Secondary interventions following endovascular repair of abdominal aortic aneurysm

CURRENT TOPICS REVIEW ARTICLE

Secondary interventions following endovascular repairof abdominal aortic aneurysm

Naoki Toya • Yuji Kanaoka • Takao Ohki

Received: 15 July 2013 / Published online: 22 October 2013

� The Japanese Association for Thoracic Surgery 2013

Abstract Endovascular aneurysm repair (EVAR) of the

abdominal aortic aneurysms is an attractive alternative to

open surgery with significantly improved perioperative

outcomes. However, EVAR is accompanied by a higher

rate of graft-related complications and secondary inter-

ventions. Therefore, life-long surveillance and manage-

ment of secondary treatment is essential for successful

EVAR. Endoleaks are one of the most crucial problems

after EVAR. Persistent endoleaks are classified into five

types and its management depends on the type and sever-

ity. Most persistent endoleaks are detectable by contrast-

enhanced computed tomography; however, in some cases,

two different endoleak types may coexist. Determining

whether an endoleak requires any treatment or not is an

important consideration. Most if not all type I and III en-

doleaks require prompt and definitive secondary treatment.

While type II endoleaks are most commonly encountered

during follow-up, not all type II endoleaks require invasive

treatment. When secondary treatment is required, it can be

treated endovascularly in most cases, even if there is no

endoleak. Following EVAR, due to the decompression of

the sac, the integrity of the aneurysmal wall strength

reduces. Therefore, sudden sac expansion/rupture may

occur when an endoleak is encountered following a period

of complete aneurysmal exclusion. If diagnosed promptly

most late complications can be treated in a less invasive

manner, but it could lead to catastrophic event if it is

missed. Therefore, adequate and life-long radiographic

follow-up is as important as the appropriate patient and

device selection as well as the EVAR procedure itself.

Keywords Endovascular aneurysm repair �Secondary intervention � Endoleak � Abdominal

aortic aneurysm

Introduction

Large randomized studies have concluded that in patients

with large abdominal aortic aneurysms (AAAs) treated

with endovascular aneurysm repair (EVAR) had reduced

30-day operative mortality compared with open repair [1,

2]. Short-term follow-up revealed a perioperative survival

benefit in favor of EVAR; however, this benefit was lost

after 2-year midterm follow-ups [3]. Crude annual sec-

ondary intervention rates from the United States population

registries was found to be 3.7 % per year, and re-inter-

vention-free survival estimates demonstrated a linear

progression with 89.9 % of grafts without secondary pro-

cedures at 2 years [4].

The rates of late conversion to open repair after EVAR

ranged from 0.4 to 22 %, and of 1.9 % AAA patients

undergoing EVAR required late conversion with a 10 %

mortality rate [5].

Postoperative complications after EVAR include endo-

leak, migration, graft limb occlusion, stentgraft infection

and aneurysmal rupture. Endoleaks are one of the most

common and crucial problems after EVAR. Most persistent

This review was submitted at the invitation of the editorial committee.

N. Toya � Y. Kanaoka � T. Ohki

Division of vascular Surgery, Department of Surgery,

Jikei University School of Medicine, Tokyo, Japan

N. Toya (&)

163-1, Kashiwashita, Kashiwa-shi, Chiba 277-8567, Japan

e-mail: [email protected]

T. Ohki (&)

3-25-8, Nishi-shinbashi, Minato-ku, Tokyo 105-8461, Japan

e-mail: [email protected]

123

Gen Thorac Cardiovasc Surg (2014) 62:87–94

DOI 10.1007/s11748-013-0333-2

endoleaks are diagnosable by enhanced computed tomog-

raphy (CT). Persistent endoleaks are classified based on the

cause into five types with endotension as type V. An

appropriate diagnosis of endoleak type is critical when

considering additional treatment.

Type I and III endoleaks require prompt, definitive,

secondary treatment. Incomplete initial graft expansion,

further arterial dilatation, endograft migration, component

separation, and tears within the graft fabric are all possible

causes of type I and III endoleaks [6].

Type II endoleaks are reportedly most common, occur-

ring at a rate of 14 % at 1 month and decreasing to 10.3 %

after 1 year [7]. An analysis of the database at Jikei Uni-

versity Hospital, which includes retrospective data on

1,100 patients, revealed that type II endoleaks were not

associated with an increased risk of rupture. Incidence of

persistent type II endoleaks was 14 %, and only one

patient with a type II endoleak experienced rupture

(0.6 %) and required conversion to open repair. Notably,

this patient was hemodynamically stable and only com-

plained of abdominal pain after AAA rupture and safely

underwent open repair. Thus, we take a conservative

approach in the management of t type II endoleaks and

only treat them when it is associated with significant sac

enlargement or the presence of abdominal pain.

Type I endoleak

In type I endoleaks, poor apposition is observed between

the attachment sites of a stent graft and the native aortic or

iliac artery wall, allowing blood to leak through the defect

into the aneurysm sac. Type I endoleaks are further sub-

classified by their location. Type IA endoleaks occur at the

proximal aortic attachment site, whereas type IB endoleaks

occur at one of the distal iliac artery attachment sites [8].

Type IA endoleaks have been described as the main cause

of late rupture [9]. Type IA and IB endoleaks require

prompt, definitive, additional treatment.

Endovascular treatment options for type IA endoleaks

includes securing of the attachment site with a touch-up

balloon, stent graft extension [10], placement of a Palmaz�

XL stent (Cordis Co. a Johnson & Johnson Company,

Miami Lakes, FL, USA) at the proximal attachment site

[11], or embolization [10, 12]. More recently, endostaples

to secure the position of the proximal cuff to the primary

endograft have been developed [13–15]. Most of these re-

interventions are treatable endovascularly, however, some

require conversion to open repair [10, 16–18].

The first treatment option for secondary interventions

for type IA endoleaks is the catheter-based placement of an

aortic cuff extension. Excluder� (W.L.Gore & Associates,

Inc., Flag-staff, AZ, USA) aortic extensions are effective

because of strong radial force. Endurant� (Medtronic, Inc.,

Minneapolis, MN, USA) aortic extension components are

capable of covering a length of 45 mm, which can provide

a long overlap between the main body, reducing the risk of

type III endoleaks, and the number of aortic cuffs.

Arthurs et al. [19] evaluated the effect of the Palmaz�

XL stent placement for type IA endoleaks on delayed en-

doleak formation and migration. The combined use of

Palmaz� XL stent after deployment of the Excluder has

also been successful in preventing type IA endoleaks and

distal migration [20].

When type IB endoleak is expected prior to EVAR

based on iliac artery pathology, embolization of the

hypogastric artery with limb extension to the external iliac

artery is recommended [21].

Type II endoleak

Type II endoleaks occur when there is retrograde blood

flow into the aneurysm sac via an excluded aortic branch,

most commonly the lumbar or inferior mesenteric artery

(IMA). Type II endoleaks can be managed conservatively

if the aneurysm is shrinking or remains stable [22].

Independent predictors of type II endoleaks are mural

thrombus, patent lumbar arteries, aneurysmal length, and

iliac length [23]. A previous study has demonstrated that

patients with a large, patent IMA, or more than two lumbar

arteries identified on preoperative CT angiography, are at a

higher risk for persistent type II endoleaks [24].

Batti et al. [25] concluded that not all type II endoleaks

are benign and recurrent as well as persistent type II en-

doleaks are prone to life-threatening complications. How-

ever, Patatas et al. [26] revealed that the management of

most isolated type II endoleaks should be conservative

with close radiological follow-up even when persistent,

with intervention restricted to significant sac enlargement

of [5 mm over a 6-month period or [10 mm when com-

pared with the pre-EVAR diameter.

Secondary interventions include transarterial emboliza-

tion [10, 17, 27–29], translumbar embolization [30, 31],

transcaval embolization [32], direct thrombin injection

[33–35], and endoscopic or open ligation of the lumbar and

IMAs [36, 37]. A risk of ischemic colitis has been reported

with the use of liquid embolization materials [34]. Some

patients require multiple re-interventions to treat type II

endoleaks: furthermore, lumbar artery embolization carries

a low midterm success rate [23].

Transarterial embolization

The IMA or iliolumbar arteries are the typical endoleak

feeding vessels. Transarterial embolization is performed

88 Gen Thorac Cardiovasc Surg (2014) 62:87–94

123

via the common femoral artery. Endoleaks occurring from

the IMA are catheterized through the middle colic artery

and Riolan’s arcade from the superior mesenteric artery

(SMA) (Fig. 1). Endoleaks from lumbar arteries or the

median sacral artery are accessed through collateral vessels

of the hypogastric artery, mostly iliolumbar arteries [38]. If

hypogastric embolization has already been performed at

the time of initial EVAR, then the endoleaks from the ili-

olumbar artery are catheterized through the deep femoral

artery or the circumflex iliac artery, using either prograde

or retrograde puncture of the common femoral artery.

The most important detail of this procedure involves

guiding the microcatheter to the endoleak cavity, referred

to as the nidus. It is not effective to embolize a single

feeding artery, such as the IMA or iliolumbar artery,

because of the redistribution of blood flow through the

other collateral vessels such as the lumbar arteries, which

can continue to supply the nidus and pressurize the aneu-

rysm sac [39]. Therefore, the best way to achieve a per-

manent cessation of flow is to occlude the entire nidus in

order to interrupt the communicating aortic side branches

[38, 40]. With the advent of modern hydrophilic guide-

wires and microcatheters that are very trackable, direct

catheter access to the endoleak nidus within aneurysm sac

has become more feasible via collateral pathways. If direct

access to the nidus is possible, transarterial embolization

can be an effective technique [39].

If a direct access to the endoleak nidus is not achievable,

a translumbar embolization should be considered. Galla-

gher et al. [23] revealed that for type II endoleaks with an

isolated IMA identified as the source, initial success for

transarterial embolization at 2 years was 72 %, however,

with a lumbar source, the initial success rate decreased to

17 % at 2 years.

Recently, several studies reported liquid embolic agents

such as n-butyl 2-cyanoacrylate (NBCA) and ethylene

vinyl alcohol copolymer (Onyx) being used to embolize the

nidus [38, 39]. However, NBCA has critical disadvantages

of low viscosity and a short polymerization time, which

increase the risk of unintended vessel embolization and

necrosis [38]. Bowel ischemia after endoleak embolization

using NBCA has been reported [40]. Onyx is a strong

solvent and can cause degradation of conventional catheter

materials: therefore, special Onyx compatible microcath-

eters are needed when using this agent [38].

The most widely used embolic material is coil, although

coil embolization of the nidus may be fraught with recan-

alization through the interstices of the coils [39].

Translumbar embolization

Taranslumbar sac puncture and embolization is a method

that we primarily perform to occlude the nidus; however,

transarterial approach has been increasingly attempted due

to the availability of the latest microcatheters and hydro-

philic wires.

Prior to translumbar embolization, diagnostic angiogra-

phy is performed via trans-femoral access to confirm the

presence of type II endoleak and to determine which ves-

sels are involved. Trans-femoral catheter should be kept in

place during the procedure, in order to evaluate the com-

pleteness of the embolization. Following diagnostic

angiogram, the patient is then placed in a prone position

and local anesthesia is administered. Pre-operative CT and

angiography findings are used to determine the optimal

entry point and the depth for sac puncture (Fig 2a).

An 18-gauge percutaneous transhepatic cholangiodrai-

nage (PTCD) needle (Hanako Medical, Saitama, Japan) is

used to directly access the aneurysm sac. Distance from the

puncture site to the nidus is measured, and the depth is

marked on the PTCD needle using silk sutures. It is

important not to advance the needle more deeply than the

Fig. 1 Transarterial

embolization Inferior

mesenteric artery were

catheterized through the middle

colic artery and Riolan,s arcade

from the superior mesenteric

artery (SMA)

Gen Thorac Cardiovasc Surg (2014) 62:87–94 89

123

marking silk thread (Fig. 2b). A lateral view is effective to

confirm the puncture depth. Digital subtraction angiogra-

phy is performed to localize the nidus and feeding vessels

(Fig. 3a).

Once the PTCD needle enters the nidus, blood return

from the sac is encountered. Sac blood pressure is mea-

sured at this point. In many cases, the nidus pressure is

almost half of that of systemic pressure and the pulse wave

is low. Direct angiography from the needle sometimes

reveals small iliolumbar arteries connecting the nidus that

were not recognizable preoperatively. If there is no return

of blood, the needle tip exists in the thrombus, and, angi-

ography should not be considered. A 0.035 in. Radifocus�

(Terumo, Tokyo, Japan) guide wire is advanced through

the needle into the nidus. After the needle is removed, a

Slip-Cath� KMP (Cook Medical, Inc., Bloomington, IN,

USA) catheter is placed over the guidewire into the nidus.

We preferentially used 0.018-in. detachable coils (Fig. 3b).

After embolization is completed and stasis confirmed by

angiography from the trans-femoral angiographic catheter,

the KMP catheter is removed. Patients are then kept in a

supine position for 4 h to promote hemostasis.

Studies evaluating the success of type II endoleak repair

using translumbar embolization compared with transarte-

rial embolization reported a low recurrence rate in the

translumbar group [31, 40]. Stavropoulos et al. [40]

recently reported, however, that there was no significant

difference in clinical success between the two groups with

two (3.2 %) complications in the translumbar group and no

complications in the transarterial group.

Direct percutaneous sac injection (DPSI)

DPSI is performed using thrombin, coils, Gelfoam�, glue,

or a combination thereof. Uthoff et al. [41] reported the

total incidence of recurrent endoleaks to be 50 % after

DPSI, and the occurrence of recurrent endoleaks was sig-

nificantly associated with dual antiplatelet medication. In

this study, cases of pulmonary artery embolism and graft

puncture have been reported as complications of DPSI.

Fig. 2 Translumbar

embolization: a CT and

angiography findings were

reviewed to determine the

optimal entry point and depth

for sac puncture; b: an 18-gauge

percutaneous transhepatic

cholangiodrainage (PTCD)

needle was used to directly

access the aneurysm sac. After

confirmation of blood return

from the sac (arrow), blood

pressure should be measured

Fig. 3 Translumbar

embolization: a digital

subtraction angiography (DSA)

was performed to localize the

nidus and feeding vessels,

b 0.018 in. detachable coils

were preferentially used


123

Type III endoleak

Type IIIA is a junctional leak or modular disconnect, and

IIIB is fabric disruption. Like type I endoleaks, type III

endoleaks are considered to be high-pressure, high-risk

leaks that require urgent management and there is little

debate regarding the need for treatment of type III en-

doleaks [8]. The management of type III endoleaks

includes additional iliac limb grafts [10] or an additional

bifurcated stent graft [42].

Aortic remodeling after EVAR may lead to junctional and

attachment site leaks: nevertheless, sac regression is

obtained. We have advocated the ‘‘anatomical deployment’’

technique where the stent graft is deployed to fit the original

aortic configuration in an attempt to avoid complication

related to remodeling. Occasionally, there are cases in which

a fabric disruption is misdiagnosed as endotension (Fig. 4).

Type IV endoleak

Most type IV endoleaks occur intra-operatively, caused by

fabric porosity and subside within 30 days. No specific

treatment is required. Type IV endoleaks have been

attributed largely to material porosity, recognized more

commonly with stent grafts made with thinner fabric such

as the Endurant and not with the Excluder low-perme-

ability device.

Angiography obtained by placing a pigtail catheter

below the proximal attachment and inside the stent graft is

useful in differentiating type IV from type IA endoleaks.

The existence of an intraoperative type IV endoleak indi-

cates that sac pressure and systemic pressure are almost

equal during the perioperative period and this may lead to

decreased occurrence of type II endoleaks due to the

absence of pressure gradient.

Type V endoleak (endotension)

Type V endoleaks, or endotension, is characterized by

continued growth of an excluded aneurysm sac without

evidence of an endoleak. There are many possible etiolo-

gies of type V endoleaks [43]. Some investigators assume

that direct pressure transmission via thrombus between the

aortic wall and the stent graft can be a cause of type V

endoleak [44, 45]. Lin et al. [46] suggested that very low-

flow endoleak channels contribute to the development of

type V endoleaks. Generally, patients with type V endoleak

are asymptomatic and do not require secondary interven-

tion [43] as type V endoleaks rarely result in serious events

such as rupture [47]; however, one must be careful that

there are no hidden type I or III endoleak.

We have experienced a case of late rupture in which we

made such a misdiagnosis. This patient was diagnosed as

type V endoleak but following aneurysm rupture, it was

recognized as fabric disruption due to a mid-graft hole

(type IIIB endoleak) (Fig. 4). During the follow-up period,

we did not recognize the endoleak on CT probably due to

absence of pressure gradient inside and outside of the stent

graft. However, the undetected endoleak became obvious

following aneurysm rupture. If indicated due to mass

effect, treatment of endotension includes an endovascular

relining of the stent graft [22] or open conversion.

Migration

Migration results in a gradual loss of aortic approximation

and eventual repressurization of the sac [48]. There is a

tendency for migration to occur in patients with a large

neck diameter ([28 mm) [49]. Brevetti et al. [50] reported

improved aortic sac shrinkage with perirenal fixation of the

stent graft and a trend toward fewer endoleaks. When

Fig. 4 A case of late rupture

from a determination of

nonurgent type V endoleak.

Actually, it was recognized

fabric disruption due to midgraft

hole in this case to be diagnosed

with type IIIB endleak: a:

preoperative CT, b angiography

showed fabric leak


123

possible, perirenal fixation with the main body of the stent

graft should be performed.

In case of migration, large balloon-expandable stents

can be used to augment the fixation or extend the sealing/

fixation zone with additional cuffs. More recently, staples

to secure endovascular grafts to the aortic wall have been

developed with good early outcome [48]. Ohki et al. [15]

also reported the use of an independent endovascular fix-

ation device.

For any type of endoleak, the use of wireless pressure

sensor may be useful in prompt detection and also in

reducing the need for CT that exposes the patient to radi-

ation [51].

Endograft limb occlusion

A previous study has shown that most endograft limb

occlusions occurred less than 2 months after EVAR, and

rarely after 1 year [52]. We experienced 11 endograft limb

occlusions, during a 5-year period all of which were treated

successfully. The duration between EVAR and the sec-

ondary procedure averaged 9.1 months. Most patients with

limb occlusions were initially treated with the Zenith�

stent graft (Cook Medical, Inc. Bloomington, IN, USA).

Femoro-femoral bypass is a less invasive and safe pro-

cedure for limb occlusion and it is our preferred procedure.

Percutaneous transluminal angioplasty with or without

thrombolysis as well as open access thrombectomy has also

been reported with acceptable outcome.

Thrombectomy is useful for occlusion of limb deployed

in the external iliac artery (EIA), however, when the limb is

landed in the common iliac artery with patent internal iliac

artery, one must be careful not to embolize the internal iliac

artery with clots. Conway et al. [53] reported that

deployment of endograft limbs into the EIA led to a higher

rate of occlusion and leg amputation.

A more liberal intraoperative and early postoperative

secondary intervention strategy may reduce the occlusion

rates and improve outcomes [52]. When stenosis of the EIA

is suspected, a self-expandable stent should be deployed.

Karthikesalingam et al. [54] showed that an increase in

the peak systolic velocity in the stent graft limbs is asso-

ciated with an increased risk of limb occlusion. Intravas-

cular ultrasound is useful for the determination of stenosis.

Conclusion

In conclusion, the first treatment options for most second-

ary interventions after EVAR are treatable with endovas-

cular techniques. Type II endoleaks should be treated only

if they are associated with significant sac enlargement or

the existence of an abdominal pain. However, type I and III

endoleaks require prompt, definitive secondary treatment.

The increased use of EVAR as well as longer follow-up

period has led to increased incidence of late complications

and the need for secondary interventions. If diagnosed

promptly most late complications can be treated in less

invasive manner, but it could lead to catastrophic event if it

is missed. Therefore, adequate and life-long radiographic

follow-up is as important as the appropriate patient and

device selection as well as the EVAR procedure itself.

Conflict of interest The authors have declared that no conflict of

interest exists.

References

1. Greenhalgh RM, Brown LC, Kwong GPS, Powell JT, Thompson

SG, EVAR trial participants. Comparison of endovascular aneu-

rysm repair with open repair in patients with abdominal aortic

aneurysm (EVAR trial 1), 30-day operative mortality results:

randomised controlled trial. Lancet. 2004;364(9437):843–8.

2. Prinssen M, Verhoeven ELG, Buth J, et al. A randomized trial

comparing conventional and endovascular repair of abdominal

aortic aneurysms. N Engl J Med. 2004;351(16):1607–18.

3. Ohki T, Veith FJ, Shaw P, et al. Increasing incidence of midterm

and long-term complications after endovascular graft repair of

abdominal aortic aneurysms: a note of caution based on a 9-year

experience. Ann Surg. 2001;234(3):323–34 (discussion 334–5).

4. Nordon IM, Karthikesalingam A, Hinchliffe RJ, Holt PJ, Loftus

IM, Thompson MM. Secondary interventions following endo-

vascular aneurysm repair (EVAR) and the enduring value of graft

surveillance. Eur J Vasc Endovasc Surg. 2010;39(5):547–54.

5. Moulakakis KG, Dalainas I, Mylonas S, Giannakopoulos TG,

Avgerinos ED, Liapis CD. Conversion to open repair after

endografting for abdominal aortic aneurysm: a review of causes,

incidence, results, and surgical techniques of reconstruction.

J Endovasc Ther. 2010;17(6):694–702.

6. Powell A, Benenati JF, Becker GJ, Katzen BT, Zemel G,

Tummala S. Postoperative management: type I and III endoleaks.

Tech Vasc Interv Radiol. 2001;4(4):227–31.

7. Drury D, Michaels JA, Jones L, Ayiku L. Systematic review of

recent evidence for the safety and efficacy of elective endovas-

cular repair in the management of infrarenal abdominal aortic

aneurysm. Br J Surg. 2005;92(8):937–46.

8. Bashir MR, Ferral H, Jacobs C, McCarthy W, Goldin M. En-

doleaks after endovascular abdominal aortic aneurysm repair:

management strategies according to CT findings. AJR Am J

Roentgenol. 2009;192(4):W178–86.

9. Schlosser FJV, Gusberg RJ, Dardik A, et al. Aneurysm rupture

after EVAR: can the ultimate failure be predicted? Eur J Vasc

Endovasc Surg. 2009;37(1):15–22.

10. Faries PL, Cadot H, Agarwal G, Kent KC, Hollier LH, Marin ML.

Management of endoleak after endovascular aneurysm repair: cuffs,

coils, and conversion. J Vasc Surg. 2003;37(6):1155–61.

11. Tzortzis E, Hinchliffe RJ, Hopkinson BR. Adjunctive procedures

for the treatment of proximal type I endoleak: the role of peri-

aortic ligatures and Palmaz stenting. J Endovasc Ther.

2003;10(2):233–9.

12. Kirby L, Goodwin J. Treatment of a primary type IA endoleak

with a liquid embolic system under conditions of aortic occlusion.

J Vasc Surg. 2003;37(2):456–60.


123

13. Deaton DH, Mehta M, Kasirajan K, et al. The phase I multicenter

trial (STAPLE-1) of the Aptus endovascular repair system:

results at 6 months and 1 year. J Vasc Surg. 2009;49(4):851–7

discussion 857–8.

14. Bail DHL, Walker T, Giehl J. Vascular endostapling systems for

vascular endografts (T)EVAR—systematic review—current

state. Vasc Endovascular Surg. 2013;47(4):261–6.

15. Ohki T, Deaton DH, Condado JA. Aptus AAA repair system.

Endovascular Today 2006;Nov:29–35.

16. Cao P, Verzini F, Parlani G, et al. Predictive factors and clinical

consequences of proximal aortic neck dilatation in 230 patients

undergoing abdominal aorta aneurysm repair with self-expand-

able stent-grafts. J Vasc Surg. 2003;37(6):1200–5.

17. Veith FJ, Baum RA, Ohki T, et al. Nature and significance of

endoleaks and endotension: summary of opinions expressed at an

international conference. J Vasc Surg. 2002;35(5):1029–35.

18. Forbes TL, Harrington DM, Harris JR, DeRose G. Late conver-

sion of endovascular to open repair of abdominal aortic aneu-

rysms. Can J Surg. 2012;55(4):254–8.

19. Arthurs ZM, Lyden SP, Rajani RR, Eagleton MJ, Clair DG.

Long-term outcomes of Palmaz stent placement for intraoperative

type Ia endoleak during endovascular aneurysm repair. Ann Vasc

Surg. 2011;25(1):120–6.

20. Ghouri M, Krajcer Z. Endoluminal abdominal aortic aneurysm

repair: the latest advances in prevention of distal endograft

migration and type 1 endoleak. Tex Heart Inst J. 2010;37(1):

19–24.

21. Ahn JH, Kim JY, Jeon YS, et al. Successful treatment of type I

endoleak of common iliac artery with balloon expandable stent

(Palmaz XL stent) during endovascular aneurysm repair.

J Korean Surg Soc. 2012;82(1):59–62.

22. Bendermacher BLW, Stokmans R, Cuypers PW, Teijink JAW,

Van Sambeek MRHM. EVAR reintervention management strat-

egies in contemporary practice. J Cardiovasc Surg (Torino).

2012;53(4):411–8.

23. Gallagher KA, Ravin RA, Meltzer AJ, et al. Midterm outcomes

after treatment of type II endoleaks associated with aneurysm sac

expansion. J Endovasc Ther. 2012;19(2):182–92.

24. Arko FR, Rubin GD, Johnson BL, Hill BB, Fogarty TJ, Zarins

CK. Type-II endoleaks following endovascular AAA repair:

preoperative predictors and long-term effects. J Endovasc Ther.

2001;8(5):503–10.

25. El Batti S, Cochennec F, Roudot-Thoraval F, Becquemin J-P.

Type II endoleaks after endovascular repair of abdominal aortic

aneurysm are not always a benign condition. J Vasc Surg.

2013;57(5):1291–7.

26. Patatas K, Ling L, Dunning J, Shrivastava V. Static sac size with

a type II endoleak post-endovascular abdominal aortic aneurysm

repair: surveillance or embolization? Interact Cardiovasc Thorac

Surg. 2012;15(3):462–6.

27. Bonvini R, Alerci M, Antonucci F, et al. Preoperative emboli-

zation of collateral side branches: a valid means to reduce type II

endoleaks after endovascular AAA repair. J Endovasc Ther.

2003;10(2):227–32.

28. Kasirajan K, Matteson B, Marek JM, Langsfeld M. Technique

and results of transfemoral superselective coil embolization of

type II lumbar endoleak. J Vasc Surg. 2003;38(1):61–6.

29. Hansen CJ, Kim B, Aziz I, et al. Late-onset type II endoleaks and

the incidence of secondary intervention. Ann Vasc Surg.

2004;18(1):26–31.

30. Stavropoulos SW, Carpenter JP, Fairman RM, Golden MA, Baum

RA. Inferior vena cava traversal for translumbar endoleak

embolization after endovascular abdominal aortic aneurysm

repair. J Vasc Interv Radiol. 2003;14(9 Pt 1):1191–4.

31. Baum RA, Carpenter JP, Golden MA, et al. Treatment of type 2

endoleaks after endovascular repair of abdominal aortic

aneurysms: comparison of transarterial and translumbar tech-

niques. J Vasc Surg. 2002;35(1):23–9.

32. Mansueto G, Cenzi D, D’Onofrio M, Petrella E, Gumbs AA,

Mucelli RP. Treatment of type II endoleaks after endovascular

repair of abdominal aortic aneurysms: transcaval approach. Car-

diovasc Interv Radiol. 2005;28(5):641–5.

33. Ellis PK, Kennedy PT, Collins AJ, Blair PH. The use of direct

thrombin injection to treat a type II endoleak following endo-

vascular repair of abdominal aortic aneurysm. Cardiovasc Interv

Radiol. 2003;26(5):482–4.

34. Gambaro E, Abou-Zamzam AM, Teruya TH, Bianchi C, Hope-

well J, Ballard JL. Ischemic colitis following translumbar

thrombin injection for treatment of endoleak. Ann Vasc Surg.

2004;18(1):74–8.

35. van den Berg JC, Nolthenius RP, Casparie JW, Moll FL. CT-

Guided thrombin injection into aneurysm sac in a patient with

endoleak after endovascular abdominal aortic aneurysm repair.

AJR Am J Roentgenol. 2000;175(6):1649–51.

36. van Nes JGH, Hendriks JM, Tseng LNL, van Dijk LC, van

Sambeek MRHM. Endoscopic aneurysm sac fenestration as a

treatment option for growing aneurysms due to type II endoleak

or endotension. J Endovasc Ther. 2005;12(4):430–4.

37. Wisselink W, Cuesta MA, Berends FJ, van den Berg FG, Rau-

werda JA. Retroperitoneal endoscopic ligation of lumbar and

inferior mesenteric arteries as a treatment of persistent endoleak

after endoluminal aortic aneurysm repair. J Vasc Surg.

2000;31(6):1240–4.

38. Muller-Wille R, Wohlgemuth WA, Heiss P, et al. Transarterial

embolization of type ii endoleaks after EVAR: the role of eth-

ylene vinyl alcohol copolymer (Onyx). Cardiovasc Interv Radiol.

2013;36(5):1288–95.

39. Massis K, Carson WG, Rozas A, Patel V, Zwiebel B. Treatment

of type II endoleaks with ethylene-vinyl-alcohol copolymer

(Onyx). Vasc Endovascular Surg. 2012;46(3):251–7.

40. Stavropoulos SW, Park J, Fairman R, Carpenter J. Type 2 en-

doleak embolization comparison: translumbar embolization ver-

sus modified transarterial embolization. J Vasc Interv Radiol.

2009;20(10):1299–302.

41. Uthoff H, Katzen BT, Gandhi R, Pena CS, Benenati JF, Gei-

sbusch P. Direct percutaneous sac injection for postoperative

endoleak treatment after endovascular aortic aneurysm repair.

J Vasc Surg. 2012;56(4):965–72.

42. Teutelink A, van der Laan MJ, Milner R, Blankensteijn JD.

Fabric tears as a new cause of type III endoleak with Ancure

endograft. J Vasc Surg. 2003;38(4):843–6.

43. Toya N, Fujita T, Kanaoka Y, Ohki T. Endotension following

endovascular aneurysm repair. Vasc Med. 2008;13(4):305–11.

44. White GH, May J, Petrasek P, Waugh R, Stephen M, Harris J.

Endotension: an explanation for continued AAA growth after

successful endoluminal repair. J Endovasc Surg. 1999;6(4):

308–15.

45. Parodi JC, Berguer R, Ferreira LM, La Mura R, Schermerhorn

ML. Intra-aneurysmal pressure after incomplete endovascular

exclusion. J Vasc Surg. 2001;34(5):909–14.

46. Lin PH, Bush RL, Katzman JB, et al. Delayed aortic aneurysm

enlargement due to endotension after endovascular abdominal

aortic aneurysm repair. J Vasc Surg. 2003;38(4):840–2.

47. Kougias P, Bismuth J, Huynh TT, Lin PH. Symptomatic aneu-

rysm rupture without bleeding secondary to endotension 4 years

after endovascular repair of an abdominal aortic aneurysm.

J Endovasc Ther. 2008;15(6):702–5.

48. Deaton DH. Improving proximal fixation and seal with the He-

liFx Aortic EndoAnchor. Semin Vasc Surg. 2012;25(4):187–92.

49. Jim J, Rubin BG, Geraghty PJ, Criado FJ, Fajardo A, Sanchez

LA. A 5-year comparison of EVAR for large and small aortic

necks. J Endovasc Ther. 2010;17(5):575–84.


123

50. Brevetti LS, Nackman GB, Graham AM. Perirenal fixation as an

independent factor in aortic remodeling after endovascular aortic

aneurysm repair. Ann Vasc Surg. 2004;18(2):138–42.

51. Ohki T, Ouriel K, Silveira PG, et al. Initial results of wireless

pressure sensing for endovascular aneurysm repair: the APEX

Trial–Acute Pressure Measurement to Confirm Aneurysm Sac

EXclusion. J Vasc Surg. 2007;45(2):236–42.

52. van Zeggeren L, Bastos Goncalves F, van Herwaarden JA, et al.

Incidence and treatment results of Endurant endograft occlusion.

J Vasc Surg. 2013;57(5):1246–54.

53. Conway AM, Modarai B, Taylor PR, et al. Stent-graft limb

deployment in the external iliac artery increases the risk of limb

occlusion following endovascular AAA repair. J Endovasc Ther.

2012;19(1):79–85.

54. Karthikesalingam A, Kumar S, Anandarajah JJ, et al. Predictive

value of peak systolic velocity for the development of graft limb

complications after endovascular aneurysm repair. J Endovasc

Ther. 2012;19(3):428–33.


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Secondary interventions following endovascular repair of abdominal aortic aneurysm