Management of endoleaks associated with endovascular treatment of descending thoracic aortic diseases

Article Outline

• Abstract
• Methods
• Results
  • Type I distal endoleak
    • Nonintervention group
    • Intervention group
  • Type I proximal endoleak
    • Intervention group
    • No intervention
  • Type II endoleaks
  • Type III
  • Open conversions
• Discussion
• Conclusion
• Author contributions
• References
• Copyright

Objective

Endoluminal grafting is emerging as a less invasive alternative to the treatment of descending thoracic aorta diseases. Endoleaks (continued pressurization of the treated aorta external to the endoluminal graft) are a potential complication. We reviewed our cumulative endovascular experience for descending thoracic aorta pathologies with respect to the management of endoleaks and associated patient outcomes.

Methods

As part of a single-site investigational device–exemption protocol, 249 patients (146 men, 103 women) with thoracic aortic diseases underwent attempted delivery of a TAG endoprosthesis (W. L. Gore & Associates, Flagstaff, Ariz) between February 2000 and August 2005. Indications for study enrollment included 111 atherosclerotic aneurysms (44.6%), 67 aortic dissections (26.9%), 27 penetrating aortic ulcers (10.8%), 14 contained ruptures (5.6%), 11 pseudoaneurysms (4.4%), 9 acute aortic transections (3.6%), 7 aortobronchial fistulas (2.8%), 2 endoleaks (0.8%) after prior thoracic endoluminal grafting, and 1 (0.4%) adult coarctation. Endoleak surveillance was performed using serial computed tomography scans.

Results

Mean patient age was 68 years (range, 23-91 years). Endoleak developed in 38 patients (15.3%): 15 distal type I (39.5%), 13 proximal type I (34.2%), 8 type II (21.1%) and 2 type III (5.3%). No surgical intervention was performed in 26 patients (68.4%), in which the endoleak spontaneously resolved in 14 (53.8%), 8 (30.8%) are being monitored and are asymptomatic, 3 (11.5%) died of unrelated causes, 2 (7.7%) withdrew from the study, and 1 (3.8%) was lost to follow-up. Twelve patients (31.6%) required reintervention using an additional endoluminal graft: 8 (66.7%) with a proximal type I endoleak, 2 (16.7%) with a distal type I endoleak, 1 (8.3%) with both distal type I and type III endoleaks, and 1 (8.3%) with a type III endoleak. Open conversions were necessary secondary to device deployment difficulties in two patients (0.8%), and due to expansion of a thoracoabdominal aneurysm and rupture of an aneurysm secondary to a type II endoleak in one patient (0.5%) each.

Conclusion

Endoleaks are an infrequent, yet important, complication after thoracic endografting. Many endoleaks will resolve spontaneously, but some patients may require another endovascular intervention. Close surveillance is recommended for these patients; however, open conversion is rarely indicated. Because more diseases of the thoracic aorta are being treated using an endovascular approach, a standardized treatment algorithm is essential to safely and effectively manage associated endoleaks.

An endoleak occurs when blood flows outside the stent graft lumen and may complicate endovascular treatment of abdominal and thoracic aortic disease by contributing to enlargement or rupture of an aneurysm. Although there are considerable data regarding endografting in the abdominal aorta, the etiology of endoleaks remains controversial.¹, ², ³, ⁴ The thoracic aortic stent graft is a relative newcomer for use in endovascular intervention, and the anatomic and pathologic challenges in this vascular region differ from those in the abdominal aorta. As yet, the precursors of endoleak after thoracic aortic endovascular interventions are poorly understood. In this article, we report the different types of endoleaks encountered during a single-center study and describe their relationship to the pathologies treated.

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Methods 

This report analyzes thoracic aortic endovascular repair at our institution (Arizona Heart Institute) from February 2000 to August 2005, with special emphasis on endoleaks. Indications for study enrollment included atherosclerotic aneurysms, aortic dissections, penetrating aortic ulcers, contained ruptures, pseudoaneurysms, acute aortic transections, aortobronchial fistulas, endoleaks after thoracic endoluminal grafting, and coarctation.

All patients were enrolled in a single-center investigational device–exemption protocol approved by an Institutional Review Board. Before the procedure, patients signed an informed consent for use of the TAG endoprosthesis (W. L. Gore & Associates, Flagstaff, Ariz). Between February 2000 and May 2001, patients received the original TAG configuration with two longitudinal nitinol spines for columnar support. The device manufacturer voluntarily recalled the device from clinical studies in mid-2001 to investigate device fracture rates; a new version of the TAG without longitudinal spines was introduced in February 2003 and used during the remainder of our study. Patient demographics, associated comorbidities, clinical presentation, operative management, procedural details, complications, and reinterventions were monitored prospectively.

All procedures were performed in the operating endovascular suite under general anesthesia. Serum levels of blood-urea nitrogen and creatinine were evaluated before scanning with contrast to assess the risk of dye administration. Digital subtraction angiography was obtained in all the cases, and intravascular ultrasound was used to confirm vessel measurements and examine aortic pathologies. After TAG deployment, an angiogram was obtained. Before discharge, high-resolution computed tomography (CT) scanning was used to evaluate device performance and determine the presence of endoleaks.

Patients were offered treatment of endoleaks as follows: type I proximal and distal endoleaks as well as type III endoleaks were treated at the time of discovery. An exception was the case of type I distal endoleak in patients with dissection in whom follow-up was performed, unless the patient was symptomatic or a pseudoaneurysm had formed. Type II endoleaks were monitored. CT scans of the chest (with and without contrast) were done at 1, 6, and 12 months the first year, and annually thereafter. If an endoleak was discovered in follow-up, CT scanning was performed every 3 months.

An endoleak was defined as the persistence of blood flow outside the lumen of the endograft and within the aneurysm sac or the adjacent vascular segment treated by the graft.⁵, ⁶ Endoleaks were classified into five categories according to the time of occurrence relative to the operative procedure and the site of origin.⁶

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Results 

During a 5-year period, 249 patients underwent TAG implantation. Demographics, indications for stent grafting, and type of endoleaks and outcomes are described in Table I.

Table I. Demographics and results

Variable	Value
Demographics, No.	249
Age, mean (range) years	68(23-91)
Sex, No. (%)
Men	146(58.6)
Women	103(41.4)
Follow-up, mean ± SD months (range)	20.0±19.4 (1-60)
Indications for TAG, No. (%)
Atherosclerotic aneurysms	111(44.6)
Aortic dissections	67(26.9)
Penetrating aortic ulcers	27(10.8)
Contained ruptures	14(5.6)
Pseudoaneurysms	11(4.4)
Acute aortic transections	9(3.6)
Aortobronchial fistulas	7(2.8)
Endoleak	2(0.8)
Coarctation	1(0.4)
Type of endoleaks, No. (%)	58
Type I distal	15(39.5)
Type I proximal	13(34.2)
Type II	8(21.1)
Type III	2(0.5)
Type IV	0
Type V	0
Fate of endoleak, No. (%)	38
Spontaneously resolved	14(36.8)
Required reintervention	12(31.6)
Under surveillance	8(2.3)
Type I proximal	5
Type I distal	2
Type II	1
Withdrew from study	2(0.5)
Died (cause not related to endoleak)	1(0.4)
Lost to follow-up	1(0.4)

Type I distal endoleak 

In 15 patients with type I distal endoleaks, 13 had no intervention, and two had further procedures (Table II).

Table II. Outcome of type I distal endoleak in 15 patients^a

In eight of the patients with chronic dissections (with or without pseudoaneurysm formation) in whom the distal endoleak was a result of persistent perfusion of the false lumen from the distal re-entry site, the endoleak spontaneously resolved in seven (≤1 month, n = 6; ≤1 year, n = 1). An endoleak was seen in the eighth dissection patient at 48 months. This patient remains asymptomatic and is being monitored. In two patients with descending thoracic aortic aneurysms, endoleaks thought to be present immediately after the procedure were not seen in follow-up scans before discharge. In the patient with the aortobronchial fistula, a distal endoleak was seen at 60 months; the patient remains asymptomatic and is currently being monitored. One patient was lost to follow-up, and one died unrelated to endoleak.

Two patients with distal type I endoleak required further reintervention. Both patients had been treated for descending thoracic aortic aneurysms. In one patient, an endoleak and an increase in aneurysm sac size became apparent 6 months after the initial procedure, and an intervention with two additional endoprostheses was performed successfully. In the other patient, the distal endoleak was seen during a 6-month follow-up exam as well. The patient had Hodgkin lymphoma and was reluctant to undergo further surgery initially; however, 2 months later he had back pain and the aneurysm sac size had increased, and he agreed to deployment of an additional TAG. This procedure was complicated by small iliac artery size, vessel tortuosity, and prior common femoral artery patch angioplasty. Ultimately, the TAG could not be inserted. Balloon angioplasty was performed on the existing graft with coil embolization of the aneurysm sac. Two days later, the patient presented with significant coagulopathy and renal failure, and his family withdrew supportive measures.

Type I proximal endoleak 

Type I proximal endoleaks occurred in 13 patients; 4 had been treated for chronic dissections, 7 for aneurysms, 1 for contained rupture and pseudoaneurysm, and 1 for chronic dissection and pseudoaneurysm (Table III).

Table III. Outcome of type I proximal endoleak in 13 patients

Reintervention with an additional TAG or treatment with balloon angioplasty and coils, or both, was performed in eight patients with type I proximal endoleaks. In three patients with aneurysmal pathology, proximal endoleaks were identified at 6, 22, and 37 months, respectively. The endoleak found at 6 months was associated with proximal expansion of the aneurysm, and an open procedure using aortic arch debranching and antegrade delivery of an additional TAG was performed. An additional TAG was placed in each of the other two patients, and the endoleaks resolved. In the four patients with chronic dissections, endoleaks at day 5 (n = 1), at 3 months (n = 2), and at 16 months (n = 1) after the primary intervention were treated with an additional TAG. The patient treated at 16 months also received coils to the left subclavian artery. In the patient with chronic dissection and pseudoaneurysm formation, a proximal endoleak was treated at day 5 after the primary procedure with two additional TAG devices and coverage of the left subclavian artery.

Five of the patients with a type I proximal endoleaks had no further intervention; four had been treated for aneurysms in the descending thoracic aorta and one patient for contained rupture with pseudoaneurysm formation. Despite our recommendations for further intervention, all five refused additional procedures and are under surveillance. Endoleaks were identified at 30 days in the patient with the contained rupture and at 6 months (n = 1) and 48 months (n = 3) in the aneurysm patients. No expansion of the aneurysm sac was seen in any of the cases.

Type II endoleaks 

Type II endoleaks occurred in eight patients (21%); seven had been treated for aneurysms and one for chronic dissection. There were no reinterventions (Table IV).

Table IV. Outcome of type II endoleaks in eight patients

Three patients left the operating room with type II endoleaks. One resolved ≤1 month, and two resolved ≤1 year. Three more endoleaks were identified at 6 months, 16 months, and 48 months, respectively; the two discovered at 6 and 16 months resolved, and the later is being monitored and shows no significant change 4 years after the procedure. One endoleak was seen at 24 months, but the patient died before additional follow-up of causes unrelated to the endoleak. Another patient was lost to follow-up at 36 months.

Type III 

Two type III endoleaks were identified, one at 6 months in a patient with an existing distal type I endoleak (diagnosed at 3 months) and the other at 1 year. The patient with type I and III endoleaks was treated after discovery of the type III leak and received an additional TAG device and coils between the graft and the aneurysm sac; both endoleaks resolved.

The patient with the solo type III endoleak was at high risk for intervention because of comorbidities and was reluctant to undergo further treatment; his aneurysm sac was stable until 33 months, when an enlargement was seen. An additional TAG was placed to line the inner lumen of the previous graft site and bridge the separation. The endoleak resolved, but a possible type II endoleak was seen at 45 months at the level of T8-T9 at another facility. The patient had a syncopal episode, and a rupture of the descending aneurysm sac was suspected. He underwent an open conversion and repair. His intercostal arteries were found to be supplying the ruptured aneurysmal sac. The patient survived the procedure.

Open conversions 

Five patients had open conversions; all of them had originally received TAG devices for aneurysmal disease. One of the patients, who had type I and III endoleaks, has already been described; details of the other 4 are provided below.

The delivery sheath perforated the aneurysm sac and caused extensive hemorrhaging in one patient with a very tortuous aorta and a 10-cm aneurysm extending distal to the subclavian artery. A successful open conversion was performed, but the patient died 2 weeks later of multiorgan failure. In another patient, TAG deployment for an aneurysm adjacent to the left subclavian artery was complicated by severe arch angulation. The orientation of the graft and severity of the endoleak required open conversion the day after the initial procedure; the patient did well and had no complications. In the other two patients, aneurysmal dilation was seen proximal to the graft with involvement of the arch vessels; an arch vessel transposition was performed with antegrade delivery of TAG endograft with good results.

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Discussion 

Despite recent advances in endovascular technology, endoleaks remain the Achilles heel of stent grafting and are a complication not seen with open repair. Management and treatment of endoleaks associated with endovascular intervention for abdominal aortic aneurysms have been described, but those after thoracic aortic stent grafting are less studied.², ³, ⁴, ⁵, ⁶, ⁷, ⁸, ⁹, ¹⁰, ¹¹ Still, rates of endoleak after thoracic aortic stent grafting have been thought to be lower than those in the abdominal aorta, where 10% to 25% of patients are affected.¹², ¹³, ¹⁴, ¹⁵, ¹⁶, ¹⁷, ¹⁸, ¹⁹ In the European Collaborators on Stent-Graft Techniques for Thoracic Aortic Aneurysm and Dissection Repair (EUROSTAR) and United Kingdom Thoracic Endograft registries of thoracic aortic stent grafting, endoleaks were relatively infrequent and usually related to graft fixation (type I).¹⁸ Similar reports indicate most endoleaks were seen early at junctional connections and proximal and distal sites.¹², ¹³ Our own results in a previous series were comparable¹⁹; nevertheless, 15% of patients in the present study had endoleaks.

Most were type I distal endoleaks in patients with an aortic dissection, and these were detected ≤30 days of the procedure and resolved spontaneously. Such endoleaks were the result of distal perfusion of the false lumen through re-entry tears, and thrombosis of the false lumen at the level of the stent sealed the leaks. Song et al,¹⁶ in their published experience of endograft exclusion of both acute and chronic descending thoracic aortic dissections, noted thrombosis of the false lumen in 61% of patients at 30 days, with 88% completely thrombosed at 12 months.¹⁶ These results are similar to those of others.¹⁷, ²⁰ When endoleaks develop >30 days in patients with dissections, they may be from reperfusion of the false lumen. In these patients, the distal end of the graft is at risk of eroding through the dissection flap, allowing flow into the false lumen.²¹ Pseudoaneurysm formation and the presence of symptoms are the main causes of failure necessitating secondary intervention.

Accurate placement in the arch can be very challenging, and even a tiny distal migration during deployment of the stent graft can result in inadequate proximal fixation; placement of a proximal cuff or an additional endoluminal graft can further complicate the repair.²² We suspect that a curved, tortuous aortic arch resulted in an inadequate proximal landing zone in three of our patients with thoracic aneurysms who required reintervention for proximal endoleaks. Graft detachment and pressurization of the aneurysm sac have also been reported to cause proximal endoleak, but we did not see this complication in our study.¹⁴

Although relatively few reports of type II endoleaks have been published, they comprised 21% of the endoleaks in our study.¹², ¹⁸, ²³, ²⁴ The causes of type II endoleaks may include the presence of small intercostal branches within the excluded aneurysm sac or coverage of the left subclavian artery.²³, ²⁴ We saw only two type III endoleaks (<1%). Junctional endoleaks secondary to modular disconnection or fabric disruption are not reported frequently,¹² and the newer generation of grafts feature a more aggressive overlapping design.¹³

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Conclusion 

The long-term consequences of endoleaks after endografting in the thoracic aorta are somewhat unclear at this time. Distal type I endoleaks in patients treated for thoracic dissection are likely to resolve spontaneously and may be monitored with CT scanning. When pseudoaneurysm formation occurs or the patient becomes symptomatic, reintervention is indicated.

A distal type I endoleak that develops in a patient with an aneurysm should be treated with an additional graft when the endoleak is discovered. Open conversion with visceral debranching may be necessary if the additional stent grafts don't resolve the endoleak, there is expansion of the sac and the patient is symptomatic. We also recommend aggressive treatment of proximal type I endoleaks with an additional cuff or stent graft. Adequate landing zones are necessary and subclavian–carotid bypass may also be indicated. When the left subclavian artery is covered, coiling should be considered to prevent retrograde endoleak. Aortic arch debranching should be performed if all the above fail, the sac is expanding and/or the patient is symptomatic.

Type II endoleak may be monitored with serial CT scans unless the dimension of the aneurysm sac changes significantly. Additional treatment may include ballooning with coil embolization between the aortic endograft and the sac. CT-guided coil embolization may be helpful in such cases.

Type III endoleaks should be treated aggressively at the time of discovery to prevent increases in the aneurysm sac size. In some cases, deployment and adequate ballooning of an additional endoluminal graft to reline the existing stent graft may ensure complete apposition of the graft to the vessel wall (Table V).

Table V. Recommendations for different types of endoleaks associated with endovascular repair of descending thoracic aortic diseases

•Proximal type I: aggressive treatment with additional stent/cuff With or without carotid–subclavian bypass or transposition Coverage of left subclavian: coiling Open conversion only if all the above fail, expansion of the aneurysm sac and patient symptomatic •Distal type I: additional cuff/stent (descending thoracic aneurysms) Pseudoaneurysm formation and/or symptomatic patient: additional cuff/stent Open conversion only if all the above fail, expansion of the aneurysm sac and patient symptomatic •Distal type I: watch and wait (thoracic aortic dissection) •Type II: follow-up (balloon, coiling, guided by computed tomography scan, if needed) •Type III: additional graft

Endoleaks represent a significant complication after endovascular treatment of the thoracic aorta. More data are needed to determine the risk of endoleak over time, and long-term CT surveillance of patients with endografts remains extremely important.

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Author contributions 

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