Surgical correction of failed thoracic endovascular aortic repair

Article Outline

• Abstract
• Methods
  • Patients
  • Preoperative diagnostic evaluation
  • Surgical protocol
• Results
• Discussion
• Conclusions
• Author contributions
• References
• Copyright

Objective

The number of thoracic aortic endovascular procedures is increasing rapidly, and the clinical outcome largely depends on the underlying aortic pathology. When primary stent grafting is unsuccessful, secondary endovascular solutions are most often feasible. However, in recurrent endovascular failure without further minimally invasive options, conservative treatments or conversion to open surgery are the only remaining therapeutic strategies.

Methods

In our experience, 106 patients received thoracic aortic endovascular treatment. Five of these patients and three from other centers underwent conversion to open repair because of 4 type Ia endoleaks (3 thoracic aortic aneurysms, 1 traumatic rupture), 2 retrograde type A dissections, 1 type Ib endoleak with contained rupture, and 1 secondary false aneurysm rupture due to stent graft migration. The latter four were surgical emergencies; the other four were urgent or elective procedures. Three patients underwent supracoronary arch replacement through sternotomy. One patient had arch and proximal descending aortic replacement, three had hemiarch and descending aortic replacement, and one had descending aortic replacement through left thoracotomy. Five stent grafts were totally removed, and three endografts were left in situ. All conversions were performed according to a protocol including total extracorporeal circulation (n = 7) or left heart bypass (n = 1), cerebrospinal fluid drainage and monitoring motor-evoked potentials, transcranial Doppler, and electroencephalography.

Results

All patients survived the surgical procedure. Six patients had an uneventful postoperative course, whereas necrotic cholecystitis developed in one patient who required cholecystectomy and prolonged intensive care stay. One polytrauma patient died from secondary rupture due to prosthesis infection 24 days after stent graft explantation. No stroke, paraplegia, renal failure, or other major complication occurred. With a mean follow-up of 14 months (range, 4-71 months), seven patients are alive without any sign of recurrent aortic problems.

Conclusion

Failure of thoracic endovascular aortic repair comprises a new aortic pathology. Secondary endovascular treatment is feasible in most patients; however, some patients will require open surgery to repair failures of thoracic endovascular aortic treatment. These procedures constitute a large surgical trauma and require an extensive protocol, including extracorporeal circulation, neuromonitoring, and adjunctive modalities to provide organ protection. We recommend that these procedures be performed in centers with experience and the infrastructure to offer these protective measures.

The initial experiences with endovascular treatment of thoracic aortic pathologies are promising, showing acceptable mortality and paraplegia rates.¹ The indications for thoracic aortic endovascular repair include thoracic aortic aneurysms (TAA), acute and chronic expanding type B dissection, traumatic aortic rupture, and penetrating aortic ulcer. The exact number of annual thoracic stent graft procedures is unknown due to lacking mandatory registries. Voluntary registries like the European Collaborators on Stent/Graft Techniques for Aortic Aneurysm Repair (EUROSTAR) registry or the United Kingdom Thoracic Endograft Registry are certainly the largest compendium of collected thoracic procedures¹, ² but only represent part of the entire implantation market. Sales figures of commercially available thoracic stent grafts show >1000 implantation procedures annually worldwide.

In contrast to endovascular abdominal aortic repair (EVAR), less is known about complications and conversions after thoracic endovascular aortic repair (TEVAR). Depending on the different aortic pathologies, procedure- related complications frequently occur. Serious complications include primary or secondary type I endoleak, retrograde type A dissection, stent collapse, and rupture with subsequent death. Series involving stent grafting of TAAs have shown that endoleaks occur in 3% to 29 %,³, ⁴ and about 50% of these are life threatening type I endoleaks with unchanged pressurized aneurysm sack. The risk of retrograde type A dissection after TEVAR is approximately 6.8%, with a procedure-related mortality of 40%.⁵ Incomplete or total collapsed endografts in the thoracic aorta have only been published in case reports.⁶

Fortunately, most of the described complications can be managed by means of additional endovascular interventions. However, patients will remain in whom repeat endovascular techniques will not be feasible owing to inadequate landing zones that do not allow extension devices, inappropriate apposition, and progressive dissection or aneurysmal disease. We have encountered eight patients with threatening pathology related to their thoracic endograft in whom secondary endovascular procedures were not possible. We present our surgical management in these patients who required conversion to open repair.

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Methods 

Patients 

Between June 2001 and June 2007, we performed 316 thoracic and thoracoabdominal aortic operations, including 106 TEVAR and 210 open procedures. The ascending aorta and proximal arch were not involved as target areas. Five of the 106 patients and three patients referred from other centers presented with life-threatening complications of failed TEVAR that were not amenable for repeat endovascular correction. Initial endovascular therapy was considered appropriate in these patients because of the underlying pathology, including acute type B dissection, rupture, and aneurysm formation after type B dissection. The mean age of the five men and three women was 51.7 years (range 40-63 years). The initial indications for TEVAR (Table I) included acute symptomatic type B dissection in 2 patients, expanding chronic type B dissection in 2, expanding chronic arch and descending dissection after a previous Bentall procedure for type A dissection in 1, chronic false aneurysm after aortic patch plasty in childhood in 1, and traumatic rupture in 2.

Table I. Survey of thoracic conversion procedures

ABF, Aortobronchial fistula; TAA, thoracic aortic aneurysm; TIA, transient ischemic attack; Ttc, time to conversion; TEVAR, thoracic endovascular aortic repair.

The indications for surgical correction of failed TEVAR included retrograde type A aortic dissection in 2 (patients 1 and 2 in Table I), type 1b endoleak with contained rupture in 1 (patient 3), false aneurysm rupture due to distal stent migration in 1 (patient 4), and type 1a endoleak in 4 (patients 5 through 8). The first four patients were operated on as emergencies, and the latter four were elective conversions.

Both patients with retrograde type A dissection underwent emergency surgery. In one patient, the initial endograft was implanted for complicated acute retrograde type B dissection with mesenteric and leg ischemia. The acute retrograde type A dissection (Fig 1, A and B) was caused 38 days later by an intimal tear induced by the bare springs of the endograft. The retrograde dissection in the second patient occurred at the third day after implantation for acute expanding type B dissection, also caused by bare spring–induced intimal injury.

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• Fig 1. 

  A, Computed tomography scan of patient 1 38 days after thoracic endovascular repair for acute type B dissection shows retrograde extension in the aortic arch. B, Intraoperative image after sternotomy shows the endograft in the descending thoracic aorta. The arch is already resected, and bypasses have been anastomosed to the innominate and left carotid artery. Antegrade cerebral perfusion is performed through the grafts.

The third patient operated on in emergency setting was previously treated with an endograft for chronic expanding type B dissection, and a contained rupture developed due to a distal type I endoleak and a repressurized false lumen. The distal descending aorta had aneurysmal disease that did not allow endovascular extension to exclude the endoleak.

The fourth patient presented with polytraumatic injuries, including a contained aortic rupture induced by thoracic blunt trauma. After initial successful endovascular repair, he had to undergo emergency conversion because of delayed rupture 31 days later. Direct preoperative computed tomography (CT) scan had confirmed a device migration.

The electively treated patients all had life-threatening type Ia endoleaks with still vascularized aneurysm sacks. In patient 5, a distal arch and proximal descending aortic aneurysm had developed as a consequence of a previous type A dissection that was initially treated with a Bentall procedure 4 years earlier (Fig 2, A) After carotid–carotid bypass, an endograft was implanted just distally to the origin of the brachiocephalic artery. The scarred dissection membrane prevented complete deployment of the endograft, causing a type Ia endoleak (Fig 2, B). Successful conversion to arch and proximal descending aortic replacement combined with complete endograft removal followed 1 week later. Fig 2, C demonstrates the situation 6 months postoperatively.

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• Fig 2. 

  A, Patient 5 presented with an expanding distal arch and descending thoracic aneurysm. B, Image shows incomplete deployment and apposition of the endograft due to stiff fibrous septum (thick arrow). Note the prior to TEVAR implanted patent carotid–carotid bypass (thin arrow). C, A control magnetic resonance angiography 6 months after conversion shows conventional aortic arch and proximal descending thoracic aortic prosthesis.

A growing distal arch and descending thoracic aneurysm developed in patient 6 after type B dissection in 2002. He was treated in 2006 with an endograft, and the covered proximal part was deployed just distally to the left carotid artery. He presented 9 months later with a small proximal type Ia and a large type II endoleak caused by left subclavian artery back bleeding. Despite successful sealing of the subclavian artery by means of an occluder device (Fig 3, A and B), the aneurysm sack was still pressurized by the type Ia endoleak, with subsequent enlarging of the arch and descending aneurysm (Fig 3, C). Repeat attempts to achieve apposition in the arch or endovascular extension as part of a hybrid procedure were considered inappropriate in this relatively young patient, and conversion to hemiarch and descending aortic replacement was decided. The patient's postoperative course was uneventful.

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• Fig 3. 

  A, Patient 6 had endovascular type II endoleak repair. B, The backbleeding left subclavian artery was closed by means of a transbrachially introduced occluder device. C, A large type I endoleak occurred despite a successfully placed occluder in the left subclavian artery before conversion.

Patient 7 (Table I), who had a type 1a endoleak, also had recurring cerebral embolization owing to proximal stent migration into the ostium of the left carotid artery and hemoptysis caused by an aortobronchial fistula. This patient had previously undergone several procedures, including a left thoracotomy and aortic patch plasty at age 11 for a false aneurysm after traumatic isthmus rupture. He presented 33 years later with paralysis of the left recurrent laryngeal nerve caused by a large false aneurysm at the aortic patch, which was treated with a thoracic endograft. Three years later he was referred to our department with cerebral embolizations and hemoptysis. The entire device had migrated proximally, and the bare stent protruded in the ostium of the left carotid artery, causing recurrent embolizations. In addition, he had a large proximal type I endoleak and an aortobronchial fistula. This young patient refused further endovascular repair because this would indicate sternotomy with debranching of the supra-aortic vessels and extension of the endograft.

Patient 8 was a morbidly obese 49-year-old man with pre-existing aneurysmal disease of the thoracic aorta who had hypertension. An extreme rise in blood pressure that occurred while he was changing a tire resulted in a rupture of the proximal descending thoracic aorta. In a lifesaving procedure, the leakage close to the left subclavian artery was overstented using an endograft, and 3000 mL blood was drained from the left chest. Despite an uneventful postoperative course, the control CT scan showed a small type Ia endoleak due to steepness of the aortic arch causing malalignment of the device in the inner arch. Unfortunately, the patient had ascending and arch dilatation with a diameter that did not allow endovascular extension and required supracoronary ascending and aortic arch replacement with preservation of the aortic valve. The supra-aortic arteries were reattached, and the graft was sewn to the endograft in an end-to-end fashion.

Preoperative diagnostic evaluation 

Patients were all relatively young and fit for open repair. Morphologic assessment of the entire aorta was performed by means of high-quality multislice CT and, since 2006, dual-source spiral CT. Cardiac evaluation included echocardiography for detection of valve insufficiency or stenosis and left ventricular ejection fraction. Dipyridamole-thallium scanning was performed to analyze myocardial perfusion before and after stress testing. In case of detected ischemia, coronary angiography followed. The four emergency patients only had echocardiography before surgery. Coronary heart disease was diagnosed in one patient; no patient had valve disorders. All patients had normal renal function (mean serum creatinine level, 88 μmol/L). Further risk factors were hypertension in five patients and obesity in two.

Surgical protocol 

Three patients underwent sternotomy (2 with retrograde type A dissection, 1 with proximal type 1a endoleak in the arch), and total extracorporeal circulation was initiated in the usual manner at a temperature of 28°C in six patients. Patients 4 and 8 (Table I) were operated on under deep hypothermia (18°). After the aortic arch was opened, selective cardioplegia was administered and cerebral protection was achieved by means of selective antegrade perfusion through catheters with an inflatable balloon at the tip in the brachiocephalic and left carotid artery. These perfusion catheters (Edwards, Irvine, Calif) are connected to the extracorporeal system and are equipped with pressure channels allowing pressure-controlled perfusion of the brain. Furthermore, volume flow in each catheter is assessed with ultrasound flow meters (Transonic, Ithaca, NY). Total antegrade cerebral flow is approximately 10 mL/kg/min, with a mean arterial pressure of 60 mm Hg. Transcranial Doppler and electroencephalography are used to monitor cerebral perfusion continuously.

Surgical access in five patients was through a left thoracotomy (fourth or fifth intercostal space) because of descending thoracic aortic pathology. In four of these patients, however, cardiac arrest and antegrade cerebral perfusion were necessary because the aortic disease extended proximally to the brachiocephalic artery, which precluded proximal aortic clamping and necessitated an open anastomosis.

Extracorporeal circulation was performed by cannulation of the left femoral vein and artery, and a vent was inserted through the left pulmonary vein. Antegrade cerebral perfusion was provided in the same manner as described previously. A Foley catheter inserted in the ascending aorta (n =2) or ascending aortic graft (n =1) was inflated and cardioplegia administered. In one patient, cardiac arrest was induced using only profound hypothermia. One patient was operated on with left heart bypass cannulating the left femoral artery and left pulmonary vein (limited heparinization of 0.5 mg/kg). Cerebrospinal fluid (CSF) drainage was performed in the four elective to reduce the risk of paraplegia. In addition, motor evoked potential monitoring was done to assess spinal cord integrity, guiding intraoperative strategies to prevent neurologic deficits. The details of this technique have been described in detail before.⁷

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Results 

All patients survived the surgical procedure. In both patients with retrograde type A dissection, the intimal tear caused by the bare springs could be identified. Fig 1, B demonstrates the opened aortic arch and the stent graft in the distal part. In both patients, as well as in patient 8, the ascending and arch prosthesis was sewn to the endograft after removal of the bare metal parts of the device. Antegrade cerebral perfusion could be applied in these three patients, and their postoperative neurologic outcomes were uneventful.

Two of five left thoracotomies were redo procedures. Because of severe adherence of the left lung with the chest wall, surgical access was chosen one intercostal space higher and one lower than the previous approach. After complete dissection and collapse of the left lung, the entire arch and descending aorta could be exposed without difficulty. In four patients, the proximal anastomosis was performed in an open end-to end-fashion (1 proximal to the brachiocephalic artery and 3 at the level of the left carotid artery) under continuous antegrade cerebral perfusion. The clamp in one patient was positioned between the left carotid and left subclavian arteries. The distal clamp was at the diaphragm in three patients and at the mid-thoracic level in two: distal aortic perfusion through the left femoral artery guaranteed lower body perfusion.

Urine output continued in all patients. Motor evoked potentials were normal, with a mean distal aortic pressure of 60 mm Hg. The endograft in all five patients was removed. Operative data are reported in Table II. The average cardiac arrest time was 50 minutes (range, 35-121 minutes), mean extra corporeal circulation time was 175 minutes (range, 123-292 minutes), and surgical time was 373 minutes (range, 330-455 minutes).

Table II. Procedural characteristics

NA, Not available.

Seven patients were extubated ≤48 postoperative hours. Patient 1 (Table I) presented postoperative sepsis due to necrotic cholecystitis and had to undergo open cholecystectomy. This patient was on ventilatory support for 4 days. Patient 4 (Table I) died 24 days after uneventful conversion as a consequence of a rupture. Autopsy confirmed prosthesis infection and distal septic anastomotic leakage.

No patients presented with renal failure, pulmonary insufficiency, or myocardial infarction, and no acute or delayed paraplegia occurred. During a mean follow-up of 14 months (range, 4-71 months) all surviving patients were in good clinical condition and CT surveillance showed patent aortic side branches and absence of new or false aneurysms.

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Discussion 

This study describes the surgical treatment of failed TEVAR, demonstrating low morbidity, acceptable mortality, and excellent late outcome. These complex open procedures, however, require adjunctive measures, however, including extracorporeal circulation and selective perfusion to provide acceptable outcome. Neuromonitoring can assist in surgical strategies to prevent spinal cord ischemia.

It is to be expected that with increasing use of thoracic endografts, the demand for open surgical repair of unsuccessful endovascular procedures will increase. Since Dake et al⁸ published their first results with transluminally placed homemade nitinol-Dacron endografts for the repair of descending TAA in 1994, this therapeutic approach has achieved wide acceptance in the treatment of different thoracic aortic pathologies. Considering the data from the EUROSTAR and United Kingdom thoracic endograft registry, a high primary endovascular success rate of 87% in TAA and 89% in dissection can be obtained.¹ Further results including 213 TAA patients have shown a cumulative 83% rate of freedom from intervention at 2 years.² Another well-accepted indication for endovascular repair includes the emergency treatment of traumatic aortic rupture, with verified reduced morbidity and mortality rates compared with open repair.⁹ Consequently, an increasing use of TEVAR is documented¹⁰, ¹¹ and more procedures will follow in the near future.

Nevertheless, complications such as endoleaks,⁴ retrograde type A dissection,⁵ rupture,¹¹, ¹² stent migration,¹³ and stent collapse⁶, ¹⁴ after this minimally invasive therapy have been described, but only limited information exists on the incidence of secondary interventions or conversion to open repair. Table III reports a compilation of recently published studies or case reports dealing with thoracic conversions after TEVAR. Altogether, we identified 37 patients in 11 publications, including 1 meta-analysis,¹⁵ 2 series from voluntary registries,², ¹² retrospective data from 4 centers,³, ⁵, ¹¹, ¹⁶ and 3 case reports.¹³, ¹⁷, ¹⁸ One report evaluated causative anatomic or device factors that may increase the probability of stent graft collapse.⁶

Table III. Reported thoracic conversions to open repair

ABF, Aortobronchial fistula; El, elective; Em, emergency; MC, major complication; NS, not specified; retro A, retrograde type A dissection.

The main cause of conversion were 3 early and 2 late type I endoleaks, 2 retrograde type A dissections and 1 rupture. Access failure did not occur. Comparable results in the few published series are presented. Zipfel et al¹¹ reported 172 patients who underwent thoracic endografting, of whom 15 had endograft failure and six had conversion to open repair. Three were converted immediately because of retrograde type A dissection, access failure, and type Ia endoleak causing rupture after deployment. Reasons for conversions at a later date, but before discharge, were initial access failure in two cases and aortic perforation by bare spring penetration. One death and one major complication occurred. Grabenwoger et al³ published four cases, including three type Ia endoleaks and one retrograde type A dissection. All patients had an uneventful postoperative course. Both authors used extracorporeal circulation to perform open repair. Neuhauser et al⁵ described their experience focused on five cases of retrograde type A dissection, including three conversions. Causative reasons were tears in the aortic wall at the proximal landing zone in three patients, but in two, the retrograde dissection was not related to the endografts.

In our series, aortic dissection was the primary pathology in five of eight patients. Acute and chronic dissections are possible risk factors for stent graft failure, particularly when devices with bare springs are used in acute type B dissection. We believe that endografts with uncovered bare springs should not be used for acute type B dissection. In addition, chronic dissections often contain a strong fibrotic septum that may cause inadequate deployment of the devices with incomplete apposition. This can usually be solved by additional stent placement; in some cases, however, endovascular attempts might not provide the solution.

As reported in Table I, six patients had to undergo correction of failed TEVAR ≤6 weeks of intervention. Immediate or short-term failure is a multifactorial event. Anatomic and technical factors, including quality and length of the landing zones and appropriate devices, are crucial. Particularly, the inner curve of the distal aortic arch causing malalignment of current stent grafts is an unsolved endovascular challenge, especially in younger patients with small aortic diameters.¹⁴ In only two patients of our series was a mid-term failure, at 10 and 37 months, observed. Possible cause for mid- or long-term failure after initial successful endografting might be a continued aneurysmal expansion at the level of the landing zones due to proximal or distal type I endoleaks, as described by Bakaeen et al.¹⁸ This well-known problem of time-related morphologic changes emphasizes the necessity of lifelong surveillance in TEVAR patients.

The published cases and our experience identify some factors that mandate open repair after failed TEVAR. The most obvious is retrograde type A dissection requiring emergency repair. Other factors include type 1 endoleaks that cannot be corrected by additional endovascular means and stent complications such as migration, perforation, fistula, collapse, or fracture that, for some reasons, cannot be treated endovascularly. It should be stated, however, that type 1 endoleaks are primarily treated with endovascular techniques.

A major problem can be caused in chronic dissections in which complete deployment, especially in angulated areas, is troublesome. If endovascular treatment of proximal type 1 endoleak is not feasible, hybrid procedures with debranching of supra-aortic vessels and subsequent endografting can be performed. In case the latter is not possible owing to anatomic issues (eg, ascending aortic disease, inadequate proximal area for bypass anastomosis, or inappropriate distal landing zone), resternotomy, or patient wishes, conversion to open surgery with a left thoracotomy should be considered.

We found that the complexity of the conversion procedures was not more extensive compared with normal open repair. In general, removal of thoracic endografts can be accomplished without difficulty. We identified one endograft with neointima-covered bare springs in the left common carotid ostium that was not easy to remove without damaging the vessel. The excellent surgical outcome of these complex challenges can be attributed to the infrastructure and multidisciplinary approach of the procedure comprising extracorporeal circulation, antegrade cerebral perfusion, distal aortic perfusion, and cerebral and spinal cord monitoring.

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Conclusions 

Endovascular treatment of thoracic aortic diseases constitutes a complex procedure, and associated pitfalls are not uncommon. Neither the total number of annually performed endovascular procedures nor conversion rates to open surgery is known, but it is highly probable that the number of procedures and conversions will increase in the future. If endovascular repair fails and open surgery is required, we believe that these procedures should be centralized in dedicated centers in which the above described experience and infrastructure is available.

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Author contributions 

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References 

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