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192
ab
S. Kumar and A. Mukherjee
patent or partially thrombosed false lumen. An early
TEVAR/open surgical repair can be offered in these
group of patients.
5. Few patients with uncomplicated chronic TBAD
develop aneurysmal dilatation of false lumen.
Denitive management should be done if the false
lumen diameter exceeds 60mm.
18.3.2.4 Imaging Options
A. Transesophageal Echocardiography (TEE)
1. It is an excellent modality to visualize the majority of
the thoracic aorta with the exception of a small segment near innominate artery origin due to tracheal air
column.
2. There are a few limitations of this modality including
the need of conscious sedation, patient co-operation,
and possible risk of structural damage by probe.
There can be other limitations in terms of availability
and expertise in the emergency setting.
B. Transthoracic Echocardiography (TTE)
1. It is a freely available modality and can be used as a
rst-line investigation for patients presenting with
acute aortic syndrome.
2. The aortic root and proximal ascending aorta can be
examined; however, aortic arch of most of the
descending thoracic aorta cannot be adequately
assessed.
C. CT angiography (CTA)
1. CT remains the investigation of choice in many centers because of its advantages like operator independence and ability to assess the aortic pathology
comprehensively. CT images are required in most
of the cases to decide the management plan
depending on the type and extent of dissection
(Fig.18.4).
2. The major limitation of CT is radiation exposure and
is relatively contraindicated in acute kidney injury
(AKI) or chronic kidney disease (CKD).
D. MR Angiography (MRA)
1. MRA is an alternative to the CTA and can provide all
the information a CTA can. It has an advantage of
being radiation free, and non-contrast MRA can be
carried out safely in patients with AKI or CKD.
2. However, limited availability in the emergency setting and longer scan time remain the major limitations of this modality.
E. Catheter Angiography
1. Catheter angiography is rarely used for the diagnosis
of aortic pathologies being invasive in nature and
availability of other non-invasive modalities.
18.3.2.5 Indications forTreatment
1. Complicated TBAD (as mentioned above)
2. Uncomplicated TBAD with
Fig. 18.4 Sagittal reformat
CT (a) and 3D VRT (b)
images showing dissection
ap extending from distal to
LSCA up to aortic
bifurcation—Type B
dissection
cd
18 Interventions oftheAorta
193
ab
Fig. 18.5 Sagittal reformat (a) and axial CTA (b) showing Type B aortic dissection with peripheral thrombus and left pleural effusion. Sagittal
CTA (c) and 3D VRT (d) post aortic stent-graft showing patent and expanded true lumen and exclusion of false lumen of dissection ap
• Primary entry tear greater than 10mm
• Diameter of total aorta greater than or equal to 40mm
• False lumen (FL) diameter≥20mm
• Partially thrombosed or patent FL
18.3.2.6 Conventional Management Plan
1. Medical (Impulse) Therapy
• The objective of medical therapy is to delay or halt the
disease process. It reduces the abnormal shear stress
on the aortic wall.
• Best medical therapy remains the integral part of aortic
dissection management (complicated and uncomplicated) with β-blocker, angiotensin-converting enzyme
inhibitors (ACEIs), or calcium channel blockers (CCBs).
• Medical management aims to maintain the systolic
blood pressure (SBP) in the range of 100–120mmHg
and heart rate<60/min.
• Along with medical therapy, patients should be
encouraged for lifestyle medications to maintain blood
pressure.
• Statin therapy can be started in patients pre- operatively,
as few studies have suggested favorable outcomes in
terms of reduced post-operative mortality, cardiac, and
renal complications [7].
• Vasodilator should be avoided in the acute setting
because it can cause reux tachycardia with increased
stress on the aortic wall, resulting in the progression of
the disease.
2. Endovascular Management (Fig. 18.5)
• In endovascular management, the objective is to
cover the primary entry tear, thereby promoting the
expansion of true lumen expansion and causing
thrombosis of false lumen. It results in an increase in
true lumen perfusion of abdominal viscera as well as
lower limbs.
• Endovascular management options include thoracic
endovascular repair of aorta (TEVAR), fenestrated
endovascular repair of aorta (FEVAR), and TEVAR
chimney technique.
Table 18.1 Prerequisites for endovascular management
Proximal
landing zone
Distal
landing zone
At least 15mm of normal (disease free) aorta. In
case of unavailability of proximal landing zone,
debranching of arch vessels maybe required
In case of severe angulation of proximal or distal
aorta, longer landing zones maybe necessary
15–20mm normal aorta proximal to the celiac
artery
• In cases with inadequate proximal or distal landing
zone, a fenestrated device or chimney technique can
be used.
• The ideal time for TEVAR is after 2weeks of inciting
event as the TEVAR done in hyperacute phase is more
likely to result in retrograde TAAD in 3–4% of cases
[8, 9]. These can occur intra-procedurally or in immediate post-procedure period.
18.3.2.7 Prerequisites forEndovascular
Management (Table18.1)
18.4 Aortic Aneurysms
18.4.1 Overview
• An aneurysm, also known as a true aneurysm, refers to an
increase in the diameter of an artery, where the diameter
of the enlarged artery is at least 1.5 times the normal
expected diameter of the artery. A true aneurysm involves
all the layers of the arterial wall.
• In a pseudoaneurysm, there is injury to the arterial wall
with resultant extravasation of blood contained by periarterial connective tissue rather than arterial wall layers.
18.4.2 Classication
• Thoracic aneurysm: Involves the supradiaphragmatic
aorta, includes the ascending aorta/arch/DTA.
194
S. Kumar and A. Mukherjee
• Thoracoabdominal aneurysm (TAA): Involves both DTA
and abdominal aorta.
• Abdominal aortic aneurysm (AAA): Affects the aorta
below the diaphragm.
18.4.3 Indication forRepair ofDescending
Thoracic Aortic Aneurysm (Tables 18.2
and18.3)
• Intervention is recommended for aneurysms with a diameter of ≥55mm.
• This cut-off can be lowered to 50–55mm in connective
tissue disorders or women.
• However, there are no randomized trials present to choose
between surgical repair and TEVAR.
Open repair: Reserved for t patients unsuitable for
TEVAR due to the following reasons:
1. Inadequate access site for safe delivery of stent-graft sys-
tem, even for aortic/iliac conduit graft placement (e.g.,
severe aorto-iliac disease).
2. Inadequate landing zones for stent-graft, either proximal
or distal.
3. Aneurysms in patients with connective tissue disorders,
e.g., Marfan.
4. Symptoms related to compression of adjacent mediastinal
structures such as left bronchus (leading to dyspnea), vertebral bodies (causing chronic pain syndrome), or esophagus.
Endovascular Intervention (Figs.18.5 and 18.6)
1. Studies have shown patients treated by TEVAR have a
lower rate of mortality at 30 days compared to open
surgery.
2. TEVAR is also associated with a signicant reduction in
peri-operative mortality and lower major neurological
complications.
3. In case of ruptured DTA aneurysm, endovascular management is the treatment of choice provided the anatomy
is appropriate (Figs.18.7, 18.8, 18.9, and 18.10).
18.4.4 Thoraco-Abdominal Aortic Aneurysm
18.4.4.1 Classication
They are classied under the Crawford system which
depends on the level of involvement of the aorta:
Table 18.2 Summary of guidelines and management
SVS
Society
Anti-hypertensive with
β-blockers
Anti-hypertensives with
β-blockers and ACEI or ARBs
Statins in atherosclerotic aortic
aneurysms
Smoking cessation I
Table 18.3 Guidelines of invasive interventional management (descending thoracic artery aneurysms) - ESVS 2017, ESC 2014, AHA 2022
TEVAR when anatomy is suitable in complicated
DTA aneurysm (rather than surgery)
TEVAR with DTA aneurysm with
diameter≥55mm (rather than surgery)
TEVAR with DTA aneurysm with
diameter≥60mm (rather than surgery)
When TEVAR is not possible, surgery in DTA
aneurysm with diameter is≥55–59mm
When TEVAR is not possible, surgery in DTA
aneurysm with diameter is≥60mm
Intervention in case of Marfan or other
elastopathies, surgery should be done instead of
TEVAR
TEVAR Thoracic endovascular aortic repair, DTA Descending thoracic
aorta, ACEI Angiotensin-converting enzyme inhibitors, ARB
Angiotensin receptor blocker, SVS Society of Vascular Surgery, ESVS
European Society of Vascular Surgery, ESC European Society of cardiology, AHA American Heart Association
2018
ESVS
2017
ESC
AHA
2014
2022
IB
IIa
IIa
IIa CI
IIb BIIa CI
IIa
B
IIb
C
IIa CIIa
C
IIa
C
B
B
• Type I: Arises above the sixth intercostal space up to the
celiac and SMA.They do not extend into the infrarenal
aortic segment.
• Type II: Same as type I but extends into the infrarenal
abdominal aorta.
• Type III: Arises below the sixth intercostal space and
extends into the abdominal aorta.
• Type IV: Entire abdominal aorta from diaphragm up to
aortic bifurcation is involved.
• Type V: Arises below the sixth intercostal space, extend-
ing into the abdominal aorta; however, it is limited to the
involvement of visceral artery segment.
18.4.4.2 Indications ofRepair
Indications for repair of thoracoabdominal aortic aneurysms
(TAAA) include surgical repair for low-to-moderate surgical
risk patients with TAAA larger than 60mm (less for patients
with connective tissue disorders), rapid growth (>10mm/
year), or with symptoms.
The treatment guidelines of TAAA are summarized in
Table18.4.
18.4.4.3 Endovascular Repair Can
BePerformed via Two Approaches
• The rst approach is the hybrid approach, which involves
safeguarding visceral perfusion by means of surgical
ab
18 Interventions oftheAorta
Fig. 18.6 (a and b): Sagittal
reformat CT (a) and 3D VRT
images showing large Type B
aortic aneurysm with
peripheral thrombus
195
ab c
Fig. 18.7 Coronal MIP (a) and axial CTA (b) showing infrarenal abdominal aortic aneurysm with peripheral thrombus. 3D VRT image (c) post
endovascular stent-graft deployment showing exclusion of the aneurysm sac
bypass followed by exclusion of the aneurysm using a
stent-graft placed via an endovascular route. The advantage of this approach is that the patient does not have to
undergo a thoracotomy; however, it still carries consider-
preserve visceral ow by using branches or fenestrations
on the stent-graft body deployed. This approach is indicated for patients who are unt for open repair of TAAA,
in particular older patients.
able risk in unt patients. Hence, this technique is usually
restricted to patients, such as high-risk patients or in
emergency situations who have an unfavorable anatomy
18.4.5 Abdominal Aortic Aneurysm (AAA)
for a branched endovascular device.
• The other approach is a total endovascular repair using
specially designed branched aortic stent-grafts, which
It is characterized by the diameter of the abdominal aorta
exceeding 3.0cm in adults.
196
Fig. 18.8 (a and b): Sagittal
reformat CT (a) and 3D VRT
image (b) showing large type
B aortic aneurysm with
peripheral thrombus
S. Kumar and A. Mukherjee
DTAA
Fig. 18.9 Summary of
management for TAAA
Symptomatic
(Back pain, ruptured)
1. Favourable anatomy
for TEVAR and not a
k/c/o connective tissue
1.TEVAR
with BMT
disorder
YES NO
1.Open Repair
with BMT
TAAA
YES
Asymptomatic
1.Size->60mm
(Males),
>50-55mm
(females)
NO
1. BMT with
surveillance
Moderate
1. Open
Repair with
BMT
Symptomatic (Back
pain, ruptured)
1. Surgical
Risk
Low to
1. FEVAR/BEVAR 1. Hybrid Approach
High
1. Endovascular
YES
Asymptomatic
1. Size->6cm
Rapid growth
>1cm/yr
NO
1. BMT with
surveillance
18 Interventions oftheAorta
197
AAA
1.Symptomatic
2.(Abdominal / back pain or
3.Ruptured AAA)
1.Surgically fit,
2.Long life expectancy
YES NO
1.Open
Repair
1.EVAR
YES
1.Asymptomatic
1. > 4cm and interval
growth of >1cm/year
2. > 5.5 cm (M), > 5cm (F)
NO
BMT with Surveillance
25 - 25 - USG every 5 years
30–39 mm – USG every 3 years
ESVS 2024
40 - 49 mm - Annualy
>= 50 mm - Every 6 months
Fig. 18.10 Summary of management of AAA
Table 18.4 Summary of guidelines for TAAA
Society ESVS 2017 ESC 2014 AHA 2022
Anti-hypertensive with β-blockers
Anti-hypertensives with β-blockers and ACEI or ARBs
I B
IIa
Statins in atherosclerotic aortic aneurysms IIa
Smoking cessation I
Individuals who have thoracoabdominal aortic aneurysms caused by atherosclerosis or degeneration,
IIa C
and whose aneurysm has a diameter of 60mm or greater, exhibit fast aneurysm expansion of more
than 10mm per year, or experience symptoms associated with the aneurysm, and who have a low to
moderate risk of surgery, should undergo an assessment for either endovascular or open repair
Elective surgery is recommended for patients with thoracoabdominal aneurysms if endovascular
I C
stent-graft options are restricted and the surgical morbidity is high. Surgery should be considered if
the aortic diameter exceeds 6.0cm, or if there is a connective tissue disorder like Marfan or
Loeys-Dietz syndrome present, and the diameter is smaller
Patients with thoracoabdominal aneurysms and concurrent atherosclerotic visceral artery disease
I B
resulting in end-organ ischemia or signicant stenosis may require an additional revascularization
procedure
Consider endovascular procedures for repairing thoracoabdominal aneurysms in patients who are not
IIa C
suitable for open repair
Consider a hybrid approach for repairing thoracoabdominal aneurysms in patients who are unt for
IIa C
open repair and have aortic anatomy that is unsuitable for a branched or fenestrated endograft
198
S. Kumar and A. Mukherjee
The classication of AAA is based on the extent of its
involvement, which includes the following:
• Suprarenal AAA: This type involves the origins of one or
more visceral arteries but does not extend into the thorax.
• pararenal aaa: in this type, the renal artery (ra) arises from
the aneurysmal segment of aorta, but the aorta at the level
of the superior mesenteric artery (sma) is not
aneurysmal.
• Juxtarenal AAA: This type is located just beyond the origins of the RA and does not have a segment of nonaneurysmal aorta distal to the RA.However, the aorta at
the level of the RA is not aneurysmal.
• Infrarenal AAA: This type originates distal to the RA and
has a segment of non-aneurysmal aorta that extends distal
to the RA origin.
The classication of AAA based on the size of aneurysm
is given in Table18.5.
18.4.5.1 Abdominal Aortic Aneurysm: Natural
History
• The natural history of AAA is of progressive expansion.
• This is variable and depends upon aneurysm diameter.
• AAAs expand, on average, at a rate of 3mm to 4mm per
year, more in smokers.
• The risk of rupture based on the diameter of AAA is given
in Table18.6.
18.4.5.2 Indications forManagement (ESVS
2024)
• Men with an AAA diameter more than 55 mm; women
with an AAA more than 50 mm
• Growth of aneurysm ≥10mm/year
• In symptomatic AAA, but not ruptured—urgent repair is
indicated
Table 18.5 Classication of AAA based on the size of aneurysm
Aneurysm Size (diameter)
Small <40mm
Medium 40 and 55mm
Large >55mm
Very large
Table 18.6 Risk of rupture
Risk Diameter
<1% 3.0–3.9cm
Up to 1% 4.0–4.9cm
1–11% 5.0–5.9cm
10–22% 6.0–6.9cm
30–33% >7.0cm
≥60mm
However, the decision to intervene should also be individualized. AAA in women has a higher rupture risk at a
given size and thus repair maybe considered at lower threshold. Before deciding to intervene, an important consideration
is the patient’s life expectancy.
18.4.5.3 Endovascular Intervention
Endovascular repair of abdominal aortic aneurysms can be a
viable alternative to traditional surgical repair.
• In patients having complex aortic anatomy or in those
who have aneurysms located close to or involving the
renal vessels, endovascular repair may not be a suitable
option, and open repair is still the standard treatment.
• While endovascular repair can reduce operative mortality
by 66% in patients with appropriate anatomy, this benet
diminishes during follow-up and may come with an
increased need for re-intervention. Hence, endovascular
intervention is not favored by some in patients who have
a longer life expectancy, of more than 15years, ahead of
them.
• Open repair is still the reference standard management for
all other abdominal aortic aneurysms which are not favor-
able for endovascular repair.
Summary of recommendations in AAA is described in
Tables 18.7 and 18.8.
18.4.6 Intramural Hematoma andPenetrating
Atherosclerotic Ulcers
Intramural hematoma (IMH) and penetrating atherosclerotic
ulcers (PAU) are two types of acute aortic syndromes that
occur other than aortic dissection.
IMH is identied by non-enhancing crescentic or circular
thickening of the aortic wall, without the typical intimal ap
seen in aortic dissection. It is thought to occur due to rupture
of vasa-vasorum in the medial layer. PAU occurs when an
ulceration of an atherosclerotic plaque penetrates the intima
of the vessel into the media.
Table 18.7 Recommendations for medical management of AAA
Society
Anti-hypertensive with
β-blockers
Anti-hypertensives with
β-blockers and ACEI or ARBs
Statins in atherosclerotic aortic
aneurysms
Smoking cessation
NICE
2020
✓
✓
✓
✓
ESVS
2024
lb I B
lb IIb B IIa
lb I B I
ESC
AHA
2014
2022
IIb B IIa
18 Interventions oftheAorta
199
Table 18.8 Recommendations for endovascular management of AAA
NICE
ESVS
ESC
Society
Patients with abdominal aortic
aneurysm (AAA) with a maximum
diameter of less than 55mm and slow
growth, typically less than 10mm per
year, may be safely monitored through
surveillance
For patients who have a reasonable life
expectancy and a suitable anatomy,
endovascular repair should be
considered the preferred modality for
elective AAA repair
If a large aneurysm is not anatomically
suitable for EVAR, open surgical repair
is recommended
For patients with asymptomatic AAA
who are not suitable for open repair,
EVAR, along with the best available
medical treatment, may be considered
Consider repair in patients with
symptoms, asymptomatic patients (with
aneurysms larger than 40mm and
growth>1cm/yr), asymptomatic
(55mm or larger)—Surgical repair
unless contraindicated and EVAR if
surgery is contraindicated
Ruptured AAA—Open repair
(>70years) and EVAR (<70years)
EVAR Endovascular aortic aneurysm repair, AAA Abdominal aortic
aneurysm
2020
✓
✓
✓
2024
IIa BI A
2014
I C
I C
IIb
B
AHA
2022
18.4.6.1 Epidemiology
IMH is present in 6%–20% of acute aortic syndrome cases,
with higher incidences in Asian population [10], while the
exact incidence of PAU is unknown.
Although PAUs are usually seen in older patients with
multiple cardiovascular risk factors and diffuse atherosclerotic disease, patients with IMH are older having a higher
number of multiple cardiovascular risk factors. On the other
hand, in younger patients, PAUs can occur in connective tissue disorders. Among the acute aortic syndromes, 2.3% to
7.6% may have isolated PAUs [11].
18.4.6.2 Classication
Both IMH and PAU are classied similarly to aortic dissection, using the Stanford and DeBakey classications.
18.4.6.3 Pathophysiology
The pathophysiology of IMH involves long-standing hypertension, leading to smooth muscle hyperplasia and hypertrophy. This, in turn, causes occlusion and constriction of the
vasa vasorum. This causes an ischemic insult to the outer
media which become stiffened, while the inner medial layer
remains normal. Thus, there is a difference in elasticity
between the stiff outer media and normal inner media leading to increased shear stress at their interface, causing tear
and aortic dissection or IMH [12, 13]. IMH and aortic dissection are similar entities, but there are some differences,
such as the location and size of the intimomedial tear and the
presence of a reentry tear in aortic dissection.
18.4.7 PAU
The rst step toward PAU is the development of atheromatous ulcers in advanced atherosclerotic plaque. In this
stage, however, the lesion is silent and restricted to the
intimal layer. Progressively, the ulcer becomes deeper,
with penetration of the deep ulcer into the media of the
vessel wall. There is hematoma formation within the
media which may extend, resulting in the appearance of a
thrombosed aortic dissection. In severe cases, the hematoma may cause stretching of the aortic wall and forming
an aortic aneurysm. This aneurysm may eventually rupture. Spontaneous, although rare, may occur due to perforation through the plaque.
18.4.7.1 Imaging
• TTE or echocardiography has a lower sensitivity for
detecting IMH compared to aortic dissection (AD), with a
sensitivity of less than 40% for IMH.Pericardial effusion
may be seen in up to 60% of patients with Type A IMH
and is associated with worse prognosis. TTE can also
evaluate aortic valve and aortic regurgitation, with 35% of
patients with Type A IMH having some grade of aortic
regurgitation. PAUs may be demonstrated on transesophageal echocardiography as localized ulcer craters protruding from the aortic lumen into the aortic wall.
• CT imaging can show IMH as a crescentic or circular
aortic wall hyperdensity (better seen in an NCCT acquisition) and may also show displacement of calcications of
the intima. CT angiography may demonstrate the diameter of the aortic lumen (Figs. 18.11 and 18.12). PAUs
appear as a contrast-lled outpouching from the lumen of
the aortic into the aortic wall, with adjacent IMH often
noted. CTA can delineate the extent of the PAU, ulcer
dimensions, associated IMH, and presence of dissection
if any (Fig.18.13).
18.4.7.2 Prognosis
Prognostic factors on imaging include Stanford classication, with Type A IMH resulting in increased risk for pericardial effusion, pleural effusion, dissection, aneurysm, and
death compared to Type B IMH.
Maximum aortic diameter (more than 48–55mm in Type
A, more than 40–41 mm in Type B) and maximum IMH
thickness (more than 11mm) are also independent risk factors for adverse outcomes.
200
ab
ab
Fig. 18.11 (a and b): Axial
NCCT (a) showing the
crescentic hyperdense IMH in
ascending aorta. Axial CTA
(b) showing the crescentic
area in ascending aorta; it
measured 65 HU
Fig. 18.12 (a and b): Type B
IMH
S. Kumar and A. Mukherjee
Focal contrast enhancement within IMH, such as ulcerlike projections (ULP), may also be associated with a poor
prognosis.
Intramural blood pool without visible connection with the
lumen or with a small connection (<2mm) is more likely to
occur in the descending aorta and may be associated with
incomplete resorption of hematoma.
Finally, pleural and pericardial effusions have a positive
coils or vascular plugs may also be needed if there is an
enlarging or large blood pool intramurally.
• In cases of Type A IMH, a recent study involving 101
patients who were initially treated non-surgically found
no difference in mortality in comparison to patients who
received immediate surgical treatment. Emergent surgery
was required in 16% of IMH patients, and 29% ultimately
needed surgery [14].
correlation with adverse outcomes.
18.4.7.3 Management
• For patients with Type B intramural hematoma (IMH),
the rst-line management involves non-surgical treatment
to decrease stress on the aortic wall using β-blockers.
Surveillance imaging using CT or MR is recommended
before discharge and at regular intervals afterward, such
as 1month, 3months, 6months, and 12months after the
acute event, and annually thereafter if the patient’s condition is stable. However, endovascular or surgical management may be necessary if there are complications such as
aortic diameter enlargement, development of ULP, or progression of hematoma. Endovascular embolization using
18.4.8 PAU
1. Due to the controversies surrounding the natural history
of PAU, there are differing opinions on whether surgical
or endovascular management is warranted. However,
most experts recommend surgical treatment with graft of
the affected region [15]. Unfortunately, many patients
with PAU are not suitable candidates for surgery due to
their comorbidities and overall physical condition, and
conventional surgery has been associated with mortality
rates as high as 15.9% [16].
2. PAU is often a localized lesion in the aorta and therefore
lends itself well to endovascular stent-graft treatment.
18 Interventions oftheAorta
201
Fig. 18.13 Axial and oblique
CTA images (a and b)
showing PAU in the arch of
the aorta. Axial CTA images
of another patient (c and d)
showing PAU in DTA and
abdominal aorta (arrow)
ab
cd
Early mortality rates for TEVAR (thoracic endovascular
aortic repair) are lower, estimated to be around 7.2%.
However, careful planning is necessary as the presence
of associated IMH increases the risk of failure, rupture,
or death.
3. Stent-grafts are recommended for high-risk PAU cases
with features such as symptomatic patients or asymptomatic patients with increased pleural effusions, the presence of IMH, PAU depth greater than 10mm and diameter
greater than 20mm, or a high growth rate [16].
18.5 Procedure forAortic Stent-Graft
(Fig.18.14)
Procedures for stent-graft deployment are specic to each
device, and manufacturer’s instruction for use must be read
in detail before using the device. The general outline for
device deployment is as follows:
18.5.1 Access Site
The preferred route of access is the common femoral artery;
however, other vessels such as the external iliac artery, common iliac artery, or distal abdominal aorta may also be used
via a conduit. The vessel may be accessed via percutaneous
puncture of surgical exposure and arteriotomy.
18.5.2 Procedure
• The intervention is usually done under general anesthesia.
Elective intubation provides for better respiratory control
during device placement.
• The patient is positioned supine on the table, and the
access sites (typically bilateral groin) are prepared and
sterile drapes are placed over the patient.
• The common femoral artery contralateral to the vessel
chosen for stent-graft delivery may be accessed for periprocedural angiography purposes. A brachial artery may
also be used for this purpose.
• After sheath placement, a marker pigtail is advanced into
the proximal arch of the aorta.