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32 Renal Artery Angioplasty andStent Insertion: AnOverview ofModern Practice
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increases with the degree of pre-existing iliac and aortic disease, factors which should be noted on pre-procedural imaging. In patients with a large burden of aortic or iliac disease,
a brachial artery approach might be required.
Finally, heparinisation during the procedure increases the
risk of cerebral haemorrhage and bleeding elsewhere in the
body. ACTs should be regularly checked as a marker of
bleeding risk.
Outcomes
The reported outcomes of patients treated with renal angioplasty and stenting are variable. Analysis of the available
data reveals considerable complexity; it is evident that many
patients with renal artery stenosis gain no benet from intervention above that achieved with best medical therapy alone;
however, certain subsets of patients can benet dramatically
from intervention. Detailed critique of the evidence is beyond
the scope of this chapter; however, the key concepts are outlined here.
Angioplasty inFibromuscular Disease
Angioplasty for patients with hypertension caused by bromuscular disease has consistently been shown to be highly
effective. Patients with bromuscular disease rarely have
resultant renal impairment, and as such, hypertension is the
sole indication for treatment. The most recent cohort studies
report levels of technical success consistently over 95%, and
around 75% of patients were deemed to have had their hypertension either cured or improved [23]. Reported complication rates for this cohort are also lower than for patients with
ARAS.
Atherosclerotic Renal Artery Stenosis
A number of randomised controlled trials comparing renal
artery stenting (with best medical therapy) to best medical
therapy alone have been conducted, including the STAR,
ASTRAL and CORAL studies [4]. The primary and secondary endpoints investigated varied across the trials; however,
none of these studies have demonstrated a benet of renal
artery stenting over best medical treatment, either for control
of hypertension or for improved renal function [3].
These trials represent the highest quality of evidence;
however, there are several recurring limitations. The most
commonly cited limitation is that patients with the most
high-risk renal artery stenosis were seldom included in the
trials, as clinicians proceeded straight to intervention. Lowrisk patients were therefore overrepresented; many of the
patients were found to have less than 70% stenosis on angiography, and indeed 25% of patients in the ASTRAL trial
had a normal eGFR and so would be considered unlikely to
benet from revascularisation [1, 3, 5].
Despite the limitations, the studies provide strong evidence that the majority of patients with renal artery stenosis
can be effectively treated with best medical management
alone, without exposing them to the risks associated with
renal artery stenting. Appropriately therefore, since the publication of the CORAL trial in 2014, rates of renal artery
stenting have declined considerably [5].
There are a number of studies which have identied
cohorts of patients who derive benet from revascularisation. The HERCULES trial included patients with hypertension refractory to two antihypertensives and who had
stenosis of >60% on angiography, treated with the Herculink
(Abbott) stent. The study demonstrated signicant blood
pressure improvements amongst the cohort of patients who
were likely to have been underrepresented in the larger
RCTs [22].
Additional studies have demonstrated the importance of
timely intervention and, by extension, the futility of treatment past a certain stage. Patient’s with rapidly deteriorating
eGFR or who experience ash pulmonary oedema have been
found to benet considerably from timely revascularisation
[5]. Furthermore, a sub-analysis of the cohort of CORAL
patients with low urinary protein excretion rates also demonstrated improved outcomes (reduced cardiovascular events
and mortality) in the patients who underwent revascularisation [3]. Conversely, more recent studies of patients who
have undergone revascularisation have demonstrated poorer
outcomes in those with low eGFR and proteinuria, concluding that there is a point beyond which revascularisation is
unable to affect hypertension and renal function [1].
These ndings, alongside a body of case reports and
smaller cohort studies, indicate that revascularisation is a
crucial tool that can have good results when chosen for the
correct cases, at the correct timepoint. The modern clinical
recommendations detailed above in the ‘Indications’ section
reect this conclusion. Assessment of patients for revascularisation involves signicant complexity and should be
determined by an experienced multidisciplinary team on a
case-by-case basis.
Case Outcome
Following initial consultation with the Interventional
Radiology team, an MRA of the renal arteries is obtained,
which conrms severe right renal artery stenosis with an
ostial lesion. A review of historical blood results demonstrates previously stable renal function with quite rapid
decline in the last 3months. After further discussion between

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the renal team and interventional radiology, it is agreed that
prompt renal artery stenting is in the patient’s best interests.
The patient is pre-assessed and deemed suitable to
undergo the procedure under local anaesthetic as a day case.
A review of the MRA demonstrates relatively conventional
anatomy, with the vessel distal to the stenosis measured at
6mm. The case is arranged for the following day.
Access is gained to the right common femoral artery, and
a 5 fr 45 cm Destination sheath is inserted. The no-touch
technique is used to carefully cannulate the right renal artery
with a 0.014in Command wire. The Destination sheath is
allowed to gently engage the ostium of the artery, and a DSA
run is taken from the sheath (Fig. 32.1). IVUS is then
deployed to measure the renal artery. The healthy renal artery
distal to the ostial stenosis is conrmed to be 6 mm. The
IVUS catheter also allows the required length of the stent to
be calculated. A landing position for the stent is marked with
a uoro-grab of the IVUS catheter.
A 6mm×15mm Cook Formula balloon-mounted stent is
then deployed, with the proximal aspect of the stent protruding into the aorta roughly 2mm. IVUS demonstrates a small
dissection of the vessel following stent deployment, so an
additional 6mm× 12mm Cook Formula balloon-mounted
stent is deployed (Fig.32.2). A nal DSA run is undertaken
from the sheath to check for complications. There is no evidence of perforation or embolisation of debris, and the stent
appears well positioned. The sheath is removed, and haemostasis is achieved with a closure device.
At discharge the patient is instructed to keep taking his
daily aspirin. He is also given a 3-month prescription for
clopidogrel. At follow-up with the renal team, the patient’s
renal function is noted to have stabilised, and the patient’s
Fig. 32.1 Initial angiogram of the right renal artery demonstrating
severe ostial stenosis
M. Gregory and T. Sabharwal
Fig. 32.2 Angiogram post-stent insertion. The proximal aspect of the
6mm ×15 mm Cook Formula balloon-mounted stent extends around
2mm into the aortic lumen. An additional 6mm×12mm stent has been
deployed to treat a small dissection distal to the initial stent. The angiogram is closely scrutinised for complications, including pseudoaneurysm or embolus in the distal renal artery branches
blood pressure is now well controlled with two antihypertensive medications.
References
1. Textor SC, Misra S, Oderich GS. Percutaneous revascularization
for ischemic nephropathy: the past, present, and future. Kidney Int.
2013;83(1):28–40. https://doi.org/10.1038/ki.2012.363.
2. Textor SC, Lerman L. Renovascular hypertension and ischemic
nephropathy. Am J Hypertens. 2010;23(11):1159–69. https://doi.
org/10.1038/ajh.2010.174.
3. Herrmann SM, Textor SC. Current concepts in the treatment of
Renovascular hypertension. Am J Hypertens. 2018;31(2):139–49.
https://doi.org/10.1093/ajh/hpx154.
4. Cooper CJ, Murphy TP, Cutlip DE, Jamerson K, Henrich W, Reid
DM, Cohen DJ, Matsumoto AH, Steffes M, Jaff MR, Prince MR,
Lewis EF, Tuttle KR, Shapiro JI, Rundback JH, Massaro JM,
D’Agostino RB Sr, Dworkin LD, Investigators CORAL.Stenting
and medical therapy for atherosclerotic renal-artery stenosis.
N Engl J Med. 2014;370(1):13–22. https://doi.org/10.1056/
NEJMoa1310753. Epub 2013 Nov 18.
5. Mousa AY, Bates MC, Broce M, Bozzay J, Morcos R, AbuRahma
AF.Issues related to renal artery angioplasty and stenting. Vascular.
2017;25(6):618–28. https://doi.org/10.1177/1708538116677654.
Epub 2017 Aug 7.
6. Funaki B.Renal ostial angioplasty and stenting. Part 1: the routine
procedure. Semin Intervent Radiol. 2009;26(1):74–81. https://doi.
org/10.1055/s- 0029- 1208385.
7. Jokhi PP, Ramanathan K, Walsh S, Fung AY, Saw J, Fox RS,
Zalunardo N, Buller CE.Experience of stenting for atherosclerotic
renal artery stenosis in a cardiac catheterization laboratory: technical
considerations and complications. Can J Cardiol. 2009;25(8):e273–
8. https://doi.org/10.1016/s0828- 282x(09)70121- 7.

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8. Kok HK, Leong S, Govender P, et al. Percutaneous renal artery
angioplasty and stenting: indications, technique and results. Ir J Med
Sci. 2013;182:351–6. https://doi.org/10.1007/s11845- 012- 0887- 5.
9. Erwin PA, Shishehbor MH.Renal artery stenting: indications, techniques, and devices. Minerva Cardioangiol. 2013;61(2):189–99.
10. Campbell JE, Stone PA, Bates MC.Technical discussion of diagnostic angiography and intervention of atherosclerotic renal
artery stenosis. Semin Vasc Surg. 2013;26(4):150–60. https://doi.
org/10.1053/j.semvascsurg.2014.06.002.
11. Caridi JG, William Stavropoulos S, Hawkins IF. Carbon dioxide
digital subtraction angiography for renal artery stent placement. J
Vasc Interv Radiol. 1999;10(5):635–40. https://doi.org/10.1016/
S1051- 0443(99)70094- 1.
12. Beek FJ, Kaatee R, Beutler JJ, et al. Complications during renal
artery stent placement for atherosclerotic ostial stenosis. Cardiovasc
Intervent Radiol. 1997;20:184–90.
13. Franz RW, Tanga CF, Herrmann JW.Treatment of peripheral arterial disease via percutaneous brachial artery access. J Vasc Surg.
2017;66(2):461–5. https://doi.org/10.1016/j.jvs.2017.01.050. Epub
2017 Apr 19.
14. Goldstein JA, Kolluri R, Rocha-Singh KJ.Technical considerations
for renal artery stenting. J Vasc Dis Manag. 2006.
15. Walker C, Kowalski J, Knan M, etal. Proximal protection before
distal protection: preventing large atheroemboli during renal intervention. Am J Cardiol. 2002;90:28.
16. Holden A, Hill A, Jaff MR, Pilmore H.Renal artery stent revascularization with embolic protection in patients with ischemic
nephropathy. Kidney Int. 2007;70:948–55.
17. Hiramoto J, Hansen KJ, Pan XM, etal. Atheroemboli during renal
artery angioplasty: an ex-vivo study. J Vasc Surg. 2005;41:1026–30.
18. Henry M, Klonaris C, Henry I, etal. Protected renal stenting with
the PercuSurge Guardwire device: a pilot study. J Endovasc Ther.
2001;8:227–37.
19. Thatipelli MR, Misra S, Sanikommu SR, etal. Embolic protection
device use in renal artery stent placement. J Vasc Interv Radiol.
2009;20:580–6.
20. Misra S, Thatipelli MR, Howe PW, etal. Preliminary study of the
use of drug-eluting stents in atherosclerotic renal artery stenoses
4mm in diameter or smaller. J Interv Radiol. 2008;19:833–9.
21. Textor SC, McKusick M.Renovascular hypertension and ischemic
nephropathy: angioplasty and stenting. In: Therapy in nephrology
and hypertension: a companion to Brenner & Rector’s the kidney,
expert consult—online and print. Elsevier; 2008. p.660–74. https://
doi.org/10.1016/B978- 141605484- 9.50060- 5.
22. Colyer W Jr. RX Herculink elite® renal stent system: a review of its
use for the treatment of renal artery stenosis. Med Devices (Auckl).
2012;5:67–73. https://doi.org/10.2147/MDER.S25150.
23. Slovut DP, Olin JW.Current concepts: bromuscular dysplasia. N
Engl J Med. 2004;350:1862–71.

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CalebSolivio, ZaeemBillah, AustinShinagawa,
KartikKansagra, andGeogyVatakencherry
33
Case Presentation
A 63-year-old male was transferred from an outside hospital
where he presented with back pain and acute urinary obstruction. As part of the workup on presentation a CT scan was
performed, incidentally showing a 4×5cm hepatic artery
visceral aneurysm, 6.8 cm inammatory infrarenal aortic
aneurysm, and 3.1 cm inammatory right common iliac
artery aneurysm. The patient underwent nephrostomy tube
placement to relieve the obstruction and clear any potential
infection. Despite urinary diversion and conrmation of no
underlying infection, his back pain persisted, and the decision was made to treat his multiple aneurysms in a staged
fashion. Given his chief concern of back pain, the decision
was made to treat the aortoiliac pathology rst. His abdominal and iliac aneurysms were rst repaired using a Gore
Excluder Iliac Branch Endoprosthesis (WL Gore &
Associates Flagstaff, Az). Given the size of the hepatic artery
aneurysm (HAA) the decision was made to treat this in an
endovascular fashion as opposed to continue surveillance.
Continued at page 359
Introduction
Visceral artery aneurysms (VAA) are historically uncommon
disorders that are now being detected with increased frequency due to the ubiquitous utilization of cross-sectional
imaging. Though they are typically asymptomatic, VAAs are
of high clinical signicance given their potential for rupture,
which may result in mortality.
C. Solivio
California University of Science and Medicine, Colton, CA, USA
e-mail: SolivioC@cusm.org
Z. Billah · A. Shinagawa · K. Kansagra · G. Vatakencherry (*)
Division of Vascular and Interventional Radiology, Kaiser
Permanente, Los Angeles, CA, USA
Though uncommon and usually clinically silent, aneurysms of the visceral arteries, namely the celiac axis, renal
arteries, superior mesenteric artery (SMA), inferior mesenteric artery (IMA), and its branches, are of clinical concern
given the potentially high mortality rate associated with their
rupture (25–70%) [1]. While open surgical treatment models
for VAAs remain a viable option in the treatment of VAAs,
modern advances in endovascular technology and interventional physician technical skill sets have propelled endovascular therapy to become the rst-line therapy for many
VAAs.
It is imperative for the modern vascular and interventional physician who takes care of patients with VAAs to
master the clinical knowledge required to guide and counsel
patients with VAAs and to develop the technical expertise to
offer treatment when deemed appropriate. It is also imperative that the vascular interventional physician continue to
follow up with these patients indenitely after endovascular
repair.
Classication
VAA can be classied as true aneurysms, which are outpouchings of vessels with integrity of all three vascular layers, or pseudoaneurysms, which are outpouchings of vessels
lacking integrity of all three vascular layers. True aneurysms
are due to an inherent weakness of the vessel wall, often
because of changes in elastin and collagen, such as in bromuscular dysplasia (FMD), or vascular degenerative diseases, such as in Ehlers-Danlos syndrome or vasculitides.
Pseudoaneurysms are associated with damage to the vessel
layers and can be further subdivided by etiology including
inammatory, infectious, traumatic, and iatrogenic. In addition, VAAs can also be categorized by their morphology such
as saccular (focal dilation of one side of the vessel) vs. fusiform (circumferential dilation of the vessel) and wide neck
vs. narrow neck, referring to the interface with the parent
vessel.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
G. Geroulakos et al. (eds.), Mastering Endovascular Techniques, https://doi.org/10.1007/978-3-031-42735-0_33
343

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C. Solivio et al.
Special Considerations
Special attention should be paid to women who are pregnant
or of childbearing age. There is an increased risk of rupture
in pregnancy due to factors such as hormonal changes, an
increase in relaxin, and a higher volume state. The rupture of
VAAs in pregnancy is associated with high mortality rates
for both the mother and the fetus. Additionally, for reasons
poorly understood, orthotopic liver transplants (OLTs) are
associated with higher rates of VAA rupture, and thus the
treatment for VAAs in individuals expected to receive OLTs
should be considered [2].
Workup
Generally, the workup for VAAs is similar. Though most are
found incidentally, the preferential method for the diagnosis
of VAAs is CT angiography (CTA), followed by other
modalities such as MR angiography (MRA) for patients with
high radiation exposure risks (especially younger patients).
Current literature indicates that some VAAs may present
with concomitant aneurysms in other vascular beds. For such
VAAs, it is recommended to perform one-time head-topelvis imaging. If aneurysms are found in multiple beds,
genetic workup for congenital conditions such as vasculartype Ehlers-Danlos, Marfan’s syndrome, Loeys-Deitz syndrome and aneurysm osteoarthritis (AOS) should be
performed. Given the diseases’ autosomal dominant inheritance, families should also be evaluated and counseled. One
should consider other etiologies such as FMD and other collagen vascular disorders as well. It is critical to take a thorough family history to identify genetically transmitted
disorders and have a low threshold to send patients with multiple visceral aneurysms for genetic testing and family
counseling.
head- to- pelvis imaging. After renal artery aneurysms are
identied, indications for intervention include pseudoaneurysm, rupture, symptomatic RAAs, size >3cm, or presentation in a premenopausal female. Medical management
includes consideration of single antiplatelet therapy such as
low-dose aspirin and follow-up surveillance imaging at
6months followed by serial imaging every 1–2years. This
can be further increased to every 3–5years once stability
has been demonstrated over a longer period of time. It is
important to note that the typical natural history of true
aneurysms of the renal artery is usually of slow growth of
<1mm/year. Most renal artery aneurysms can be repaired
using a consortium of endovascular techniques similar to
what is used for the treatment of intracranial aneurysms.
Surgical management of RAAs is typically reserved for
those that have complex distal branch lesions and includes
ex vivo surgical repair, autotransplantation, or even
nephrectomy. Endovascular vs. surgical approaches for the
more complex renal artery aneurysms will often be determined by local surgical and endovascular expertise
(Fig.33.1).
Vascular Beds: Renal
Renal artery aneurysms (RAAs) occur in about 0.1% of the
population with rupture rates up to 5% and an associated
mortality rate of less than 10%. However, this mortality
rate greatly increases for both mother and fetus (55% and
85%, respectively) if rupture presents in the third trimester.
In women, RAAs may be associated with bromuscular
dysplasia (FMD), which increases the risk for concomitant
aneurysms. Renal artery pseudoaneurysms may be associated with procedures such as renal biopsy and percutaneous
nephrostomy tubes. Current guidelines suggest that women
with RAAs also be screened via CTA/MRA for aneurysms
of the cerebrovascular, mesenteric, and iliac arteries with
Fig. 33.1 Angiographic image demonstrating a saccular aneurysm
arising from the left main renal artery. The beaded appearance of the
renal artery is identied as a result of underlying FMD

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Vascular Beds: Splenic
Splenic artery aneurysms (SAAs) constitute 60% of all
VAAs. They most commonly occur in women and are associated with multiparity. Many SAAs present with rupture
upon diagnosis with a rupture mortality rate of 25%. In
pregnant women, rupture of SAAs is associated with maternal and fetal mortality rates as high as 80 and 90%, respectively. A study by Lee etal. [3] showed high rupture rates of
splenic artery aneurysms in the setting of orthotopic liver
transplant. Due to its high spatial resolution, CTA is the preferred imaging modality for the diagnosis of SAAs.
Indications for intervention include pseudoaneurysm, symptomatic or ruptured SAAs, size >3 cm, rapid growth
(>0.5 cm/year), patients undergoing liver transplantation,
and SAAs in premenopausal females. A surveillance regimen for untreated SAAs includes shorter-term imaging
between 3 and 6 months for 1 year followed by annual
cross-sectional imaging. If stability for 5–10years is demonstrated, the timespan between surveillance scans can be
extended to every 3–5years.
Endovascular intervention is the preferred method for
SAA repair, as supported by much of the current literature,
including a multicenter, retrospective study by Qiu et al.,
demonstrating a 90% technical success rate in endovascular
repair of 70 aneurysms in 65 patients by covered stent with
or without coil embolization, 23 of which were SAAs.
Vascular Beds: Hepatic
Hepatic artery aneurysms (HAAs) represent 20% of all
VAAs [4], with reported rupture rates as high as 80% [5].
Hepatic artery pseudoaneurysms constitute up to 80% of all
HAAs, most commonly caused by iatrogenic injury or blunt
trauma. These aneurysms may present with rupture into the
biliary tree and hemobilia/melena or as an intraperitoneal
bleed and hemoperitoneum. After diagnosis, those with
HAAs should also receive a one-time head-to-pelvis screening CTA to evaluate for aneurysms in additional vascular
beds to identify associated pathologies such as bromuscular
dysplasia, vasculitis, and connective tissue disorders, and
genetic testing should also be considered. Indications for
intervention include symptomatic HAAs, pseudoaneurysms,
inammatory aneurysms, size >2cm, or growth rate>0.5cm/
year. Endovascular repair is the preferred HAA therapy, and
current literature exhibits primary technical success rates for
endovascular HAA repair of up to 98% [6–8]. Surgical
345
Fig. 33.2 Patient with pancreatic cancer who presented with melena
and hemobilia after a biliary drain. A hepatic artery pseudoaneurysm
was identied after pulling the biliary drain back over a wire
intervention may be necessary in rare cases of unfavorable
aneurysmal anatomy (Fig.33.2).
Vascular Beds: Celiac
Celiac artery aneurysms (CAAs) represent 4% of all VAAs
[9] but reported associated rupture mortality rates near
100% [10]. Additionally, they may present with concomitant aortic aneurysms and other VAAs. Most CAAs are
found incidentally. Indications for intervention include
pseudoaneurysms, rupture, symptomatic CAAs, and size
>2cm. Endovascular management is the rst-line treatment
for CAAs though surgical management may be considered
in anatomically unfavorable cases. If surveillance is performed, annual cross-sectional imaging is recommended to
assess for CAA growth, and in younger patients, MRA
should be considered for follow-up. Three retrospective
analyses, totaling 26 CAAs, demonstrated the safety and
efcacy of endovascular management of CAAs with technical success rates ranging from 84.2 to 98% [6–8].
Complications on follow-up included type 1a endoleak [8],
mild restenosis [8], and a persistent but improving CAA
which shrunk from 39mm to 29mm [7]. No reported cases
warranted further surgical intervention. Postoperative
annual imaging is recommended to check for endoleaks and
residual CAA growth (Fig.33.3).

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Fig. 33.3 5cm celiac artery aneurysm arising from the main trunk
Vascular Beds: Superior Mesenteric Artery
Superior mesenteric artery aneurysms (SMAAs) are relatively rare, and true statistics regarding their prevalence
vary greatly. SMAA rupture mortality rates vary in the literature between 30 and 90% [10]. The natural history of
SMAAs is thought to be one of expansion and rupture. All
true and false SMAAs should be considered for intervention with endovascular management when possible over
open surgical management because of reported improvements in mortality rates [10]. Elective SMAA repair is
associated with mortality rates less than 15%; such rates
improve with endovascular techniques compared to open
surgical repair methods. When considering endovascular
repair, it is critical to maintain the patency of the major
tributaries of the SMA to prevent intestinal infarction,
which could result in fatality.
C. Solivio et al.
with gastric or gastroepiploic artery aneurysms have presented with rupture [11]. Intervention is reasonable for all
gastric and gastroepiploic artery aneurysms, and an endovascular approach should be considered as rst-line
therapy.
Vascular Beds: Pancreatoduodenal
andGastroduodenal Arteries
Together pancreaticoduodenal artery aneurysms (PDAA)
and gastroduodenal artery aneurysms (GDAA) represent
6% [12] of all VAAs and are often associated with celiac
artery stenosis or occlusion, which increases ow through
the pancreaticoduodenal arcades as it is the primary collateral network between the superior mesenteric and celiac
axes. Inammatory conditions such as pancreatitis can
result in pseudoaneurysms of these beds, and given their
associated high mortality rates, they should be treated
endovascularly when feasible. Given the high reported rupture rate in the current literature, it is recommended that
PDAA and GDA aneurysms be treated endovascularly. If
there is median arcuate ligament compression on the celiac
artery, a laparoscopic ligament release can be considered
(Fig.33.4).
Vascular Beds: Gastric andGastroepiploic
Arteries
Gastric and gastroepiploic artery aneurysms represent only
4–5% of all VAAs, and given their rarity, their natural histories are not as clear. It is reasonable to perform head-to- pelvis
imaging and consider genetic testing if multiple aneurysms
are noted. Their rarity limits current data regarding their
rupture rates, but some data reports up to 90% of patients
Fig. 33.4 Pancreaticoduodenal aneurysms arising from a patient with
liver arteriovenous malformations (AVMs) and median arcuate ligament compression of celiac trunk

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347
Vascular Beds: Jejunal, Ileal, andColic
Together, jejunal, ileal, and colic artery aneurysms represent less than 3% of all VAAs. In patients whom jejunal,
ileal, or colic artery aneurysms are found, a head-to-pelvis CTA or MRA should be performed. Though natural
history is not clear, the current literature suggests a high
rupture rate between 30 and 70%, and collective mortality
rates between 20 and 50%.[10] Though these may be
repaired with endovascular approaches, it is critical for
the vascular interventionalists to ensure that they are able
to effectively exclude the aneurysm while preserving ow
to the intestines. Bannur etal. demonstrated a successful
endovascular intervention of VAAs, four of which were
colic or right colic artery aneurysms, without periprocedural morality [6]. Patients who received embolization
should be monitored every 12–24months with cross-sectional imaging to assess for vascular remodeling or aneurysm reperfusion.
Technical Considerations
Overall, the goal of VAA treatment, whether endovascular,
laparoscopic, or open surgical, is to prevent aneurysm (or
pseudoaneurysm) rupture while maintaining adequate endorgan perfusion. Endovascular approaches to VAA repair
are generally preferred over their laparoscopic and open surgical counterparts, but determination of endovascular candidacy should be considerate of inow vasculature, outow
vasculature, branch vessels arising from the aneurysm, as
well as morphology of the aneurysm. Depending on which
organ is involved, the etiology of the aneurysm, and individualized patient anatomies, various endovascular
approaches can be considered, such as coil embolization,
liquid embolization, and vascular plugs. For more challenging vascular anatomy, balloon- or stent-assisted coiling can
be performed. Various types of stents can be used to exclude
aneurysms including stent grafts and ow-diverting stents.
In order to overcome some of the technical challenges from
a transfemoral approach due to some of the downward angulations from the visceral vasculature, one can consider a
torqueable guidesheath from a transfemoral approach or
radial, brachial, or even axillary access. For excessive tortuosity, as seen in the splenic bed, one can also consider using
exible neuro distal access catheters. General anesthesia
may be needed to minimize patient movement and obtain
high- quality imaging, which is often necessary to ensure
clinical and technical success with complex endovascular
repairs.
Coil Embolization
Coil embolization represents the most popular endovascular
VAA repair technique given its cost-effectiveness and aptitude for a wide array of saccular aneurysms in which the
aneurysm neck is sufciently narrow to prevent coils from
extruding into the parent artery, thus maintaining vascular
patency and end-organ perfusion. There is a growing array of
microcatheters and various shapes, diameters, stiffnesses,
and widths of coils that enable dense packing of aneurysms
of varying sizes and morphologies. Online tools exist which
can guide the interventionalist in calculating the number of
packing coils needed to produce sufcient packing density
based on aneurysm morphology and volume, depending on
the length, shape, diameter, and stiffness of coils used.
Balloon-Assisted Coiling
Balloons can supplement coil embolization in cases where
the neck of the saccular aneurysm is too wide allowing for
high-density coil packing while simultaneously preventing
coil prolapse into the parent vessel.
Stent-Assisted Coiling
Stents can assist coil embolization similarly to balloons but
also can act as a scaffold to prevent the coils from prolapsing
into the parent vessel. The microcatheter can be placed in the
aneurysm sac through the interstices of the stent or alongside
an undeployed or deployed stent. However, stent-assisted
coiling usually requires that the patient remain on a duration
of antiplatelet therapy to mitigate thrombogenicity of stents
and maintain stent patency. Some have even described using
retrievable stents employed for strokes as a temporary scaffold which can be removed once the coil mass has been
deployed (Figs.33.5 and 33.6).
Liquid Embolics
Liquid embolics can be used to obliterate aneurysms or as an
adjunctive technique to add to coils in the treatment of aneurysms. Adhesive (also known as n-butyl cyanoacrylate) and
non-adhesive liquid embolics (ethyl vinyl alcohol polymer)
act in the same way but differ in their material properties.
Newer non-adhesive agents coming up the pipeline include
Squid (Balt USA, Irvine, California) and PHIL (MicroVention
Terumo, Aliso Viejo, CA). Additional liquid embolics cur-

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Fig. 33.5 Stent-assisted coiling performed on a complex bilobed RAA
to preserve ow to both branches
C. Solivio et al.
placement of a balloon-expandable covered stent in the
smaller visceral beds, off-label use of coronary stents may be
considered.
Covered stents allow for total aneurysm exclusion but are
susceptible to endoleaks. However, due to thrombogenicity of
the covered stent material, dual antiplatelet therapy must often
be administered for 3–12months following placement. Flowdiverting stents are adapted from neurointerventional radiology and have been introduced in the treatment of VAAs. Their
design partially excludes aneurysmal sacs, facilitating laminar
ow through the parent arteries and turbulent, thrombogenic
ow within the aneurysmal sac (Fig.33.7). In general, if there
is concern that the aneurysm is mycotic in nature, stent grafts
should be avoided (Fig. 33.8).
Future Directions
Some future directions in product development for VAA
management include the Barrel Vascular Reconstruction
Device by Medtronic, detachable neck-bridging devices, and
the Woven EndoBridge (WEB) by Subsequent Medical/
Biovention [14]. The Barrel Vascular Reconstruction Device
is purported to provide additional control for stent-assisted
aneurysms at bifurcations and branch origins; detachable
neck-bridging devices exclude ow across aneurysms with a
hope for gradual endothelization; and WEB is a nitinol mesh
device that is intended to plug aneurysms with stability
across their necks. Research regarding long-term outcomes
for the aforementioned future directions is lacking, and thus,
their uses are currently limited.
rently being studied include the Embrace hydrogel embolic
system, ionic strength-triggered chelation, thermoresponsive
gels, pH-sensitive embolic agents, and shear-thinning hydrogels [13].
Stent Grafts and Flow Diverting Stents
The use of stents in endovascular repair of the VAAs is limited by vessel diameter and tortuosity. Various types of stents
are currently used in VAA repair including balloonexpandable covered stents, self-expanding covered stents,
and ow-diverting stents. The splenic artery can be exceedingly tortuous, making stent graft deployment in the distal
bed quite challenging. In those instances, a lower-prole
ow-diverting stent may be utilized. When considering
Percutaneous andSurgical Options
Both open surgical and percutaneous VAA repair options
exist. Open surgical methods, which have historically been
used to treat VAAs, include aneurysmectomy, ligation, and
bypass with venous graft or prosthetic vascular graft. In
certain situations, direct sac access can be obtained via
percutaneous approach, and a combination of thrombin,
liquid embolics, and coils can be administered under uoroscopic guidance to embolize the aneurysm while maintaining the patency of the parent vessel. Given the rapid
advancements in endovascular technology and expanding
skill set of vascular and interventional physicians, the need
for open or laparoscopic surgical techniques is diminishing (Fig.33.9).

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Fig. 33.6 Renal artery aneurysm excluded with a balloon-expandable covered stent graft
Fig. 33.7 Stent-assisted coiling with a neuro ow-diverting stent in a large common HAA in a patient with multiple aneurysms (aorta/iliac)
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