken with caution and perhaps should not be performed at all. If active infection is evident at the time of device implantation, lifelong antibiotic coverage should be considered. Similarly, late remote infections need to be promptly diagnosed and treated as late endograft seeding may be more common with thoracic endoprostheses than with sewn in grafts.

The stroke rate of 8.6% in this report is on the higher end of the spectrum compared with other series including those with open surgical repair.³, ¹⁸, ²⁶ This may be due to the relatively high percentage of patients treated for very proximal disease in this series. Thoracic aortic disease that is adjacent to the great vessels requires manipulation of the arch with wires, catheters, and the device prior to device deployment. This can result in disturbance or disruption of atherosclerotic plaque within the aorta and can lead to cerebral embolic events. This is particularly true in patients with disease that is within close proximity to the great vessels so caution must be exercised.

Our stroke rate was highest in the earlier part of our series and strokes occurred in four patients who were treated with custom-made grafts. Other authors have described a higher incidence of stroke with the use of custom-made devices. This is likely related to the size and stiffness of the delivery system.¹⁷, ¹⁹ The stroke rate in the second half of our series was reduced to 2.6% after developing an aggressive policy regarding minimal wire and catheter manipulation in the arch and routine branch vessel revascularization and after we began to deploy only industry-designed devices.

Posterior circulation strokes occurred alone or in combination with anterior circulation strokes in five patients in our series. We have previously reported our experience with subclavian arterial revascularization in patients requiring proximal device fixation.²⁷ Early in our series, we identified two patients with isolated posterior circulation strokes who had endograft coverage of the subclavian artery. As a result, we now routinely perform subclavian artery transposition or carotid to subclavian bypass in patients with dominant left vertebral arterial circulation, LIMA coronary bypass grafts, anticipated extensive thoracic intercostal vessels coverage, or when the potential exists for retrograde perfusion of a type B dissection via a patent subclavian artery. We suspect that this aggressive policy of arch branch reconstruction has contributed to an improvement in stroke rate over time and may also contribute to optimal spinal cord perfusion.

Paraplegia and paresis rates in our series are consistent with previous reports. Endovascular thoracic aortic repair is associated with a decreased incidence of paraplegia, compared with conventional operative repair. This complication occurred in a patient with previous abdominal aortic surgery with hypotension, and in a patient with acute rupture, persistent hypotensive shock and midthoracic aortic coverage. This patient profile is consistent with other series in which patients with compromised thoracic intercostal arterial circulation, lack of compensatory lumbar or pelvic circulation coexisting with hypotension developed paraplegia or paresis.⁸, ¹⁸, ²⁸ To prevent spinal ischemia in a high-risk subset of patients, we selectively use spinal drainage when technically feasible.

Our study is limited by its retrospective design and by the fact that this is a relatively small patient cohort. In addition, we chose not to use any standard surgical repair patients for comparison. Despite these shortcomings, we conclude that in certain patient populations, the endovascular treatment of thoracic aortic pathology is a viable alternative to open repair. We also conclude, however, that like with open repair TEVAR carries significant risk in both early and late complications.

In conclusion, advances in the endoluminal technology used to treat thoracic aortic pathology have allowed many patients to undergo life saving treatments with decreased morbidity and mortality. On the other hand, it is clear that the elderly and infirmed may not fare well, even with a “minimally invasive” therapy. Furthermore, unlike open surgical repair, the long-term durability of thoracic aortic endograft remains to be seen. Long-term imaging surveillance is required to monitor for endoleaks and repeat interventions may be required if device failure or migration should occur. Overall, TEVAR for thoracic aortic pathology is safe and efficacious, but it is not without significant high risk in the complex patient population who come to endovascular repair.

Back to Article Outline

Author contributions 

Back to Article Outline

The authors thank Daniel Amaranto for his assistance with the life table analysis.

Back to Article Outline

References 

1. Dake MD, Miller DC, Semba CP, Mitchell RS, Walker PJ, Liddell RP. Transluminal placement of endovascular stent grafts for the treatment of descending thoracic aortic aneurysms. N Engl J Med. 1994;331:1729–1734
   • View In Article
   • MEDLINE
   • CrossRef
2. Makaroun MS, Dillavou ED, Kee ST, Sicard G, Chaikof E, Bavaria J, 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
   • View In Article
   • Abstract
   • Full Text
   • Full-Text PDF (302 KB)
   • CrossRef
3. 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. J Vasc Surg. 2004;40:670–679discussion 679-80
   • View In Article
   • Abstract
   • Full Text
   • Full-Text PDF (190 KB)
   • CrossRef
4. Fattori R, Nienaber CA, Rousseau H, Beregi JP, Heijmen R, Grabenwoger M, 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
   • View In Article
   • Abstract
   • Full Text
   • Full-Text PDF (179 KB)
   • CrossRef
5. Orend KH, Scharrer-Pamler R, Kapfer X, Kotsis T, Gorich J, Sunder-Plassmann L. Endovascular treatment in diseases of the descending thoracic aorta: 6-year results of a single center. J Vasc Surg. 2003;37:91–99
   • View In Article
   • Abstract
   • Full Text
   • Full-Text PDF (228 KB)
   • CrossRef
6. Cambria RP, Brewster DC, Lauterbach SR, Kaufman JL, Geller S, Fan CM, et al. Evolving experience with thoracic aortic stent graft repair. J Vasc Surg. 2002;35:1129–1136
   • View In Article
   • Abstract
   • Full Text
   • Full-Text PDF (639 KB)
   • CrossRef
7. Patel HJ, Williams DM, Upchurch GR, Shillingford MS, Dasika NL, Proctor MC, et al. Long-term results from a 12-year experience with endovascular therapy for thoracic aortic disease. Ann Thorac Surg. 2006;82:2147–2153
   • View In Article
   • CrossRef
8. Stone DH, Brewster DC, Kwolek CJ, Lamuraglia GM, Conrad MF, Chung TK, et al. Stent-graft versus open-surgical repair of the thoracic aorta: midterm results. J Vasc Surg. 2006;44:1188–1197
   • View In Article
   • Abstract
   • Full Text
   • Full-Text PDF (213 KB)
   • CrossRef
9. Peterson BG, Longo GM, Matsumura JS, Kibbe MR, Morasch MD, Cardeira KR, et al. Endovascular repair of thoracic aortic pathology with custom-made devices. Surgery. 2005;138:598–605discussion 605
   • View In Article
   • Abstract
   • Full Text
   • Full-Text PDF (271 KB)
   • CrossRef
10. Crawford ES, Hess KR, Cohen ES, Coselli JS, Safi HJ. Ruptured aneurysm of the descending thoracic and thoracoabdominal aorta (Analysis according to size and treatment). Ann Surg. 1991;213:417–425discussion 425-6
    • View In Article
    • MEDLINE
    • CrossRef
11. Coselli JS, Bozinovski J, LeMaire SA. Open surgical repair of 2286 thoracoabdominal aortic aneurysms. Ann Thorac Surg. 2007;83:S862–S864discussion S890-2
    • View In Article
    • CrossRef
12. Wheatley GH, Gurbuz AT, Rodriguez-Lopez JA, Ramaiah VG, Olsen D, Williams J, et al. Midterm outcome in 158 consecutive Gore TAG thoracic endoprostheses: single center experience. Ann Thorac Surg. 2006;81:1570–1577discussion 1577
    • View In Article
    • CrossRef
13. Riesenman PJ, Farber MA, Mendes RR, Marston WA, Fulton JJ, Mauro M, et al. Endovascular repair of lesions involving the descending thoracic aorta. J Vasc Surg. 2005;42:1063–1074
    • View In Article
    • Abstract
    • Full Text
    • Full-Text PDF (214 KB)
    • CrossRef
14. Conrad MF, Crawford RS, Davison JK, Cambria RP. Thoracoabdominal aneurysm repair: a 20-year perspective. Ann Thorac Surg. 2007;83:S856–S861discussion S890-2
    • View In Article
    • CrossRef
15. Girardi LN, Krieger KH, Altorki NK, Mack CA, Lee LY, Isom OW. Ruptured descending and thoracoabdominal aortic aneurysms. Ann Thorac Surg. 2002;74:1066–1070
    • View In Article
    • MEDLINE
    • CrossRef
16. Greenberg R, Resch T, Nyman U, Lindh M, Brunkwall J, Brunkwall P, et al. Endovascular repair of descending thoracic aortic aneurysms: an early experience with intermediate-term follow-up. J Vasc Surg. 2000;31:147–156
    • View In Article
    • Abstract
    • Full Text
    • Full-Text PDF (249 KB)
    • CrossRef
17. Dake MD, Miller DC, Mitchell RS, Semba CP, Moore KA, Sakai T. The “first generation” of endovascular stent grafts for patients with aneurysms of the descending thoracic aorta. J Thorac Cardiovasc Surg. 1998;116:689–703discussion 703-4
    • View In Article
    • Abstract
    • Full Text
    • Full-Text PDF (118 KB)
    • CrossRef
18. Bavaria JE, Appoo JJ, Makaroun MS, Verter J, Yu ZF, Mitchell RS. 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;133:369–377
    • View In Article
    • Abstract
    • Full Text
    • Full-Text PDF (142 KB)
    • CrossRef
19. Demers P, Miller DC, Mitchell RS, Kee ST, Sze D, Razavi MK, et al. Midterm results of endovascular repair of descending thoracic aortic aneurysms with first-generation stent grafts. J Thorac Cardiovasc Surg. 2004;127:664–673
    • View In Article
    • Abstract
    • Full Text
    • Full-Text PDF (283 KB)
    • CrossRef
20. Ishida M, Kato N, Hirano T, Cheng SH, Shimono T, Takeda K. Endovascular stent graft treatment for thoracic aortic aneurysms: short- to midterm results. J Vasc Interv Radiol. 2004;15:361–367
    • View In Article
    • Abstract
    • Full Text
    • Full-Text PDF (93 KB)
    • CrossRef
21. Muhs BE, Balm R, White GH, Verhagen HJ. Anatomic factors associated with acute endograft collapse after Gore TAG treatment of thoracic aortic dissection or traumatic rupture. J Vasc Surg. 2007;45:655–661
    • View In Article
    • Abstract
    • Full Text
    • Full-Text PDF (1192 KB)
    • CrossRef
22. Neschis DG, Moaine S, Gutta R, Charles K, Scalea TM, Flinn WR, et al. Twenty consecutive cases of endograft repair of traumatic aortic disruption: lessons learned. J Vasc Surg. 2007;45:487–492
    • View In Article
    • Abstract
    • Full Text
    • Full-Text PDF (398 KB)
    • CrossRef
23. Lettinga-van de Poll T, Schurink GW, De Haan MW, Verbruggen JP, Jacobs MJ. Endovascular treatment of traumatic rupture of the thoracic aorta. Br J Surg. 2007;94:525–533
    • View In Article
    • MEDLINE
    • CrossRef
24. Semba CP, Sakai T, Slonim SM, Razavi MK, Kee ST, Jorgensen MJ, et al. Mycotic aneurysms of the thoracic aorta: repair with use of endovascular stent-grafts. J Vasc Interv Radiol. 1998;9:33–40
    • View In Article
    • Abstract
    • Full-Text PDF (7823 KB)
    • CrossRef
25. Sayed S, Choke E, Helme S, Dawson J, Morgan R, Belli A, et al. Endovascular stent graft repair of mycotic aneurysms of the thoracic aorta. J Cardiovasc Surg (Torino). 2005;46:155–161
    • View In Article
    • MEDLINE
26. Khoynezhad A, Donayre CE, Bui H, Kopchok GE, Walot I, White RA. Risk factors of neurologic deficit after thoracic aortic endografting. Ann Thorac Surg. 2007;83:S882–S889discussion S890-2
    • View In Article
    • CrossRef
27. Peterson BG, Eskandari MK, Gleason TG, Morasch MD. Utility of left subclavian artery revascularization in association with endoluminal repair of acute and chronic thoracic aortic pathology. J Vasc Surg. 2006;43:433–439
    • View In Article
    • Abstract
    • Full Text
    • Full-Text PDF (265 KB)
    • CrossRef
28. Gravereaux EC, Faries PL, Burks JA, Latessa V, Spielvogel D, Hollier LH, et al. Risk of spinal cord ischemia after endograft repair of thoracic aortic aneurysms. J Vasc Surg. 2001;34:997–1003
    • View In Article
    • Abstract
    • Full Text
    • Full-Text PDF (111 KB)
    • CrossRef