Download Factors Portending Endoleak Formation After Thoracic Aortic Stent

Factors Portending Endoleak Formation After Thoracic
Aortic Stent-Graft Repair of Complicated Aortic Dissection
Daniel Y. Sze, MD, PhD; Maurice A.A.J. van den Bosch, MD, PhD; Michael D. Dake, MD;
D. Craig Miller, MD; Lawrence V. Hofmann, MD; Robin Varghese, MD; S. Chris Malaisrie, MD;
Pieter J.A. van der Starre, MD, PhD; Jarrett Rosenberg, PhD; R. Scott Mitchell, MD
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Background—Endoleaks after stent-graft repair of aortic dissections are poorly understood but seem substantially different
from those seen after aneurysm repair. We studied anatomic and clinical factors associated with endoleaks in patients
who underwent stent-graft repair of complicated type B aortic dissections.
Methods and Results—From 2000 to 2007, 37 patients underwent stent-graft repair of acute (ⱕ14 days; n⫽23), subacute
(15 to 90 days; n⫽10) or chronic (⬎90 days; n⫽4) complicated type B aortic dissections using the Gore Thoracic
Excluder (n⫽17) or TAG stent-grafts (n⫽20) under an investigator-sponsored protocol. Endoleaks were classified as
imperfect proximal seal, flow through fenestrations or branches, or complex (both). Variables studied included coverage
of the left subclavian artery, aortic curvature, completeness of proximal apposition, dissection chronicity, and device
used. Endoleaks were found during follow-up (mean, 22 months) in 59% of patients, and they were associated with
coverage of the left subclavian artery (complex, P⬍0.001), small radius of curvature (type 1 and complex, P⫽0.05), and
greatest length of unapposed proximal stent graft (complex, P⬍0.0001). During follow-up, 10 endoleaks resolved
spontaneously, 6 required reintervention for false lumen dilatation, and 2 were stable without clinical consequences.
Conclusions—Endoleaks are common after stent-graft repair of aortic dissection and may lead to false lumen enlargement
necessitating reintervention. Anatomic complexities such as acute aortic curvature and covered side branches were
associated with endoleaks, illustrating the need for dissection-specific device development. (Circ Cardiovasc Intervent.
2009;2:105-112.)
Key Words: aorta 䡲 dissection 䡲 surgery 䡲 complications
E
curved or angulated, rendering sealing of the PIT a challenge.
Second, if the distance between the left subclavian artery
(LSCA) and the PIT in the dissected aorta is short (less than
20 mm in length), coverage of the LSCA may be required to
achieve an adequate seal.14 Coverage of large side branches
by endovascular treatment of abdominal aortic aneurysms is
associated with type 2 endoleaks, and a similar pathophysiology likely exists in the thoracic aorta.15,16
Inadequate seal or retrograde flow from branches or
fenestrations can result in persistent false lumen flow and
pressurization. The risk of subsequent false lumen enlargement and aortic rupture due to endoleak is not yet known. The
aim of this study was to assess which anatomic and clinical
conditions were associated with endoleaks in patients who
underwent endovascular stent-graft repair of complicated
type B aortic dissection and to examine the clinical consequences of these endoleaks.
ndovascular stent-graft closure of the primary intimal
tear (PIT) was introduced more than a decade ago as a
treatment option for patients with complicated type B aortic
dissection.1,2 Goals of stent-graft placement are to reestablish
arterial flow to ischemic beds and to abolish pulsatile antegrade perfusion of the false lumen, which should reduce
subsequent false lumen enlargement and rupture.3– 8 Continued pressurization and perfusion of the false lumen due to
endoleak, however, is frequently seen after stent-graft repair
of aortic dissection.9,10 Compared with endoleaks encountered after thoracic endovascular aneurysm repair, endoleak
physiology in aortic dissection is complex and incompletely
understood.
Clinical Perspective see p 112
The first prerequisite for successful sealing of the PIT is a
proximal landing zone of adequate geometry.11,12 It has long
been observed that severe angulation and curvature in the
abdominal aorta can result in endoleaks when treating aneurysms.13 Near the aortic arch, the geometry can be severely
Patients and Methods
Between January 2000 and November 2007, 37 patients underwent
endovascular stent-graft repair of acute (ⱕ14 days; n⫽23), subacute
Received September 4, 2008; accepted December 31, 2008.
From the Division of Interventional Radiology (D.Y.S., M.A.A.J.B., M.D.D., L.V.H.), Department of Cardiothoracic Surgery (M.D.D., D.C.M., R.V.,
S.C.M., R.S.M.), Department of Anesthesia (P.J.A.S.), and Department of Biostatistics (J.R.), Stanford University Medical Center, Stanford, Calif.
Correspondence to Daniel Sze, MD, PhD, H-3646 Stanford University Medical Center, 300 Pasteur Road, Stanford, CA 94305-5642. E-mail
[email protected]
© 2009 American Heart Association, Inc.
Circ Cardiovasc Intervent is available at http://circinterventions.ahajournals.org
105
DOI: 10.1161/CIRCINTERVENTIONS.108.819722
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Circ Cardiovasc Intervent
April 2009
Figure 1. Common endoleak pathophysiology
after stent-graft repair of aortic dissection. A,
Type 1a endoleak: imperfect seal at the proximal landing zone allowing blood to flow around
the stent graft, through the PIT, and into the
aortic false lumen. B, Type 2 endoleaks: persistent perfusion of the aortic false lumen through
natural fenestrations, reentry tears, or retrograde flow from branch vessels. C, Complex
endoleak, combining aspects of both type 1a
and type 2. Flow in the LSCA and in the aortic
false lumen may be antegrade, retrograde, or
more complex.
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(15 to 90 days; n⫽10), or chronic (⬎90 days; n⫽4) complicated type
B aortic dissections. Type B aortic dissections were judged to be
complicated if 1 or more of the following 3 clinical problems was
present: (1) symptomatic visceral or lower limb ischemia due to
compromise of blood flow into branch vessels, including refractory,
new, or worsened hypertension indicative of renal malperfusion; (2)
false lumen rupture; or (3) pain with documented rapid aortic
enlargement, interpreted to be impending rupture. Patients were
excluded if arterial access was inadequate (⬍7-mm diameter of iliac
or femoral arteries). Patients with connective tissue disorders (eg,
Marfan disease) were preferentially treated by open surgical methods, and only 1 patient with Marfan disease and severe ischemia of
multiple vascular beds was enrolled.
Endovascular repair was the default for all other patients. The
Gore Thoracic Excluder with the longitudinal spines (n⫽17) or the
redesigned and renamed “TAG” stent grafts (n⫽20)17 were used
under an investigator-sponsored investigational device exemption
protocol approved by the Food and Drug Administration and by our
institutional review board.
No abdominal cuffs or components were used. Informed consent
was obtained from each patient or legal representative.
Patient evaluation and selection required consensus between the
cardiothoracic surgeons and the interventional radiologists, and all
procedures were performed collaboratively as previously described.1,18 All patients underwent helical computed tomographic
angiography (CTA) before stent-graft placement to determine the
location, length and diameter of the dissection and landing zones,
and to evaluate the suitability of the iliac and femoral arteries for
vascular access. Arterial access was gained either by inguinal or
retroperitoneal exposure of the femoral or iliac artery and introduction of a 20 to 24F sheath. One hundred units per kilogram of heparin
were administered in patients without frank rupture.
Transesophageal echocardiography was used intraoperatively to
further characterize the anatomic relations between the true and false
lumens, the PIT, and the branch vessels.1 Measurements from
calibrated catheter aortography, transesophageal echocardiography,
and CTA were used to select the device size. Early practice of using
intravascular ultrasound was phased out as the quality of data from
the other modalities improved.
Diameter was chosen according to the measurements of the
nondissected aorta at the proximal landing zone, and length was
chosen to be the minimum judged necessary to cover the proximal
landing zone and extend at least 3 cm beyond the distal extent of the
PIT. After the stent graft was deployed to cover the PIT, repeat
aortography was performed to confirm the position of the device and
to evaluate the size of and flow within the aortic lumens and branch
vessels. Postdeployment balloon angioplasty was performed judiciously and only proximally in patients with acute dissections
because of the fragility of the intimal flap. Angioplasty was performed routinely in the patients with chronic dissections.
Adjunctive surgical or medical therapies included antihypertensive or vasopressor medications, resection of infarcted bowel,
thoracostomy drainage, hemodialysis, and antibiotics as needed. For
long-term management, every patient was placed on oral antihypertensive medications including at least ␤-blockers. Two patients
required long-term anticoagulation for deep venous thrombosis, 1 of
whom experienceed a pulmonary embolism.
The follow-up protocol included clinical evaluation and multiple
phase CTA with 3D reconstructions, performed at 1, 6, and 12
months after stent-graft placement, and annually thereafter. An
additional scan was performed at 3 months if any issues were raised
at the 1-month follow-up. Although not mandated in the protocol,
postprocedural CTAs were also routinely performed within 1 week
of surgery before patient discharge. In 3 patients, magnetic resonance
angiography with gadolinium contrast enhancement was substituted
for the CTA because of azotemia and/or allergy. Pathophysiology of
any thoracic false lumen filling was analyzed retrospectively on
postprocedural scans using multiplanar reformatting capabilities
(AquariusNet, TeraRecon, Redwood City, Calif) to classify endoleak
type (Figures 1 and 2). Six patients also underwent catheter angiography, in part to delineate pathophysiology and direction of flow in
these endoleaks (Figure 3). In accordance with the classification
system that exists for endoleak formation after stent-graft repair of
abdominal aortic aneurysms, we classified type 1a leaks as persistent
flow around an imperfect proximal seal and through the patent PIT,
and type 2 leaks as false lumen perfusion involving retrograde flow
through branch vessels such as the LSCA, bronchial, or intercostal
arteries9 and/or flow through natural fenestrations and reentry tears.
Endoleaks were classified as “complex” if both factors were present
(Figure 1).
Three-dimensional reconstructions of the aortic arch based on
CTA were also used to calculate the radius of the arch curvature in
each patient. The aortic arch curvature was quantified by calculating
the arithmetic mean of the lesser curve radius of curvature and the
greater curve radius of curvature at the level of the PIT. Thus,
smaller values of radius represent more severe aortic curvature
(Figure 4). From these reconstructions, the adequacy of proximal
apposition of the stent graft to the aortic wall was also assessed by
measurement of the length of lack of apposition to the lesser
curvature, sometimes termed the bird beak.
Primary technical success was defined as angiographic sealing of
the PIT, with reperfusion of previously ischemic visceral or lower
extremity arteries fed by the aortic true lumen if present. Primary end
points were incidence of endoleaks and endoleak type in relation to
LSCA coverage, aortic arch curvature, completeness of apposition,
dissection chronicity, and device used. Secondary end points were
necessity for reintervention, neurologic complications, and periprocedural mortality within 30 days. Clinically relevant baseline characteristics are reported with 95% confidence intervals. Continuous
variables are expressed as mean⫾SD. Comparison of continuous
variables before and after stent-graft placement was performed with
Student t test. For comparison of dichotomous variables, the ␹2 test
was used. P⬍0.05 was considered to indicate statistical significance.
All statistical analyses were performed with SPSS version 10.0
(SPSS Inc, Chicago, Ill).
Sze et al
Endoleaks After Repair of Aortic Dissection
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Figure 2. Imaging appearance of endoleaks. Thinslab maximum intensity projection reconstructions
of contrast medium– enhanced computed tomography scans reveal a presence of blood flow in the
aortic false lumen. Differential enhancement may
indicate direction of flow, especially when delayed
images are obtained. A, Type 1a endoleak, with no
flow in the covered LSCA but slow contrast
enhancement of the aortic false lumen (arrow) via
flow around an imperfect proximal seal. B, Type 2
endoleak, with slow retrograde flow in the covered
LSCA (arrowhead) leading into the aortic false
lumen (arrow). In this delayed image, brightly
enhanced blood has already passed through the
fast-flowing true lumen, leaving the highest attenuation enhanced blood in the slower-flowing false
lumen and LSCA. C, Complex endoleak, with flow
into the aortic false lumen from both an imperfect
proximal seal and from natural fenestrations. First
arterial phase image showed a trace of contrast
enhancement of the covered LSCA (arrow) and
retrograde filling of the aortic false lumen from natural fenestrations below the diaphragm (asterisk).
D, Oblique maximum intensity projection of a
delayed image obtained 60 seconds after the
image in panel C showed extensive patency of the
aortic false lumen (arrow), with apparent contiguity
with the covered LSCA (asterisk), later confirmed
by catheter angiography.
Results
Patient demographics are listed in Table 1. Stent-graft insertion was technically successful in all 37 (100%) patients
(Table 2). No open surgical conversions were necessary at the
time of initial treatment. Average follow-up was 28.3 months
in those who survived beyond 30 days and 22.3 months
overall (range, 0 to 92 months).
Intraprocedural type 1a endoleaks were observed in 4 acute
patients and in 1 chronic patient. All were successfully treated
by immediate proximal stent-graft extension. Postprocedural
endoleaks were detected in 11 of 23 (48%) acute patients, 8
of 10 (80%) subacute patients, and 3 of 4 (75%) chronic
patients, evenly distributed by type. There was a trend toward
greater incidence of endoleaks in subacute and chronic
patients, especially for type 2 leaks, that did not reach
statistical significance (Table 3). There were no significant
differences in endoleak formation between the earlier generation Thoracic Excluder and the redesigned TAG (Table 4).
Coverage of the LSCA was required in 20 of 37 (54%)
patients in total, including in 13 of 23 (57%) acute patients, 4
of 10 (40%) subacute, and 3 of 4 (75%) of chronic patients.
After coverage of the LSCA, the incidence of complex leaks
was 35% (n⫽7), where none were seen without coverage of
the LSCA (P⫽0.0005; Table 5). In addition, summing all
patients with at least a component of type 2 leak (including
type 2 and complicated endoleaks), coverage of the LSCA
resulted in endoleaks in 55% of patients (n⫽11), compared
with 18% (n⫽3) in those without coverage of the LSCA
(P⫽0.017). Incidence of type 1 or type 2 endoleaks alone as
a function of LSCA coverage did not reach statistical
significance.
The radius of the aortic arch curvature in patients with type
1a endoleaks was 36⫾12 mm (mean, ⫾1 SD) versus
65⫾51 mm in those without leaks (P⫽0.05; Table 6). In
patients with complex endoleaks, the radius was 37⫾14 mm,
not quite reaching statistical significance (P⫽0.06). Including
all patients with a component of poor proximal landing zone
seal (type 1a and complex leaks), the radius of curvature was
36⫾13 mm (P⫽0.05). Pure type 2 endoleaks did not seem to
be related to degree of aortic curvature.
The length of the bird beak varied from zero to 37 mm. The
length was shortest in patients who did not develop endoleaks
(6.7⫾8.8 mm) and longest in patients who formed complex
type endoleaks (22.6⫾5.1 mm, P⬍0.0001; Table 7). Although patients with type 1a and type 2 endoleaks also had
longer bird beaks than patients without endoleaks, these did
not reach statistical significance. Length of the bird beak was
weakly associated with the degree of curvature as defined as
the reciprocal of the radius of curvature, with a Pearson
coefficient r⫽0.53. The mean bird beak length without
coverage of the LSCA was 9.3⫾11.8 mm, compared with
16.2⫾10.9 mm with coverage of the LSCA (P⫽0.08). Bird
beak length tended to be longer with use of the newer TAG
design (15.6⫾12.7 mm) when compared with the older
Thoracic Excluder (9.6⫾9.6 mm), but this also did not reach
statistical significance (P⫽0.13).
Six endoleaks resulted in false lumen enlargement and
necessitated reinterventions. Interventions included embolization of the LSCA in 2 patients, surgical repair in 3 patients,
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April 2009
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Figure 3. Confirmation and treatment of a complex endoleak.
Imaging performed 9 months after the study shown in Figure 2C
and 2D showed false lumen dilatation and increase of aortic
diameter from 38 to 52 mm. A, True lumen aortogram demonstrated immediate faint antegrade filling of the covered LSCA
(arrow), suggesting a type 1a endoleak. B, False lumen aortogram showed antegrade flow into the LSCA (arrow), to and fro
in the aortic false lumen, and antegrade flow into intercostal and
bronchial branches of the aortic false lumen (arrowheads). C,
Embolization coils (Tornado, Cook Inc, Bloomington, Ind) were
placed extending from the LSCA true lumen through the PIT
into the aortic false lumen adjacent to the stent graft. D, Threemonth follow-up showed complete thrombosis and regression
of the false lumen to the level of the diaphragmatic hiatus. A
30-mm Hg drop in systolic blood pressure in the left upper
extremity after the embolization was well tolerated.
and both in 1 patient. Embolizations were performed 12
months, 4 months, and 1 week after stent-graft treatment in 3
patients, and were successful in 2. The third patient had a
preexisting retrograde propagation of the dissection into the
arch and a natural fenestration at the origin of the left
common carotid artery, which did not resolve with embolization of the LSCA and adjacent aortic false lumen. This
patient and 3 others underwent elective surgical repair at 8, 8,
6, and 3 months after stent-graft treatment, all of which were
successful in removing endoleak-related dilatation.
Ten endoleaks resolved spontaneously during follow-up at
6.5⫾5.4 months after stent-graft treatment, including in 1 of
2 patients on long-term anticoagulation for deep vein thrombosis. Two endoleaks persisted but have not been subjected to
reintervention because initial ischemia was rectified and false
lumen diameter remained stable. Two patients with endoleaks
died during their initial hospitalizations, both from multiorgan failure stemming from the limb, renal, and mesenteric
infarction originally caused by dissection.
Two patients with type 2 endoleaks were patients with
chronic dissections (14 months and 8 years from initial event)
who presented with frank ruptures of false lumen aneurysms
Figure 4. Quantitation of aortic curvature and adequacy of
apposition (bird beak length). A, Thin-slab maximum intensity
projection reconstruction of a CT scan showed a gently curved
device well conformed to a gently curved aorta. In this reformat
that approximates the center flow plane, circles were drawn to
fit the inner and outer curves. The curvature was quantitated as
center flow line radius of curvature at the level of the PIT, calculated as the mean of the radii of the inner and outer curves, in
this case 66 mm. B, Reformat of a different patient showed an
acutely curved aorta with a radius of curvature of 49 mm. Note
the imperfect apposition of the proximal stent graft to the lesser
curvature, referred to as a bird beak. The bird beak length, or
length of lack of apposition, was measured from the proximal
tip of the stent graft to the site of circumferential aortic contact,
in this case 26 mm.
and expanding hemothoraces. Despite sealing of the PITs,
angiography showed continued filling of the false lumen
through abdominal natural fenestrations and reentry tears, and
both patients died from inexorable hemorrhage and disseminated intravascular coagulation. Placement of large bare
stents extending from the stent graft to the aortic bifurcation
was performed in 1 patient but was not successful in
eliminating false lumen perfusion.
Sze et al
Table 1.
Endoleaks After Repair of Aortic Dissection
109
Demographics of the Study Population
Age, years
62 (18 to 88)
Gender, male/female
31 (84)/6 (16)
Aortic dissection chronicity
Acute
23 (62)
Subacute
10 (27)
Chronic
4 (11)
Presenting symptoms*
Mesenteric ischemia
Acute
9 (39)
Subacute
6 (60)
Chronic
0
Total
15 (41)
14 (61)
5 (50)
1 (25)
19 (51)
Extremity ischemia
6 (26)
1 (10)
0
7 (19)
Spinal cord ischemia/paralysis
2 (9)
0
0
2 (5)
False lumen rupture
6 (26)
3 (30)
2 (50)
9 (24)
Pain with false lumen enlargement (impending rupture)
9 (39)
6 (60)
2 (50)
17 (46)
Extension to type A
4 (17)
0
0
4 (11)
Renal ischemia
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Risk factors/comorbidities
Hypertension
37 (100)
Diabetes
3 (8)
Hyperlipidemia
8 (22)
Smoking
15 (41)
Marfan disease
1 (3)
Stent-graft device used
Thoracic Excluder
17 (46)
TAG
20 (54)
No. of stent grafts used
1
32 (86)
2
4 (11)
3
1 (3)
Data are presented as mean (range) or n (%).
* Percentages of presenting symptoms sum to more than 100% because of multiple ischemic beds or symptoms
in many patients.
of the paraparesis. Neurologic deficits had not improved after
9 months.
Of the 20 patients who underwent coverage of the LSCA,
only 3 developed left upper extremity ischemic symptoms.
Two patients’ symptoms were mild and improved over time
without reintervention, and 1 underwent successful carotid to
subclavian bypass grafting.
Overall 30-day mortality was 7 of 37 (19%), representing
1 procedural complication (the stroke described earlier) and 6
failures to rescue. The failures included the 2 patients with
ruptured chronic false lumen aneurysms described earlier.
Two acute and 1 subacute dissection patients died due to
visceral, renal, or extremity infarction and multiorgan failure,
and 1 acute traumatic dissection patient died of other trau-
Two strokes (5%) were observed, both in acute patients
who underwent coverage of the LSCA. One had an intraoperative type 1a endoleak and immediately underwent proximal extension. The extension partially covered the left
common carotid artery origin, requiring inflation of a trilobed
balloon (Gore) within the stent graft and dragging the device
distally. The other patient underwent an unremarkable procedure but a postprocedural CT scan of the brain showed
widespread infarction in the anterior and posterior circulation
distribution bilaterally, and care was withdrawn.
One patient (3%) developed postprocedural paraparesis of
the left lower extremity. MRI of the spine revealed an
ischemic spinal cord lesion from T3 to T8. A spinal drain was
placed on postoperative day 2 immediately after recognition
Table 2.
Clinical Outcomes of Stent-Graft Treatment
Technical success (PIT covered)
Acute Patients (n⫽23)
Subacute Patients (n⫽10)
Chronic Patients (n⫽4)
Total (n⫽37)
23 (100)
10 (100)
4 (100)
37 (100)
30-day mortality
4 (17)
1 (10)
2 (50)
7 (19)
Stroke
2 (9)
0 (0)
0 (0)
2 (5)
Paraparesis
1 (4)
0 (0)
0 (0)
1 (3)
Data are presented as n (%).
110
Circ Cardiovasc Intervent
Table 3.
April 2009
Endoleak Formation and Endoleak Type in Relation to Acuity of Dissection
Endoleak Type
Acute Patients (n⫽23)
Subacute Patients (n⫽10)
Chronic Patients (n⫽4)
Combined Subacute/
Chronic Patients (n⫽14)
P
Type 1a
4 (17)
2 (20)
1 (25)
3 (21)
0.77
Type 2
3 (13)
3 (30)
2 (50)
5 (36)
0.11
4 (17)
3 (30)
0 (0)
3 (21)
0.77
11 (48)
8 (80)
3 (75)
11 (79)
0.07
Complex (both 1a and 2)
Total
Data are presented as n (%).
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Left untreated, 36% to 72% of thoracic aortic dissection
patients die within 48 hours.19,20 Most cases of type B
dissections are uncomplicated and can be managed by medical therapy, including the use of antihypertensive and negatively inotropic drugs. Dissections complicated by ischemia,
rupture, or impending rupture have historically been treated
by surgical graft techniques, with mortality rates as high as
87% in patients with multiple comorbidities and ischemic
beds.20 –23 Stent-graft repair has emerged as a minimally
invasive alternative treatment with high initial technical
success rates ranging from 90% to 100%, 30-day mortality
rates between 6% and 16%, and encouraging midterm results.1,24 –29 Despite the high rates of endoleak (which may not
necessarily represent treatment failure), the morbidity and
mortality rates reported herein continue to support stent-graft
repair in these high-risk patients.
In addition, outcomes after stent-graft repair compare
favorably with those of percutaneous fenestration and stenting,30 a technique effective at relieving ischemia but permissive of continued false lumen pressurization and dilatation.
The technical goal of stent-graft treatment is closure of the
PIT, but clinical success is defined according to the original
clinical presentation. In patients with malperfusion, restoration of arterial flow to the ischemic beds is the primary
clinical objective, so the presence of an endoleak may have
no adverse impact on clinical success, which is distinctly
different than when treating patients with aneurysms. For
patients with impending or frank rupture, exclusion of the
false lumen is the primary clinical objective. In the latter
group, and for both groups over the long term, endoleaks are
an important issue. Endoleaks after thoracic endovascular
aneurysm repair are well described and occur in 5% to 35%
of patients,9,10,31 but endoleaks after treatment of dissections
are strikingly different.
Endoleaks were detected in 59% of patients, much more
than that reported in previous studies, reflecting several
important distinctions. First, we used a multiple (3 to 5) phase
CTA protocol, including an unenhanced phase, an arterial
contrast-enhanced phase, and multiple (up to 3) delayed
phases, with 3D reconstructions. Contrast medium was injected at 4 to 6 mL/s to maximize arterial enhancement. This
protocol was specifically designed to detect endoleaks and is
more aggressive than published techniques.32 Second, many
early endoleaks were detected when imaging studies were
performed postoperatively, before the mandated follow-up.
Ten of these early endoleaks resolved spontaneously and
would have been occult had we adhered to a less aggressive
follow-up protocol. Excluding these leaks, our overall endoleak rate was 12 of 37 (32%). Third, the follow-up period
was relatively long (up to 92 months), so the time at risk for
endoleaks was greater in our population than in previous
series. However, all but 1 documented endoleaks were
detected within the first year of follow-up.
We found that patients with LSCA coverage had a significantly increased prevalence of type 2 and complex endoleaks, supporting thoracic endovascular aneurysm repair
studies that found high rates of endoleak when the arch was
involved.10,33 Dissection flaps that extend to or into the origin
of the LSCA complicate the achievement of a seal using a
simple cylindrical device. The physiology of blood flow at
the origin of the LSCA can be extremely complex, with
communication between aortic and LSCA true and false
lumens, and directions of flow varying with different phases
of the cardiac cycle. Future use of branched endografts should
help to address this limitation.
Table 4. Incidence of Endoleak Formation and Endoleak Type
in Relation to Device Used
Table 5. Incidence of Endoleak Formation and Endoleak Type
in Relation to LSCA Coverage
matic injuries. During follow-up that averaged 22.3 months in
length, no stent-graft migration, fracture, dislocation, propagation from type B to type A, or new false lumen rupture was
documented. One case of distal device flares eroding through
the dissection flap and causing a localized false lumen ulcer
was noted 22 months after the original surgery. This was
accompanied by mild hemoptysis and was treated by surgical
graft repair through a left thoracotomy, but the patient died
postoperatively from complications of an arrhythmic arrest.
Discussion
Endoleak Type
TAG
(n⫽20)
Thoracic Excluder
(n⫽17)
P
Endoleak Type
LSCA Covered
(n⫽20)
No LSCA Coverage
(n⫽17)
P
Type 1a
4 (20)
3 (18)
0.98
Type 1a
2 (10)
5 (29)
0.16
Type 2
4 (20)
4 (24)
0.67
Type 2
4 (20)
3 (18)
0.86
Complex (both 1a and 2)
5 (25)
2 (12)
0.40
Complex (both 1a and 2)
7 (35)
0 (0)
0.0005
11 (55)
8 (47)
0.74
Total
13 (65)
8 (47)
0.29
Total
Data are presented as n (%).
Data are presented as n (%).
Sze et al
Table 6. Incidence of Endoleak Formation and Endoleak Type
in Relation to Degree of Curvature of the Aorta at the Level of
the Primary Intimal Tear
Endoleak Type
Radius of Curvature, mm
P
No leak
65⫾51
Type 1a
36⫾12
0.05
Type 2
42⫾6
0.18
Complex (both 1a and 2)
37⫾14
0.06
Type 1a and complex
36⫾13
0.05
Type 2 and complex
40⫾12
0.10
Data are presented as mean⫾SD.
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The clinical impact of covering the LSCA is still controversial. Although upper extremity ischemia and vertebrobasilar insufficiency are uncommon and generally reversible,
emerging statistics on stroke and paraplegia are raising
concern.14 –16 Both patients in our series who experienceed
strokes underwent coverage of the LSCA, and both strokes
seemed embolic on MRI and involved the anterior circulation, suggesting that manipulation in the arch rather than
compromise of left vertebral perfusion were to blame. In the
EUROSTAR registry, coverage of the LSCA was not associated with stroke, but did increase the risk of paraplegia.34
Mortality was not affected by LSCA coverage. These data
resulted in guidelines suggesting that LSCA coverage can be
managed expectantly unless anatomic conditions such as
diminutive right vertebral artery, or left internal thoracic
artery to coronary bypass are identified.14,35 We continue to
adhere to these guidelines for emergent cases, but preemptive
carotid to LSCA surgical transposition or bypass has become
our standard for elective cases.
The other factor contributing to formation of endoleaks is
the limited capability of current devices to conform to acutely
curved aortic anatomy, resulting in type 1a and complex
endoleaks. Apposition of stent grafts to the lesser curvature of
the aortic arch was generally incomplete and resulted in a bird
beak defect. This shortcoming was independent of the generation of stent graft used, but future devices in development
address this issue using more conformable and flexible
designs.
Limitations of this study includes its nonrandomized nature, limited numbers of subjects, and variety of chronicity
and symptoms within the cohort. Even optimized imaging
protocols do not always reveal direction of flow, compromising the detection, and classification of endoleaks. Furthermore, the data presented are from a single center, but reflect
Table 7. Incidence of Endoleak Formation and Endoleak Type
in Relation to Length of Lack of Apposition of the Endograft to
the Aortic Lesser Curve (Bird Beak)
Endoleak Type
Bird Beak Length, mm
P
No leak
6.7⫾8.8
Type 1a
17.7⫾14.5
Type 2
12.4⫾11.9
0.26
Complex (both 1a and 2)
22.6⫾5.1
⬍0.0001
Data are presented as mean⫾SD.
0.10
Endoleaks After Repair of Aortic Dissection
111
the performances of 10 different cardiovascular and thoracic
surgeons and interventional radiologists of different degrees
of experience.
In conclusion, these results confirm that stent-graft treatment of patients with complicated type B dissections can be
safely performed with a very high initial rate of technical
success. Factors that portend endoleak formation were related
to involvement of the distal arch, including coverage of the
LSCA, severe aortic curvature, and poor lesser curve apposition. Late false lumen dilatation necessitated reintervention
in 16% of patients, all of whom demonstrated endoleaks.
Because of flow through distal fenestrations and reentry tears,
stent-graft treatment was inadequate in treating ruptured
chronic false lumen aneurysms, a specific high risk group for
whom substantial technological improvements are needed
before stent-graft repair can become an acceptable treatment
option.
Disclosures
Dr Sze is a consultant for MediGene Inc, Jennerex Biotherapeutics
Inc, and Pain Therapeutics Inc, none of which are pertinent to this
manuscript. Dr Dake is a consultant for W.L. Gore Inc. Dr Miller is
a consultant for Medtronic Heart Valve Division Inc and speaker for
the St Jude Medical Residency Symposium. Dr Hofmann is on the
Board of Directors of Endovention Inc, on the Scientific Advisory
Board for Bacchus Vascular Inc, is a speaker for Cook Inc, and has
received research grants from StemCells Inc and Siemens Medical
Inc, none of which are pertinent to this manuscript.
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CLINICAL PERSPECTIVE
Endoleaks after stent-graft repair of aortic dissections result in continued perfusion and pulsatility of the false lumen. The
pathophysiology of these endoleaks differs from that of endoleaks after repair of aneurysms, reflecting the numerous
natural fenestrations and re-entry tears typically present in a dissection outside of the stent-grafted zone. Using an
aggressive high-sensitivity imaging protocol, we found evidence of endoleak in 59% of treated patients, but almost half of
these resolved spontaneously. Of the remaining leaks, 27% led to delayed false lumen enlargement necessitating
reintervention. In patients with dissections complicated by malperfusion, stent-graft repair resulted in a high rate of clinical
resolution even in the presence of an endoleak. Thus, the definitions of technical and clinical success need to be amended
in this patient population. In contradistinction, persistent perfusion of the false lumen after stent-graft repair in 2 patients
with ruptured false lumen aneurysms from chronic dissections proved to be fatal. Occurrence of endoleaks was associated
with coverage of the left subclavian artery, small radius of aortic curvature, and poor device apposition to the aortic lesser
curve. High rates of endoleak should be expected when treating high-risk dissection patients, and long-term surveillance
is particularly crucial in patients with documented endoleaks.
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Factors Portending Endoleak Formation After Thoracic Aortic Stent-Graft Repair of
Complicated Aortic Dissection
Daniel Y. Sze, Maurice A.A.J. van den Bosch, Michael D. Dake, D. Craig Miller, Lawrence V.
Hofmann, Robin Varghese, S. Chris Malaisrie, Pieter J.A. van der Starre, Jarrett Rosenberg and
R. Scott Mitchell
Circ Cardiovasc Interv. 2009;2:105-112; originally published online February 20, 2009;
doi: 10.1161/CIRCINTERVENTIONS.108.819722
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