1. ¤CLINICAL INVESTIGATION ¤
Intraoperative Intrasac Thrombin Injection to Prevent
Type II Endoleak After Endovascular Abdominal Aortic
Aneurysm Repair
Mario Zanchetta, MD, FSCAI; Francesca Faresin, MD; Luigi Pedon, MD; and
Salvatore Ronsivalle, MD
Department of Cardiovascular Disease, Cittadella, Padua, Italy.
¤ ¤
Purpose: To report a prospective, nonrandomized pilot study to determine whether fibrin
glue aneurysm sac embolization at the time of endovascular aneurysm repair (EVAR) is
a safe and effective procedure to primarily prevent type II endoleaks.
Methods: Between June 2003 and December 2005, 84 consecutive patients (79 men; mean
age 73.867.8 years, range 64–86) with degenerative infrarenal abdominal aortic aneurysm
underwent EVAR with bifurcated stent-grafts and fibrin glue injection into the aneurysm
sac at the conclusion of the endovascular procedure. A total of 424 imaging studies and 348
visits were recorded during the study period and reviewed.
Results: Selective catheterization of the aneurysm sac and fibrin glue injection immediately
after initial stent-graft deployment was successful in 83 (99%) of 84 cases; there was one
failure to access the excluded aneurysm sac due to severe iliac artery calcification. The
estimated primary and assisted clinical success rates at 2 years were 91.3% and 98.8%,
respectively, but the major findings were the low rate of delayed type II endoleak (2.4%)
and the statistically significant decrease in the maximum transverse aneurysm diameter
(50.4066.70 versus 42.0366.50 mm, p50.0001) at follow-up. In addition, of 31 patients
available for 24-month follow-up, 14 (45.2%) patients showed a reduction in maximum
transverse aneurysm diameter by $5 mm; 16 (51.6%) patients had no significant changes,
whereas only 1 patient showed a .5-mm enlargement.
Conclusion: This clot engineering approach to aneurysm sac embolization at the time of
endografting appears to be safe and may spare the patient a repeated catheter-based
intervention or surgical procedure.
J Endovasc Ther 2007;14:176–183
Key words: abdominal aortic aneurysm, endovascular repair, stent-graft, type II endoleak,
fibrin glue, sac embolization
¤ ¤
With an increasing demand for less invasive
procedures, endovascular aneurysm repair
(EVAR) of abdominal aortic aneurysms
(AAA) has emerged as a therapeutic alterna-
tive to conventional surgery, leading to new
complications and, consequently, to the de-
velopment of specific techniques for their
resolution. Endoleaks are one of the unique
complications of EVAR. Type II, the most
common form occurring in 5% to 17% of
patients treated in clinical trials,1
arises from
retrograde flow from the aortic side branches
with their multiple feeding and draining
vessels. The significance and treatment of
type II endoleaks have been debated for
nearly a decade. As our knowledge has
The authors have no commercial, proprietary, or financial interest in any products or companies described in this article.
Address for correspondence and reprints: Mario Zanchetta, MD, FACA, FSCAI, FESC, Dipartimento di Malattie
Cardiovascolari, Ospedale Civile, Via Riva Ospedale, 35013, Cittadella, Padova, Italy. Fax: 39-049-942-4502; E-mail:
emodinacit@ulss15.pd.it
176 J ENDOVASC THER
2007;14:176–183
ß 2007 by the INTERNATIONAL SOCIETY OF ENDOVASCULAR SPECIALISTS Available at www.jevt.org

2. increased, the areas of disagreement among
experts are now minimal.2–4
It is generally
agreed that an appropriate intervention has to
be considered when such a leak is accompa-
nied by aneurysm growth or persists for 6 to
12 months without evidence of sac shrinkage.
On the contrary, an endoleak that is present in
the setting of a shrinking aneurysm sac does
not need to be treated, even though its impact
on long-term outcome following EVAR is
unknown. The only disagreement that cur-
rently exists is whether to treat a type II
endoleak in the setting of an unchanged sac
diameter.
Today, secondary procedures are required
in up to 10% of patients per year to address
type II endoleaks.5
A variety of techniques are
employed, from early or late percutaneous
interventions6–10
(transarterial and direct
translumbar embolotherapy using coils or
liquid embolic agents) to surgical approaches
(laparoscopic retroperitoneal branch ligation11
or endoscopic aneurysm sac fenestration12
).
Intraoperative prophylaxis of type II endoleaks
may be a means of avoiding another interven-
tion or adjunctive surgical procedure, whose
morbidity and failure rates are still unknown.
We hypothesized that fibrin glue sac em-
bolization at the time of EVAR could primarily
prevent type II endoleaks instead of treating
them at their elusive origins once diagnosed;
thus, we conducted a pilot study to evaluate
the safety and midterm clinical results of this
approach.
METHODS
Study Design and Patient Population
A prospective nonrandomized study was con-
ducted between June 2003 and December
2005 to determine if fibrin glue embolization
of the aneurysm sac at the time of EVAR was
feasible, safe, and potentially effective. The
study protocol was approved by the hospital’s
Ethics Committee, and a specific informed
consent was obtained from each patient.
During the study period, 84 consecutive
patients (79 men; mean age 73.867.8 years,
range 64–86) with degenerative infrarenal
abdominal aortic aneurysm (AAA) were en-
rolled in the study; patients with fully rup-
tured aneurysms were excluded, although
contained ruptures were considered for treat-
ment. There were no restrictions to the use of
commercially prepared fibrin glue because it
has been approved for clinical use in Europe
since 1976. The preoperative patient charac-
teristics and comorbidities of the study cohort
are summarized in the Table. The first 64
patients in this study were included in a
technical note on this technique published
in 2005.13
Before the endovascular procedure, all pa-
tients underwent angiographic and contrast-
enhanced computed tomographic (CT; 3.75-
mm slice thickness) imaging to delineate
aneurysm morphology and to detect the
lumbar and inferior mesenteric arteries in
communication with the aneurysm. The ma-
jority of patent aortic side branches were the
lumbar arteries (range 1–3 paired vessels per
patient), whereas only 18 patent inferior
mesenteric arteries were detected. The mean
AAA diameter was 50.4066.70 mm (in our
institution, endovascular treatment of aneur-
ysms measuring 4.0 to 4.9 cm in diameter is
considered on the basis of aortoiliac anatomy,
vessel wall characteristics, and rapid expan-
sion .1 cm/y).
Fibrin Sealant
The fibrin sealant (Tisseel/Tissucol; Baxter-
Hyland Immuno AG, Vienna, Austria) is a non-
¤ ¤
TABLE
Characteristics and Comorbid Factors of 84
Patients Undergoing Intraoperative AAA
Sac Embolization
Male sex 79 (94.0%)
Age, y 73.867.8
Body mass index, kg/m2
26.664.1
Comorbidities
Diabetes mellitus 8 (9.5%)
Tobacco use 47 (55.9%)
Hypertension 46 (54.8%)
Hyperlipidemia 44 (52.4%)
Carotid artery disease 13 (15.5%)
Cardiac disease 39 (46.4%)
Renal disease 7 (8.3%)
Pulmonary disease 23 (27.4%)
¤ ¤
Continuous data presented as mean 6 standard
deviation.
J ENDOVASC THER
2007;14:176–183
PRIMARY PREVENTION OF TYPE II ENDOLEAK 177
Zanchetta et al.

3. cytotoxic, fully resorbable biological adhesive
matrix. The two main components of the
sealant are a fibrinogen solution containing
plasmatic proteins and factor XIII and a throm-
bin solution with calcium chloride and an
antifibrinolytic agent, such as aprotinin. The
organic components are extracted from hu-
man plasma, except for aprotinin, which
comes from bovine lungs. The fibrinogen
component, when mixed with thrombin, is
converted into polymerizing fibrin mono-
mers. Factor XIII is activated by thrombin in
the presence of calcium ions, and the pre-
mature lysis of the clot is prevented by
aprotinin.
Mixing fibrinogen and thrombin simulates
the environment of the last stages of the
natural coagulation cascade to form a struc-
tured fibrin clot similar to a physiological clot,
which may be naturally degraded by pro-
teolytic enzymes from the fibrinolytic system,
such as plasmin.14
As a result of its hemo-
static and adhesive properties, fibrin glue has
been extensively used in Europe in most
surgical specialties for over 3 decades to
reduce postoperative bleeding, to increase
tissue plane adherence, for drug delivery, and
in regenerative medicine or tissue engineer-
ing.15
The required dose of fibrin sealant to
cover 40 cm2
or 3.5 cm3
is about 5.0 mL.
However, its use as an injectable biopoly-
meric scaffold for aneurysm sac embolization
represents an off-label application.
Stent-Graft Procedure
EVAR was performed with bifurcated de-
vices in all cases: 69 Talent (Medtronic
Vascular, Santa Rosa, CA, USA), 14 AneuRx
(Medtronic Vascular), and 1 Excluder (W.L.
Gore and Associates, Flagstaff, AZ, USA).
Additionally, 33 adjunctive iliac extensions
(24 Talent and 9 AneuRx) were deployed
using the bell-bottom technique due to com-
mon iliac artery dilatation or aneurysm. All
the procedures were performed by creating
a brachial-femoral artery access; the main
body of the prosthesis with its integral iliac
leg, as well as the contralateral extension,
were deployed in the usual fashion, over-
sizing the endograft from˜ 10% to 20%.
Aneurysm Sac Embolization Technique
Selective catheterization of the AAA sac and
fibrin glue injection into the aneurysm cavity
were performed in the operating room during
endografting, as previously described.13
Briefly,
access to the aortic sac was obtained by leaving
a standard 0.035-inch guidewire in a suprarenal
position between the stent-graft and the native
aorta during the release of the main body. After
deploying the contralateral limb, a 23-mm-long
5-F Brite Tip introducer sheath (Cordis Europe,
Roden, The Netherlands) was advanced over
the guidewire into the excluded aneurysm sac.
The wire and the sheath’s vessel dilator were
removed, leaving the cannula in the aneurysm
sac. An aneurysmogram was performed to
demonstrate the patency and direction of flow
in the aortic side branches. A 25-cm-long,
double-lumen Duplocath catheter mounted on
a Duploject Y-connector (Baxter/Hyland Im-
muno) was inserted into the Brite Tip sheath.
To prevent distal embolization of the sealant,
a balloon was inflated in the limb of the main
prosthetic body to secure it to the native vessel.
Two vials containing 3000 IU/mL of aprotinin
and 500 IU/mL of thrombin solutions, respec-
tively, were attached to the 2 syringes in the
Duploject, and 5 or 10 mL of reconstituted fibrin
glue were injected into the sac. The balloon was
left in place for 1 minute after sealant injection.
Before withdrawing the introducer sheath from
the aneurysm sac, a repeated aneurysmogram
was performed to demonstrate the embolized
sac and thrombosis of type II endoleaks. In
patients with empty aneurysm sacs, aortic side
branch occlusion monitoring was also per-
formed by means of intravascular ultrasound
using the AcuNav catheter (Acuson, Siemens
Corp., Mountain View, CA, USA), a 10-F in-
tracardiac probe with a 5.5 to 10 MHz frequency
agile and full color-Doppler capability.
At follow-up, clinical examination, serum
creatinine monitoring, abdominal radiogra-
phy, CT angiography, and echo-color Doppler
were performed at discharge and at 3, 6, 12,
18, and 24 months, and annually thereafter.
Imaging Analysis
At the conclusion of the observation period,
all imaging studies were retrieved and in-
178 PRIMARY PREVENTION OF TYPE II ENDOLEAK
Zanchetta et al.
J ENDOVASC THER
2007;14:176–183

4. dependently reviewed in a blinded fashion by
two experts; differences were resolved in
consensus. The numbers of patent inferior
mesenteric as well as paired lumbar arteries
were counted; additionally, the aneurysm size
as well as the presence and type of endoleaks
were recorded. Moreover, sequential changes
in sac diameters were measured on 3-di-
mensional CT reconstructions and annotated.
The remodeling index (RI), i.e., the ratio of
serial changes in maximum transverse aneu-
rysm diameter, was defined as: positive
remodeling: RI .1.05, absence of remodeling:
RI 0.95 to 1.05, and negative remodeling: RI
,0.95.
Definitions
According to the current reporting stan-
dards for endovascular aortic aneurysm re-
pair,16
primary clinical success was defined as
freedom from aneurysm-related death, aneu-
rysm rupture, conversion to open repair, and
secondary endovascular or surgical proce-
dures, whereas our assisted primary and
secondary clinical success rates were defined
as clinical success achieved with the use of
additional or secondary endovascular or
surgical interventions, respectively. Finally,
complications were recorded according to
standardized definitions and are presented
with the severity score and treatment.
Statistical Analysis
Continuous variables are expressed as
means 6 standard deviation. The imaging
measurements before and after stent-graft
implantation were compared using the Stu-
dent t test. P,0.05 was considered to indicate
statistical significance. Kaplan-Meier analysis
was used to analyze initial, short-term, and
midterm primary and assisted primary clini-
cal success.
RESULTS
Selective sac catheterization and fibrin glue
injection immediately after initial stent-graft
deployment was successful in 83 (99%) of 84
cases; the only failure was due to severe
calcification of the common iliac artery. The
embolization took ,5 minutes at the conclu-
sion of the endovascular procedure. In these
patients, aneurysm sac embolization and
complete exclusion from retrograde perfu-
sion was achieved, as confirmed by intra-
operative aneurysmography (Fig. 1) or intra-
vascular echo-color Doppler insonation
(Fig. 2). Two patients required reintervention
Figure 1 ¤Selective angiograms of the aneurysm sac showed (A) a complex type II endoleak
from a patent lumbar artery (LA) and an inferior mesenteric artery (IMA) before fibrin glue
injection and (B) after fibrin glue aneurysm sac embolization. Note the absence of outflow vessels.
J ENDOVASC THER
2007;14:176–183
PRIMARY PREVENTION OF TYPE II ENDOLEAK 179
Zanchetta et al.

5. within 30 days: 1 for failed deployment (grade
2; conversion to open surgery) and the other
for external iliac artery rupture (grade 2;
surgical iliac artery repair). One symptomatic
patient with contained rupture died within
30 days (1.2% procedure-related mortality).
The mean follow-up was 14.468.7 months
(range 2–30); a 2-year follow-up was available
for 31 patients. A total of 424 imaging studies
(both CT and echo-color Doppler scans) and
348 visits were recorded, for a mean of 5.1
studies per patient (range 2–7) and 4.2 visits
per patient (range 1–5). The estimated prima-
ry and assisted primary clinical success rates
at 2 years were 91.3% and 98.8%, respectively
(Fig. 3). There were no early allergic-anaphy-
lactic reactions or tissue reactions in the
aneurysm sac or in the surrounding struc-
tures due to the fibrin glue injection during
the study period.
Four complications requiring reintervention
in follow-up included 2 implant-related com-
plications: 1 due to postoperative graft mi-
gration (grade 2; additional endovascular
aortic cuff) and the other to postoperative
endograft limb thrombosis (grade 3; femoro-
femoral bypass). Two systemic complications
were due to renal insufficiency because of
partial stent-graft coverage of the renal ar-
teries (grade 1; renal angioplasty and stent-
ing). Moreover, 4 late non-aneurysm-related
deaths were observed during the study
period: 2 metastatic cancers at 6 and
12 months, 1 colonic necrosis at 6 months,
and 1 sudden death at 15 months.
However, the major findings of this study
were the low rate of delayed type II endoleak
(2.4%, 2 patients) and the statistically signif-
icant decrease in the maximum transverse
Figure 2 ¤Intravascular ultrasound examples of
(A) an empty aneurysm sac at baseline, (B) a pre-
embolization sac with flow from inflow vessels,
and (C) a sac after fibrin glue injection and type II
endoleak occlusion.
Figure 3 ¤Kaplan-Meier estimates of primary and
assisted primary clinical success. Adverse events
for primary success included aneurysm-related
death, aneurysm rupture, conversion to open
repair, and secondary endovascular or surgical
procedures. Assisted primary clinical success was
defined as clinical success achieved with the use of
additional or secondary endovascular interven-
tions.
180 PRIMARY PREVENTION OF TYPE II ENDOLEAK
Zanchetta et al.
J ENDOVASC THER
2007;14:176–183

6. aneurysm diameter (50.4066.70 versus
42.0366.50 mm, p50.0001) at follow-up
(Fig. 4). Moreover, the 0.92 remodeling index
at 3 months showed that sac shrinkage was
an early phenomenon in our fibrin glue–
treated patients, without further changes at
follow-up, primarily as a result of intraopera-
tive sac embolization and type II endoleak
thrombosis. In addition, of 31 patients avail-
able for 24-month follow-up, 14 (45.2%)
patients showed a $5-mm reduction in
maximum transverse aneurysm diameter; 16
(51.6%) patients had no significant changes,
whereas only 1 patient showed a .5-mm
enlargement.
DISCUSSION
In 2000, Fry and colleagues17
were among the
first to propose embolizing the aneurysm sac
with Onyx as a means of preventing type II
endoleaks. A year earlier, Walker et al.18
reported packing the aneurysm sac with
absorbable thrombogenic sponge during the
stent-graft procedure to prevent side branch
endoleaks. Although this procedure was a re-
liable method of preventing type II endoleaks
(33 of 48 patients available for a mean 4-
month follow-up had no type II endoleaks), it
did not come into routine clinical use because
it required an aortomonoiliac stent-graft and
femorofemoral bypass grafting.
Other investigators have since explored sac
embolization with a variety of techniques in
experimental models.19–22
Rhee et al.19
eval-
uated the use of polyurethane foam to induce
thrombosis of type II endoleaks by filling the
aneurysm sac outside the bifurcated stent-
graft in a canine model. They documented
angiographic thrombosis of polyurethane
foam–treated endoleaks in all 4 animals, with
nearly complete elimination of the intrasac
pressure measured by an implanted pressure
transducer. Histological cellular infiltration
into the aneurysm sac at a mean 64 days
(range 30–90) had created a stable and
durable correction of type II endoleaks. In
another animal study, Uflacker and Brothers20
explored the use of deacetylated-poly-N-ace-
tyl glucosamine in a swine AAA model to
promote intrasac clotting with progressive
replacement by connective tissue and neo-
vascularization as a means of preventing
endoleaks.
Over the past several years, we have been
amassing experience with routine prophylac-
tic aneurysm sac fibrin glue embolization and
aortic side branch occlusion at the time of
bifurcated endografting.13
In our opinion,
intraoperative treatment is the optimal means
of preventing type II endoleaks, avoiding
much more challenging preventive or sec-
ondary interventions; moreover, this adjunc-
tive intraoperative procedure may increase
the overall success of EVAR and decrease the
need for close monitoring in the postopera-
tive period.23
In our experience, fibrin glue injection into
the aneurysm sac at the time of endografting
is easy and independent of anatomical vari-
ability or currently available endovascular
equipment. It offers certain advantages with
respect to provisional postoperative trans-
lumbar injection of other liquid embolic
agents, such as histoacryl glue and poly-
ethylene-vinyl alcohol copolymer.10
Indeed,
the application of these liquid embolic agents
can be associated with uncontrolled emboli-
zation into the downstream vessels, leading
to colonic or spinal cord ischemia.24
Addi-
tionally, artifacts and backscatter of the liquid
embolic agent itself may create a diagnostic
challenge in surveillance imaging studies,
precluding direct evaluation of perigraft en-
doleak on future CT scans of the abdomen.10
Fibrin glue, on the other hand, forms a rapidly
structured fibrin clot within the first few
minutes of reaction, physiologically similar
to naturally occurring thrombus, with slight
Figure 4 ¤Serial changes in maximum transverse
diameter after fibrin glue sac embolization.
J ENDOVASC THER
2007;14:176–183
PRIMARY PREVENTION OF TYPE II ENDOLEAK 181
Zanchetta et al.

7. diffusion to the ostia of outflow vessels. It is
completely reabsorbed after several days by
fibrinolysis with a minimum of tissue re-
action,25
allowing optimal evaluation of peri-
graft space at follow-up surveillance.
Conclusion
This clot engineering approach to aneu-
rysm sac embolization makes prophylaxis of
type II endoleaks easier to handle in the
operating theater and provides a scaffold for
natural coagulation, thus engendering occlu-
sion of the target aortic side branches, and
perhaps, biological fixation of the implanted
stent-graft. Therefore, our fibrin glue aneu-
rysm sac embolization technique should
point the way to future research in the field
of biomaterials and scaffolds for ‘‘reparative
medicine,’’ as the occlusion of potential
feeding vessels at the time of endografting
does not increase intraoperative complica-
tions, providing durable occlusion of both
inflow and outflow vessels. However, com-
prehensive evaluation of the clinical efficacy
of fibrin glue aneurysm sac embolization at
the time of endografting will require a larger
and a longer controlled study to evaluate the
true magnitude of this new approach.
REFERENCES
1. Gelfand DV, White GD, Wilson SE. Clinical
significance of type II endoleak after endovas-
cular repair of abdominal aortic aneurysm. Ann
Vasc Surg. 2006;20:69–74.
2. Veith FJ, Baum RA, Ohki T, et al. Nature and
significance of endoleaks and endotension:
summary of opinions expressed at an interna-
tional conference. J Vasc Surg. 2002;35:1029–
1038.
3. van Marrewijk C, Buth J, Harris PL, et al.
Significance of endoleaks after endovascular
repair of abdominal aortic aneurysm: the
EUROSTAR experience. J Vasc Surg. 2002;35:
461–473.
4. Faries PL, Briggs VL, Bernheim J, et al. In-
creased recognition of type II endoleaks using
a modified intraoperative angiographic pro-
tocol: implications for intermittent endoleak
and aneurysm expansion. Ann Vasc Surg.
2003;17:608–614.
5. Laheij RJ, Buth J, Harris PL, et al. Need for
secondary interventions after endovascular re-
pair of abdominal aortic aneurysms. Interme-
diate-term follow-up results of a European col-
laborative registry (EUROSTAR). Br J Surg.
2000;87:1666–1673.
6. Gould DA, McWilliams RG, Edwards RD, et al.
Aortic side branch embolization before endo-
vascular aneurysm repair: incidence of type II
endoleak. J Vasc Interv Radiol. 2001;12:337–
341.
7. Kasirajan K, Matteson B, Marek JM, et al.
Technique and results of transfemoral super-
selective coil embolization of type II lumbar
endoleak. J Vasc Surg. 2003;38:61–66.
8. Baum RA, Cope C, Fairman RM, et al. Trans-
lumbar embolization of type 2 endoleaks after
endovascular repair of abdominal aortic an-
eurysms. J Vasc Interv Radiol. 2001;12:111–
116.
9. Baum RA, Carpenter JP, Golden MA, et al.
Treatment of type 2 endoleaks after endovas-
cular repair of abdominal aortic aneurysms:
comparison of transarterial and translumbar
techniques. J Vasc Surg. 2002;35:23–29.
10. Martin ML, Dolmatch BI, Fry PD, et al. Treat-
ment of type II endoleaks with Onyx. J Vasc
Interv Radiol. 2001;12:629–632.
11. Ho P, Law WL, Tung PH, et al. Laparoscopic
transperitoneal clipping of the inferior mesen-
teric artery for the management of type II
endoleak after endovascular repair of an
aneurysm. Surg Endosc. 2004;18:870.
12. van Nes JG, Hendriks JM, Tseng LN, et al.
Endoscopic aneurysm sac fenestration as
a treatment option for growing aneurysms
due to type II endoleak or endotension.
J Endovasc Ther. 2005;12:430–434.
13. Zanchetta M, Faresin F, Pedon L, et al. Fibrin
glue aneurysm sac embolization at the time of
endografting. J Endovasc Ther. 2005;12:579–
582.
14. Sierra DH. Fibrin sealant adhesive systems:
a review of their chemistry, material properties
and clinical application. J Biomater Appl. 1993;
7:309–352.
15. Clark RA. Fibrin glue for wound repair: facts
and fancy. Thromb Haemost. 2003;90:1003–
1006.
16. Chaikof EL, Blankensteijn JD, Harris PL, et al.
Reporting standards for endovascular aortic
aneurysm repair. J Vasc Surg. 2002;35:1048–
1060.
17. Fry PD, Martin M, Machan L. Endoleaks and the
need for a paradigm shift [Letter]. J Endovasc
Ther. 2000;7:521.
182 PRIMARY PREVENTION OF TYPE II ENDOLEAK
Zanchetta et al.
J ENDOVASC THER
2007;14:176–183

8. 18. Walker SR, Macierewicz J, Hopkinson BR.
Endovascular AAA repair: prevention of side
branch endoleaks with thrombogenic sponge.
J Endovasc Surg. 1999;6:350–353.
19. Rhee JY, Trocciola SM, Dayal R, et al. Treat-
ment of type II endoleaks with a novel poly-
urethane thrombogenic foam: induction of
endoleak thrombosis and elimination of intra-
aneurysmal pressure in the canine model.
J Vasc Surg. 2005;42:321–328.
20. Uflacker R, Brothers T. Filling of the aneurys-
mal sac with DEAC-glucosamine in an animal
model of abdominal aortic aneurysm following
stent-graft repair. J Cardiovasc Surg (Torino).
2006;47:425–436.
21. Rolland PH, Vidal V, Mekkaoui C, et al. Embo-
lization-driven occlusion of the abdominal
aortic aneurysmal sac as the basis of pre-
vention of endoleaks in a new swine model.
Eur J Vasc Endovasc Surg. 2006;31:28–35.
22. Hiraki T, Pavcnik D, Uchida BT, et al. Pro-
phylactic residual aneurysmal sac emboliza-
tion with expandable hydrogel embolic de-
vices for endoleak prevention: preliminary
study in dogs. Cardiovasc Intervent Radiol.
2005;28:459–66.
23. Corriere MA, Feurer ID, Becker SY, et al.
Endoleak following endovascular abdominal
aortic aneurysm repair: implications for dura-
tion of screening. Ann Surg. 2004;239:800–807.
24. Bush RL, Lin PH, Ronson RS, et al. Colonic
necrosis subsequent to catheter-directed
thrombin embolization of the inferior mesen-
teric artery via the superior mesenteric artery:
a complication in the management of a type II
endoleak. J Vasc Surg. 2001;34:1119–22.
25. Radosevich M, Goubran HI, Burnouf T. Fibrin
sealant: scientific rationale, production meth-
ods, properties, and current clinical use. Vox
Sang. 1997;72:133–143.
J ENDOVASC THER
2007;14:176–183
PRIMARY PREVENTION OF TYPE II ENDOLEAK 183
Zanchetta et al.