During the past several decades, stent grafts have provided significant advances in the treatment of a variety of abdominal and thoracic aortic pathologic conditions. This article reviews the imaging of abdominal aortic aneurysms, the stent grafts available for treatment, management of endoleaks, and current data on the results of stent-graft placements.
are Associate Professors of Radiology, Department of Radiology,
UCSD Medical Center, and
is Chief of Interventional Radiology, Naval Medical Center, San
Transluminal placement of an endovascular stent was initially
conceived by Charles Dotter.
Previous to this time, many efforts to treat aneurysms focused on
wire embolization. The first successful resection and in situ
bypass of an abdominal aortic aneurysm (AAA) was performed by
Dubost in 1951.
Dr. Dotter's initial proposal was followed-up with feasibility
research, using animal models of AAA.
From this initial pioneering work, stent grafts have evolved into a
significant adjunct in the treatment of a variety of abdominal and
thoracic aortic pathologic conditions that will be reviewed in this
Abdominal aortic aneurysm
An aneurysm is a focal dilation >1.5 times the adjacent
normal caliber artery. Abdominal aortic aneurysms occur in 5% to 7%
of people over the age of 60 in the United States.
It is estimated that 2.7 million Americans have AAA, but only half
have been properly diagnosed. When the abdominal aorta is >3 cm
in diameter, an AAA is diagnosed. Abdominal aortic aneurysm is the
13th leading cause of death in the United States. The infrarenal
AAA is an arteriosclerotic aneurysm in 90% to 95% of patients, and
in most cases, it remains asymptomatic until rupture occurs. Other
causes of aneurysms include bacterial infection (mycotic),
traumatic, or anastomotic pseudoaneurysms; a small set of AAAs are
of the infiammatory type (<10%). Abdominal aortic aneurysms can
rarely occur in juxta- and suprarenal locations. Abdominal aortic
aneurysms predominate in men (85%), but AAAs tend to rupture in
women at an overall smaller diameter than in men. The indication
for therapy of AAA varies, but when the diameter is >5 cm (some
advocate 4 cm, the so-called "small AAA") open surgical repair is
considered. At this diameter, the risk of death from rupture over 1
year exceeds the risk of the operative repair. Most experts agree
that the annual risk of rupture for aneurysms ≥6 cm is at least 10%
per year, while with aneurysms >7.5 cm the risk may be as high
as 30%! The particular risk varies with individual patients,
however, since some patients have higher operative comorbidities.
Abdominal aortic aneurysm may also be considered for repair at
smaller sizes if they are painful, have caused distal embolization,
or are rapidly enlarging (>0.5 cm/year).
Conventional AAA therapy constitutes major surgery requiring
postoperative intensive care unit (ICU) monitoring, a 5- to 7-day
hospitalization, and 6 to 8 weeks of overall recovery. Open repairs
typically use general anesthesia. The exposed aorta is clamped
beneath the renal arteries, the AAA sac is opened, the thrombus is
removed, and side branches are controlled surgically. A Dacron
graft (DuPont, Wilmington, DE) is sutured in place, and the native
AAA sac closed over the graft. Short AAA necks may require
suprarenal clamping, which entails added risks. Procedural risks of
AAA repair include: Pulmonary, cardiac, and renal failure;
postoperative ileus; embolization into renal, mesenteric, and lower
extremities; infection; blood loss; paralysis or other nerve injury
(including sexual dysfunction); and colonic ischemia. In large
contemporary series, the hospital mortality after elective aneurysm
repair ranges from 2.8% to 6.2%; coronary artery disease is the
major risk factor for postoperative death. For ruptured AAAs, the
hospital mortality is as high as 60%. Currently, approximately
15,000 aneurysm ruptures with fatal outcomes are documented in the
United States annually. Approximately 40,000 patients undergo
aneurysmorrhaphy each year. Despite improved screening methods,
approximately 20% to 30% of all AAA repairs still occur
Image-guided diagnosis has contributed greatly to the impressive
success of modern vascular surgery for AAAs. A wide array of
imaging systems can be used in the diagnosis and characterization
of AAAs (Table 1).
Selection of the optimal AAA diagnostic imaging modality is
determined by the clinical symptoms, patient status, and
availability of equipment. In unstable patients, operative repair
may be done without imaging. In stable suspected rupture cases,
imaging findings facilitate surgical planning. Routine screening is
performed easily with ultrasound studies; although, presently,
computed tomography (CT) appears to offer many advantages.
Angiography is reserved for problem solving, such as determination
of accessory renal arteries, defining the AAA neck, evaluating for
side-branch disease, and delineating runoff status in
Because ultrasound is quick, inexpensive, and accurate, and
elective surgery has an acceptably low mortality, some researchers
have advocated screening for AAA.
The 12-fold increase in operative deaths for ruptured as compared
with nonruptured AAA clearly suggests that more emphasis needs to
be placed in identifying and repairing asymptomatic lesions.
With the advent of endovascular repair of AAA, more detailed
analysis of aneurysm anatomy is required to properly plan the
procedure than is required for conventional repair (Table 2). This
information is readily obtained with a spiral CT technique, with
supplemental information obtained with catheter angiography and
occasionally with endovascular ultrasound.
Commercially available endografts for AAA
Presently, 4 endografts have been approved by the Food and Drug
Administration (FDA) for repair of AAA, but only 3 are currently
commercially available. Ancure (Guidant Corp., Indianapolis, IN),
the first approved device, was removed from the market on October
1, 2003. The other endovascular devices are the AneuRx (Medtronic,
Inc., Santa Rosa, CA), the Excluder (W. L. Gore & Associates,
Flagstaff, AZ), and the Zenith (Cook, Inc., Bloomington, IN) (Table
3; Figures 1 through 3).
Implantation of AAA stent grafts
Stent-graft design has evolved over the past decade. The ideal
stent graft remains an elusive goal, but successive iterations have
improved deployment characteristics, reduced profiles, and improved
durability. In general terms, stent grafts can be classified in a
number of ways: 1) unibody construction (tubes, bifurcated designs,
and aorto-uni-iliac versions) versus modular; 2) supported versus
unsupported endografts; 3) hook fixation versus friction fit; and
4) infrarenal versus transrenal fixation. Considering all clinical
and morphologic prerequisites, it is estimated that only 20% to 30%
of all patients with infrarenal AAA are candidates for endovascular
repair. The technical success of stent-graft insertion has
progressively risen. Improvements in technique, patient selection,
and preoperative imaging and planning have all played a role, but
the main factor appears to be improved device performance.
The technical details describing insertion of each particular graft
exceeds the scope of this article.
Imaging follow-up of stent-graft devices
All patients who undergo stent-grafting have to be informed of
the importance of follow-up imaging, as long-term complications may
occur that may result in the patient not being adequately
protected. The various manufacturers have slightly different
follow-up schedules (Table 4).
Follow-up imaging repeatedly assesses the aneurysm size, detects
endoleaks, and monitors the structural and positional integrity of
the stent graft.
Endoleak refers to persistence of fiow within the aneurysm sac
despite an endovascular prosthesis, and these are classified by the
cause of the leak (Table 5).
The significance of endoleak is controversial and hotly debated.
Endoleaks can be detected with several imaging modalities.
Triphasic CTA is the most commonly used modality to follow-up
endovascular repair of AAAs. Noncontrast CT allows assessment of
migration by careful evaluation of the aortic and iliac deployment
sites on serial studies. These also detect calcification that may
mimic leaks. The arterial phase appraises patency of lumens and
side branches. The delayed postcontrast phase detects leaks.
Ultrasound is used in patients who are unable to receive contrast.
Catheter angiography is helpful to investigate leaks detected by
other modalities or to study suspected leaks in patients whose AAAs
do not shrink despite endoprosthesis placement. These are tailored
examinations based upon the problem at hand. In general, each
anastomosis is studied along with injections of the superior
mesenteric artery (SMA), renals, and internal and external iliacs.
Magnetic resonance angiography can also be used for endoleak
detection; some suggest this method has added sensitivity.
With CT angiograms, careful side-by-side comparisons are
imperative for accurate AAA sac size measurements. Review of
preplacement CT images may detect interval AAA growth not noticed
on sequential follow-up CTAs. If the AAA is growing and the
endoleak is identified on CT, transcatheter correction is
warranted. If the AAA sac is growing, but a leak is not seen with
CTA, angiography with careful attention to anastomotic connections
and side branches is performed.
Type I endoleak
With type I leaks, there is direct communication between the
lumen and the AAA sac and the patient is not protected from AAA
rupture; these leaks are typically detected during the procedure
and repaired immediately (Figure 4). If patient selection and
preprocedural planning is done carefully, the need to treat type I
endoleaks may be avoided. All measurements must be done carefully;
it is best to err on the side of oversizing the device diameters to
help with seals. Aortic attributes believed to infiuence these
leaks include neck diameter, length, and angulation. Infiation of a
balloon across the anastomosis with a type I leak may seal the
leak. Addition of aortic cuffs or iliac extenders may solve leaks
if additional graft material is required. If there is insufficient
room for a covered stent graft, placement of a noncovered stent may
affect a seal. If these maneuvers are ineffective, consideration of
open conversion becomes necessary. Proximal type I leaks may
develop later if the device migrates inferiorly, and these may be
treated with addition of aortic cuffs.
Type II endoleak
Management of these leaks is most controversial because one
third to one half of these eventually thrombose, typically within
the first 6 to 12 months. Apprehension occurs because direct AAA
sac pressure measurements have documented near systemic blood
pressures in some cases.
In a sac with a type II endoleak that is shrinking or stable,
conservative management is utilized, with follow-up scans at 3- to
6-month intervals. The follow-up interval depends upon the size of
the leak, the size of the feeding vessel, and the overall AAA size.
A smaller aneurysm should tolerate more growth before rupture than
would a larger AAA. If treatment is considered (ie, if the sac has
progressively increased), transcatheter embolization can be tried
(Figure 5). Type II leaks require infiow and an outfiow vessel (or
outfiow vessels) for patency. Treatment of the infiow or outfiow
artery and the sac may be needed for closure. Microcatheters allow
for precise delivery of coils and gelfoam. Injection of thrombin
has been associated with neurologic impairment that is possibly
related to embolization of spinal arteries or the lumbar plexus.
Other investigators have attempted to enter the sac by puncturing
the seal at an anastomosis (proximal or distal) and negotiating a
catheter into the sac. Direct puncture may be done with CT,
sonographic, or fiuoroscopic guidance. This allows embolization of
the endoleak with coils or glue (n-butyl-cyano-acrylate; TRU-FILL,
Cordis Neurovascular, Inc., Miami Lakes, FL).
Type III endoleaks
Like type I endoleaks, type III endoleaks are dangerous and
require treatment. Proper overlap of modular components minimizes
the occurrence of these leaks. Balloon dilation of the leaking
segments may seal these as well. If the balloon is too large, tears
in the graft fabric may result in type III leaks. Placement of
cuffs and extenders may seal these.
Type IV endoleaks
Porosity of graft material may result in an impressive leak at
the time of graft placement. The early AneuRx grafts all
demonstrated this leak at angiography and CT scanning within 24
hours of insertion. The WALLGRAFT (Boston Scientific, Natick, MA)
may also show this type of leak. One must be aware of this property
of the grafts being used, as this leak is self-limited over a few
Type V endoleaks
Open conversion is apparently required for these cases, as the
sac remains pressurized and no cause for the leak is identified. It
appears that increased pressure within the AAA sac (endotension)
can be transmitted through clot.
Results of endovascular stent grafts for AAA
Endovascular AAA repair has gained acceptance as a minimally
invasive alternative to open surgery in selected patients. While
long-term durability remains a major concern, patients and their
physicians are willing to accept a degree of uncertainty in
exchange for dramatic reductions in hospital stays, need for blood
transfusions, and postoperative recovery times.
This is clearly illustrated by a comparison of 5-year data of the
Guidant Ancure bifurcated AAA stent graft with open repair.
No aneurysm ruptures were reported in endovascular patients
followed for 5 years. (Note that ruptures did occur in patients
treated with the first-generation Ancure tube [nonbifurcated]
graft). The 30-day morbidity was 28.8% and 44.4% in the
endovascular and open arms, respectively. Patients in the
endovascular arm were more likely to have arterial trauma and
hematoma, while the surgical-arm patients were more likely to have
bleeding, and bowel, cardiac, and respiratory problems. The 30-day
mortality was 1.7% versus 2.7% (not significant [NS]) in the
endovascular and open arms, respectively. The immediate benefits of
endovascular repair compared with open repair include shorter
hospital stay (2 versus 6 days), decreased blood loss (400 versus
800 mL), and reduced ICU use (33% versus 94%). Only 9 patients
(2.8%) required late open conversion. These patients were
distributed over the 5-year period, which emphasized the necessity
of follow-up. Long-term survival rates were similar.
Various endovascular devices have been evaluated in clinical
trials designed to gain FDA approval. The devices and studies
differ in many regards, so interdevice comparisons are difficult.
One study recently published by the Cleveland Clinic summarizes
many issues with endovascular therapy of AAA.
Over a 6-year period, 703 patients underwent endovascular repair of
infrarenal AAA. Patient ages ranged from 48 to 100 years with an
average of 75 years. Five devices were used in the study: Ancure (n
= 63), AneuRx (n = 203), Excluder (n = 25), Talent (n = 39), and
Zenith (single center [n = 181] and multicenter data [n = 144]).
The operative 30-day mortality was 1.7% (12 patients). Elective AAA
repair had a 30-day mortality of 1.1%, while "urgent AAA repairs"
had a mortality of 19%. Patient survival with stent-grafting was
90% at 1 year, 78% at 2 years, and 49% at 5 years; survival did not
vary with the device used. Aneurysm-related death occurred in 12
patients (1.7%) with no device-specific differences. Three
aneurysms ruptured after device implantation, at 4, 7, and 19
months, for a rupture-free probability of 98.7% ± 0.9% at 24
months. Secondary procedures were required in 104 patients (15%).
The 12-month risk for secondary intervention did not differ between
device groups (
= 0.333), ranging from 8.8% ± 2.1% in the AneuRx to 20% ± 5.6% in
the Zenith (multicenter trial). Graft limb occlusion was more
common with the Ancure device (unsupported) (11% ± 4.6% at 12
months). Late limb occlusion was rare. The 12-month risk for
migration ranged from 0% (Ancure, Excluder, and Talent) to 8.2% ±
4.3% (Zenith), but the differences were not statistically
significant. Endoleak of any type was documented in 162 patients
(23%). Kaplan Meier risk for endoleak was 22% ± 1.9% at 6 months,
30% ± 2.3% at 12 months, and 42% ± 3.4% at 24 months. Type I leak
was found in 21 patients (3%), type II in 130 patients (18%), and
type III in 16 patients (2.3%). Interestingly, type I and III leaks
were not infiuenced by stent-graft design, although type II leaks
were (Excluder 58% at 12 months and 19% in the Talent). Aneurysm
shrinkage (diameter reduction >5 mm) was the following: 6 months
(8.3% ± 1.4%), 12 months (39% ± 2.7%), 24 months (60% ± 3.1%), and
36 months (68% ± 3.6%). Aneurysm sac enlargement was the following:
6 months (1.8% ± 0.7%), 12 months (3.5% ± 1.0%), 24 months (11% ±
2.5%), and 36 months (21 ± 4.5%).
The incidence of thoracic aortic aneurysms (TAAs) and acute and
chronic type B dissections is estimated to be as high as 10 cases
per 100,000 people per year.
The natural history of untreated disease includes progressive
enlargement, increasing risk of rupture, and, ultimately, death,
with 2-year survival rates of <30%. Traditional treatment
involves graft replacement via left thoracotomy, which improves
survival in comparison with medical therapy. Despite dramatic
improvements in the technical expertise for performing these
complex thoracic aortic surgeries, open surgery is complicated by
operative mortality rates ranging from 8% to 20% for elective cases
and up to 60% for emergencies. Survivors of open repairs still
suffer from morbidity rates of up to 50% related to renal,
intestinal, and spinal cord ischemia that substantially limit
The success of endovascular stent grafts for AAAs has provided
motivation to adapt similar technology for descending TAAs and type
B dissections. The preliminary results of such therapy appear
promising, with advantages of the endografts including shorter
operative time, avoidance of cardiopulmonary bypass, decreased need
for general anesthesia, lack of aortic cross-clamp time, and
avoidance of major thoracic or thoracoabdominal incisions. Most
reported series document high technical success along with major
reductions in morbidity and mortality. The FDA has recently granted
conditional approval of the Gore TAG thoracic endoprosthesis for
TAAs (W. L. Gore & Associates).
Since 1992, there have been at least 13 reported series of
patients undergoing endovascular repair of TAAs. Patient
populations and devices used varied, but the results have been
fairly impressive (Table 6). The Stanford Group reported 1- and
2-year survival rates of 81% and 73%, respectively.
This compares favorably with the results of traditional open
surgery, where the actuarial survival rates are estimated to be 70%
at 5 years, and 40% at 10 years in "survivors of open repair."
These comparisons are difficult since most of the patients offered
endovascular therapy have been denied surgery.
Acute and chronic aortic dissections
The endovascular approach has been applied to other thoracic
aortic pathologies, including acute and chronic dissections,
penetrating ulcers, and traumatic transections. Current indications
for open repair of type B dissections include uncontrollable
hypertension, persistent pain, expanding aneurysm, or end-organ
ischemia. Acute dissection results in 36% to 72% mortality within
48 hours if left untreated; even operative therapy is associated
with 50% to 70% mortality. With such dismal results, it is no
wonder that endovascular approaches have been applied, and early,
small series report lower mortality rates of 16% to 28%.
Stent-graft coverage of the proximal entry site of a type B
dissection should, in theory, limit the extent of the dissection,
obliterate the fiow into the entry tear, and promote thrombosis of
the false lumen.
Traumatic transections and postoperative
A small number of patients have had stent grafts used, with very
encouraging results, to treat posttraumatic aortic transections and
for postoperative pseudoaneurysms (Figure 6).
Those patients who survive aortic transaction are at particularly
high risk of dying from further hemorrhage within the first 24
hours. If endovascular repair is going to play a major role in such
cases, there is a need for the devices to be of sufficient caliber
to seal the thoracic aorta and the ability to place such devices
rapidly. Moreover, the long-term performance characteristics need
to be better delineated before use in younger trauma patients is
undertaken. Surgical repair of chronic traumatic aneurysms has been
reported to have a mortality rate of 5% to 18%, a morbidity of 11%
to 50% (related to bleeding, heart failure, renal failure, spinal
cord injury), and a 53% incidence of Horner syndrome or vocalcord
palsy. Stent grafts may potentially ameliorate these
The development of endovascular repair of AAA has now entered
its second decade with introduction of a multiplicity of designs
(>16) with only 4 devices gaining FDA approval.
There has certainly been great progress in the design of
endovascular devices, and several newer designs have completed, or
are undergoing, evaluation. Up to this point, a mortality advantage
for endovascular repair of AAA has not been convincingly shown
compared with results of open repair, although recent trials are
encouraging. Essentially, all trials thus far have shown
significant reductions in systemic complications (cardiac and
pulmonary) using the endovascular approach as opposed to open
repair. Compared with conventional surgery, endovascular repair has
shown reduced blood losses and transfusion requirements and reduced
hospital and ICU stays with more rapid return to preoperative
levels of function. Concerns about the durability of endovascular
repair still remain. Endoleaks and limb thromboses continue to
plague endovascular grafts, necessitating secondary interventions.
The annual rate of AAA rupture after endovascular repair is
approximately 1%. Performing endovascular grafts in AAA patients
who are fit for open repair and have otherwise reasonable life
expectancy seems unwise at this point. Endovascular repair of AAAs
is appropriate in patients with significant comorbidities and
suitable anatomy and in patients with relatively limited life
expectancy and larger or expanding AAAs. Technical advances in
design will allow expansion of the use of endovascular repairs for
AAAs, in ruptured AAAs, and in other thoracic aortic