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Z1
V. M. Rodriguez et al.
a
Z2
Z0
Z3
Z4
Fig. 12.11 Ischimura’s classication of zones of the aortic arch. This
classication system is widely used to determine the preferred option of
hybrid endovascular aortic arch aneurysm repair. (Courtesy of Lena
P.Abraham)
Hybrid procedures thus avoid the need for cardiopulmonary bypass or hypothermic circulatory arrest. Modications
in existing technology and new-generation devices, such as
the Conformable TAG thoracic device (C-TAG, Gore &
Associates), Valiant thoracic stent graft (Medtronic), Relay
thoracic device (Bolton Medical), and Zenith Alpha thoracic
endovascular graft (Cook Medical), have resulted in more
reliable trackability and precise deployment at the distal
margin of the innominate, left common carotid, and left subclavian arteries (LSA), or in the ascending aorta.
The arm’s rich collateral blood supply obviates the need
for mandatory revascularization, especially in an emergency setting, but restoring direct arterial ow to the subclavian artery can be important in stroke prevention as well
as in the prevention of paraplegia, depending on the extent
of coverage of the thoracic aorta. The decision to revascularize the left subclavian with left carotid–subclavian artery
bypass has been a subject of much debate in the literature
[20]. As mentioned, often the decision is based on the
amount of thoracic aortic coverage required or the presence
of a dominant or solitary left vertebral artery, or the presence of a functioning left internal mammary artery coronary artery bypass graft, all of which necessitate left
subclavian revascularization. Clinical trials are currently
underway examining the safety and feasibility of the Gore
TAG Thoracic Branch Endoprosthesis (TBE device), as
well as the Valiant Mona LSA Thoracic Stent Graft System,
both of which feature endovascular revascularization as
part of their thoracic stent graft via branches attached to
their stent graft platform (Fig.12.12). If surgical left carotid
b
Fig. 12.12 (a) GORE® TAG® Thoracic Branch Endoprosthesis.
(Reprinted with permission from W.L. Gore and Associates). (b)
Medtronic Valiant Mona LSA Thoracic Stent Graft System. (Reprinted
with permission from Medtronic)
12 Aortic Arch Aneurysms
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185
subclavian bypass is performed, either proximal surgical
ligation of the left subclavian artery or endovascular proximal occlusion of this artery is generally required to prevent
retrograde endoleak.
Chimney or snorkel grafts (Fig.12.13) have been proposed to extend the proximal xation zone in the aortic
arch during TEVAR repairs [21]. They have the advantage
of using standard, off-the-shelf materials and being technically less demanding, but their durability and ability to
effect exclusion of an arch aneurysm in the aortic arch
remains questionable, despite reported early success [22,
23]. Thoracic stent graft technology is not being devel-
oped with chimney and snorkel grafts in mind, and consequently, there are presently no ideal stent grafts for this
application. Until longer and more rigorous follow-up are
available, chimney grafts should only be considered in
emergency patients who are poor candidates for open
repair or in cases of inadvertent coverage of the supraaortic trunks.
Near-Total Arch Branched Endovascular Grafts
Near-total branched arch stent grafting offers several advantages over other approaches including avoiding the need for
sternotomy, eliminating exposure to cardiopulmonary
bypass, and circulatory arrest, and minimizing the extent of
extra-anatomic bypass of supra-aortic vessels [24]. Several
iterations of graft designs exist with the latest generation
grafts being exible enough to accommodate most arch anatomy. Branched arch endografts from Cook Medical and
Bolton are available outside the United States under special
access (Fig.
12.14).
The author (C.A.) has one of the largest experiences (15
cases) using the Cook Medical Arch Branched Graft in North
America. Over 200 cases have been performed worldwide,
and the global experience has provided valuable insight into
improving stroke and mortality rates [25]. Supra-aortic
branch target vessels must be of suitable diameter. The
innominate artery should have a minimum diameter of 8mm,
while the left common carotid artery should have a minimum
diameter of 6 mm. A custom-made branch extension limb
provided by Cook Medical is usually required for the innominate artery in order to accommodate the larger diameter of
the distal innominate artery. Commercially available covered
stents are suitable for most carotid or subclavian arteries.
Because of its accuracy and versatility, our preference is for
the Atrium/ICast covered stent graft; although Bard
Fluency™ and Gore Viabahn™ covered self-expanding
stents are also used worldwide. The balloon expandable covered stents require lining with a bare metal self-expanding
stent to add support and mitigate against tortuosity or possible kinking.
Conduct of the procedure has been described elsewhere
24]. Salient points include the need for a stiff wire buried in
[
the left ventricle, deployment during asystole, achieved with
either rapid ventricular pacing or right atrial venous balloon
occlusion, and attention to the relationship of the endograft
Fig. 12.13 (a) Snorkel Zone 1 Arch thoracic
endovascular repair. (b) Snorkel Zone 0 Arch
thoracic endovascular repair. (Courtesy of Lena
P.Abraham)
ab
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V. M. Rodriguez et al.
a
b
c
Fig. 12.14 (a) Bolton Relay Branch Thoracic Stent-Graft System. (Reprinted with permission from Bolton Medical). (b, c) Cook Arch Branched
Graft ™. (Reprinted with permission from Cook Medical)
and its branches to the coronary arteries and supra-aortic
vessels (Fig.12.15).
The largest published series of arch branch endografting
was a global experience that included 38 patients with
median follow-up of 12months [25]. The 30-day mortality
of the entire cohort was 13.2%. Comparative analysis of the
early experience (rst 10 patients) and late experience
demonstrated an interesting but not statistically signicant
difference in 30-day mortality (30% vs. 7.1%, p=0.06). No
late mortality was observed during the follow-up period.
Cause of death included perioperative cardiac arrest, myocardial infarction, hemorrhagic shock, and pulmonary complications. Early procedural success was 84.2%. Failures
included proximal type 1 endoleak, failure to catheterize
the innominate branch, and conversion to chimney technique. On discharge, 28.8% of patients were diagnosed
with an endoleak (5 Type I, 3 Type II, Type III, and 2 indeterminate), with 10.5% of patients requiring a secondary
procedure. Neurological complications occurred in 16% of
patients who survived the procedure. This compares to
4–12% neurological event rates seen in larger series of traditional open and hybrid repairs [26–28]. All patients in the
branched arch endograft series had a full neurologic recovery (4 transient ischemic attacks, 1 stroke, 1 subarachnoid
hemorrhage). In comparative analysis of the early experience (rst 10 patients) compared to the late experience,
12 Aortic Arch Aneurysms
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Fig. 12.15 Angiogram aortic arch demonstrating relationship of branch
markings (yellow and red arrows), to origins of supra-aortic vessels
(open white arrows), and proximal arch branch graft stent to origins of
coronary arteries (solid white and black arrows). Note double curved
lunderquist wire buried in left ventricle
there were signicantly fewer intraoperative complications,
less need for secondary procedures, less need for interventions for endoleaks, less operative time, and less radiation
exposure. This highlights the importance of the learning
curve involved with this complex procedure as well as the
importance of conning these procedures to high volume
regional centers.
Although a viable alternative to traditional open and
hybrid repair, near-total endovascular arch stent grafting is
still in its early development. The complexity of arch geometry and its branches poses unique challenges for endovascular devices and necessitates an individualized approach.
These complex endovascular procedures should be reserved
for patients who are not able to tolerate open or hybrid procedures for anatomic reasons, or in patients who have signicant comorbidities precluding open surgery. Stroke remains
an important risk in these procedures. Despite satisfactory
early results, mid- to long-term studies are needed before we
can recommend this treatment as a comparable alternative to
standard open arch reconstruction or hybrid arch repair.
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Thoracoabdominal Aneurysms
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AshokVenkataraman andJereyP.Schwartz
13
Introduction
Thoracic aortic disease is a complex process and a result of
several histopathologic processes. Although abdominal aortic aneurysms (AAAs) and ascending aortic aneurysms are
more common, descending thoracic aortic aneurysms
(TAAs) and thoracoabdominal (TAAAs) aneurysms are not
rare. The incidence has been steadily increasing and a recent
study suggests an estimated incidence approaching 10.4
cases per 100,000 person-years [1]. TAA repair is associated
with high morbidity and mortality. The focus of this chapter
is on TAAAs dened by anatomy, arising from the left subclavian artery to the aortic bifurcation.
The earliest report of successful repairs of a thoracoabdominal aneurysm in the United States was in 1955 by
Etheredge [2]. Cooley and DeBakey, known pioneers within
this eld, also reported total repairs via a thoracoabdominal
incision utilizing a homograft conduit initially, subsequently
involving knitted Dacron grafts as conduits [3]. Crawford is
attributed with pioneering the evolution of techniques to
include pedicled visceral segment anastomoses of celiac,
superior mesenteric, and renal vessels [4]. Over the years,
techniques performed at major centers today have evolved to
utilize cardiopulmonary bypass, hypothermic circulatory
arrest, and cerebrospinal uid drainage amongst other novel
modications.
A. Venkataraman
Department of Cardiovascular & Thoracic Surgery,
Loyola University Medical Center, Maywood, IL, USA
J. P. Schwartz (
Lung Transplant Program & Aortic Center, Department
of Cardiovascular & Thoracic Surgery, Loyola University
Medical Center, Maywood, IL, USA
*)
Denition
Thoracoabdominal aneurysms (TAAA) result from the
continuous dilation of the descending thoracic and abdominal aorta secondary to weakening and expansion of the
aortic wall. By denition, the dilatation is 1.5 times its
normal value [5]. TAAAs account for approximately 10%
when all aneurysms of the thoracic aorta are considered
[6]. Dening anatomic sizes is critical to help identify
pathologic aortic growth because aortic diameter is the
strongest predictor of rupture. The “hinge points” at which
likelihood of rupture or dissection increases precipitously
are seen at 5.5 cm for ascending and 6.5 cm for the
descending aorta [7]. The challenge is weighing the risks
of surgery versus that of continued surveillance and possible rupture or dissection.
With respect to TAAAs, multiple congurations occur
anywhere from the origin of the left subclavian artery to the
aortoiliac bifurcation. Crawford described the rst classication scheme based on the anatomic extent of the aneurysm in 1986 [8]. Type I (25%) involves most of the
descending thoracic aorta from the origin of the left subclavian to the suprarenal abdominal aorta. Type II (approximately 30% of all TAAAs) is the most extensive, extending
from the subclavian to the aortoiliac bifurcation. Type III
(<25%) involves the distal thoracic aorta to the aortoiliac
bifurcation. Type IV TAAAs (<25%) are limited to the
abdominal aorta below the diaphragm, including visceral
and renal arteries. A Type V classication was added later
referring to distal thoracic aorta extension including the
celiac and superior mesenteric origins but excluding the
renal arteries [9] (Fig.13.1).
Indications for operative repair can range from elective
interventions when aneurysmal size approaches a critical
point to urgent or emergent surgical intervention for acute
dissection, free rupture or associated complications such as
visceral and extremity malperfusion.
© Springer Nature Switzerland AG 2019
R. S. Dieter et al. (eds.), Diseases of the Aorta, https://doi.org/10.1007/978-3-030-11322-3_13
189
190
II
III IV V
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A. Venkataraman and J. P. Schwartz
Normal
I
th
6
th
6
Fig. 13.1 Clark classication for thoracoabdominal aneurysm
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191
Epidemiology
Population studies have indicated an incidence of thoracic
aortic aneurysms in the range of approximately 10 new aneurysms per 100,000 person-years [1]. Up to 80% of these will
eventually rupture, owing to a 10–20% 5-year survival of
patients who remain untreated. The increasing prevalence of
TAAAs has been attributed to several factors including an
aging population, improved and more readily accessible
imaging techniques, and increased patient and physician
awareness [10]. Females tend to develop TAAAs later in life
than men but are at a higher risk of rupture, and advanced
age confers a higher risk in both sexes [11].
Pathogenesis
Development of TAAA is multifactorial, similar to that of
other aneurysms, a complicated dynamic process involving
both cellular and extracellular processes. Evidence suggests
that extracellular matrix degradation by matric metalloproteinases (MMPs) exceeds matrix production and repair during aneurysm formation [12]. The capacitance and elasticity
of the aortic wall is largely from its medial layer composed
mainly of structural proteins such as collagen and elastin.
Degradation of these proteins leads to medial degeneration
and eventual weakening of the aortic wall [13]. Hemodynamic
forces on the aortic wall, intrinsic changes in the composition of the wall and increasing stiffness and loss of elasticity
lead to subsequent dilatation. A vicious cycle is created as
the diameter of the aorta increases as the wall tension
increases as dened by the law of Laplace, wherein the wall
tension is proportional to the pressure applied by the radius
of the conduit.
Medial degeneration, part of the normal aging process, is
worsened by clinical conditions such as atherosclerosis and
hypertension [14]. Genetic abnormalities such as Marfan’s
syndrome and other connective tissue disorders such as
Ehlers–Danlos and Loeys–Dietz syndromes also contribute
to medial degeneration [15]. Turner syndrome, polycystic
kidney disease, syphilis, arteritis, and traumatic injury are
amongst other disorders that are associated with aortic aneurysms in similar fashion [16]. Whilst 80% of TAAAs are secondary to medial degeneration, approximately 15–20% are
caused by dissection [17].
It is postulated that atherosclerosis plays a role in aneurysm formation, particularly in the descending thoracic and
abdominal aorta. True causality is unclear but the two conditions occur simultaneously in a majority of patients. Risk
factors for TAAAs are thus similar to those for atherosclerosis. These include primarily smoking, hypertension, obesity,
hyperlipidemia, chronic obstructive pulmonary disease
(COPD), and family history. Interestingly, patients with
TAAAs have a much lower incidence of coronary artery disease (CAD) (less than 30%) than those patients with abdominal aortic aneurysms (greater than 70%) [18].
Indications forRepair
The decision when to operate on a patient with a TAAA
essentially involves an assessment of the likelihood of aortic
rupture versus the operative risk of the individual patient.
Endovascular techniques with its lower short-term mortality
and morbidity continue to evolve and will in future be an
important factor in the decision making for intervention. The
patient’s physiologic reserve and vascular anatomy determine whether open or an endovascular approach would be
more suitable. Recent guidelines have been issued tailored to
the when and how to repair with descending thoracic and
thoracoabdominal aneurysms [19].
Natural history studies have documented an extremely
high risk of rupture and death if TAAAs are left untreated
and therefore all TAAAs should be considered for repair
[20]. Symptomatic aneurysms regardless of size or anatomic
extent should be addressed surgically. Symptoms usually
present as pain and pressure that may be often described as
chest pain radiating to the back or as intrascapular, with a
“stabbing” or “tearing” quality. However, few patients present with symptoms prior to an acute event [21].
Size criteria have been extensively debated in the literature, with groups advocating repair anywhere between 5 and
10 cm [22]. This is further complicated by the fact that
degenerative TAAAs are not uniform in size and involve
segments of the aorta with varying diameters and morphology. Recent literature points toward the need for adjustment
of body surface area and an evaluation of relative aortic size
rather than absolute aortic size, to be incorporated into decision making about threshold for repair and the risk of rupture [23].
Elefteriades etal. have reported extensively on the natural
history and rupture risk of thoracic aorta stratied by diameter and the guidelines outlined have remained the current
benchmark used for intervention [24].
I. Rupture
II. Acute dissection resulting in malperfusion or other life-
altering complications
III. Symptomatic states
(a) Pain consistent with rupture and unexplained by
other causes
(b) Compression of adjacent organs
IV. Documented enlargement ≥1 cm/year or substantial
growth approaching absolute size criteria
V. Absolute size >6.5cm or >6.0cm in patients with con-
nective tissue disorders
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A. Venkataraman and J. P. Schwartz
All size criteria per guidelines are based on the premise
that the ideal time to intervention is when the annual risk of
rupture exceeds the perceived mortality of the proposed
procedure.
Preoperative Workup
The physiologic stress on a patient undergoing open TAAA
repair is unparalleled and as such extensive preoperative
workup to ensure optimal tness for surgery is mandatory.
Pulmonary and renal function evaluation, in addition to cardiovascular risk evaluation is imperative.
Cardiac
The typical patient undergoing TAAA is elderly and the incidence of impaired myocardial function and the presence of
atherosclerotic coronary disease are moderate, thereby making cardiac disease the leading cause of mortality after open
TAAA repair [25]. Therefore, preoperative electrocardiogram, echocardiogram, and coronary angiography are routine. In the elective setting, coronary artery revascularization
either by coronary angioplasty and stenting or by coronary
artery bypass grafting may be indicated prior to intervention
for the TAAA.The use of bare metal stents versus drug eluting stents should be considered particularly in view of the
duration of dual antiplatelet therapy required.
outcome after operative repair [27]. Endovascular repairs
require even closer attention to preoperative renal function
given the use of nephrotoxic contrast agents during these
procedures.
Cerebral
Intracranial aneurysms are thought to share pathophysiologic
features with TAAA and clinical association between these
two conditions has been well established in recent years.
Patients with TAA have a 9% prevalence of intracranial
aneurysms, which is ninefold greater than the general population [28]. In light of this association, notable groups have
made it a policy within their practices to image the brain of
all patients prior to surgery on the thoracic aorta and obtain
neurosurgical consultations should a cerebral aneurysm be
identied [29].
Functional Status
Considering the surgical insult involved in open repair of
TAAA, preoperative functional status of the patient is a key
predictor of perioperative mortality [30]. Interestingly,
advanced age alone does not impair return to normal functional status postoperatively and thus patients with asymptomatic thoracic aneurysms should not be denied elective
replacement on the basis of age alone [31].
Pulmonary
Pulmonary complications after open TAAA are common,
and the incidence of COPD is high in this patient population
(estimated between 30% and 40%) and it is associated with
increased perioperative mortality [25]. Also, single lung
ventilation is routinely utilized in open TAAA repair. As
such, preoperative spirometry and arterial blood gas analysis is strongly recommended and performed routinely.
Smoking cessation in the weeks preceding surgery, pulmonary rehabilitation to improve lung capacity, and an attempt
to lose weight in obese patients has all been shown to be
benecial.
Renal
Chronic renal failure is the strongest predictor of perioperative renal failure and mortality after TAAA repair (increasing
risk threefold), second only to aortic rupture [26]. Routinely
assessed by laboratory tests such as blood urea nitrogen and
creatinine concentrations, recent evidence indicates calculation of glomerular ltration rate is superior as a predictor of
Anesthesia/Intraoperative Monitoring
Following induction of general anesthesia, a double lumen
endotracheal tube is inserted. Central access is then obtained
and a pulmonary artery catheter placed for hemodynamic
monitoring. A Foley catheter is placed and arterial lines are
placed in both upper and lower extremities (typically right
radial and right femoral) to monitor both proximal and distal
perfusion during aortic clamping.
Lumbar cerebrospinal uid drains are routinely used for
extensive I and II repairs, maintaining an intrathecal pressure
of less than 10mmHg (Fig.13.2). This has been shown to
appreciably lower the probability of neurological decit [9].
In the case of a bloody insertion during the initial setting,
consideration should be given for delaying surgery and
admission of patient a day prior to elective surgery and
placement of lumbar drain to reduce the risk of subsequent
intraoperative bleeding. In the majority of cases, and particularly in Type II repairs or those requiring hypothermic
circulatory arrest, electrodes are placed cranially and peripherally for monitoring of somatosensory and motor evoked
potentials to assess intraoperative spinal cord protection and
perfusion [32].
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Fig. 13.3 Right lateral decubitus position, posterior view
Fig. 13.2 Spinal drain inserted preoperatively
Surgical Approach
Exposure oftheThoracoabdominal Aorta
Regardless of the extent of the TAAA repair, the patient is
routinely placed in the right lateral decubitus position with the
operating room table exed at the waist (Figs.13.3 and 13.4).
A beanbag is utilized to maintain appropriate position is necessary; the left arm is secured over the patient using an appro-
extended arms). The hips and shoulders are taped down after
all bony prominences are appropriately padded. The shoulders
are typically rotated posteriorly 10–20° and the hips are rotated
50–60° posteriorly (attened) with a folded sheet placed
underneath the buttocks and a rolled sheet used as a shoulder
roll. The right femoral arterial line is prepped into the eld.
The procedure is started with exposure of the left femoral
vessels after an appropriate groin incision. Access to the
descending thoracic aorta and distal arch is gained by a thoracoabdominal incision (Fig.13.5). The scapular tip is identied and marked and its location is relevant the higher the
extent of the pathology is on the thoracic aorta. For exposure of the proximal descending aorta, the incision is started
two ngerbreadths beneath the tip of the scapula, curved
posteriorly—midway between the scapular edge and the
spine. The lower extent of the incision is usually midway
between the anterior superior iliac spine (ASIS) and umbilicus.
Fig. 13.4 Right lateral decubitus position, anterior view
Fig. 13.5 Thoracoabdominal incision, transection of diaphragm dem-
onstrated, followed by medial visceral rotation
The curve of the incision is along the ribs and eventually
almost parallel in a long axis direction anatomically to the
right of scapular tip. The level of the rib entry into the thoracic cavity is based on the proximal extent of the intended
repair. Typically, the fourth or fth interspace is appropriate
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