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23 Endovascular Management ofAcute Limb Ischemia
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Fig. 23.4 Patient admitted with a Rutherford IIb acute limb ischemia
due to thromboembolic complication of a popliteal artery aneurysm
(PAA). (a) Pre-procedural angiographic view of a near-complete thrombosis of PAA, arrows indicate the lumen thrombosis. (b) Pre-procedural
angiographic view of BTK vessels with thrombosis of proximal posterior tibial artery and chronic occlusion of the anterior tibial artery. (c)
Pre-procedural angiographic view of the complete thrombosis of distal
Decision Making Algorithm in Acute Limb
Ischemia
According to the most recent European Society for Vascular
Surgery (ESVS) Clinical Practice Guidelines on the
Management of Acute Limb Ischemia [65]. ALI is a medical
emergency, and it is essential that the diagnosis is established
promptly, and appropriate treatment is started in order to prevent limb loss and other severe complication.
posterior tibial artery. (d) Intraprocedural image of Indigo/Penumbra
thromboaspiration catheter CAT 6 in distal posterior tibial artery.
*Indicates the tip of the CAT 6 catheter. (e) Intraprocedural image of
Indigo/Penumbra thromboaspiration catheter CAT 3 in plantar artery.
**Indicates the tip of the catheter. (f) Post-thromboaspiration angiographic view of posterior tibial artery and plantar arch
The decision-making algorithm starts from a correct clinical assessment, that should be performed urgently by a vascular specialist, who should be responsible for planning
further investigation and management (Recommendation I
C). Diagnostic imaging is recommended to guide treatment,
provided it does not delay treatment, or if the need for primary amputation is obvious (Recommendation I C).
For patients with acute limb ischemia awaiting revascularization, heparin and supplemental oxygen is recom-
234
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G. de Donato and E. Pasqui
mended (Recommendation I C). Moreover, prostacyclin
analogues may be considered during and after revascularization (Recommendation IIb B).
Then, the guidelines remark the importance that patients
diagnosed with ALI in a non-vascular center should be transferred to a vascular center that offers the full range of open
and endovascular interventions (Recommendation I B). In
particular, all patients should have access to treatment in a
hybrid theatre, or operating theatre with C arm equipment,
and by a clinical team able to offer a full range of open or
endovascular interventions during a single procedure
(Recommendation I C).
The guidelines focus on the importance of a completion
angiography for patients undergoing open (Recommendation
I C), and of considering to remove residual thrombus after
open surgery with intra-operative local thrombolysis
(Recommendation IIb B).
The selection of the best rst-line treatment (open, lysis or
endovascular technique) is based on several factors including
patient condition and operator’s preference. However, some
recommendations are clearly stated regarding brinolysis
appropriateness and limits based on clinical presentation:
– For patients with acute onset claudication (Rutherford
grade I) that does not threaten the limb, (percutaneous)
catheter directed thrombolysis is not recommended
(Recommendation III B).
– For patients with Rutherford grade IIa acute limb isch-
emia, it is recommended that (percutaneous) catheter-
directed thrombolysis is considered as an alternative to
surgery (Recommendation I A).
– For patients with Rutherford grade IIb acute limb isch-
emia, (percutaneous) catheter-directed thrombolysis may
be considered if initiated promptly and may be combined
with percutaneous aspiration or thrombectomy
(Recommendation IIb B).
A correct decision-making algorithm for ALI is based on
combining surgery and endovascular options.
After open revascularization for acute limb ischemia, simultaneous endovascular treatment addressing inow or outow
stenosis should be considered (Recommendation IIa C).
Notably, the ESVS guidelines clearly state that for all
patients with acute limb ischemia, aspiration and mechanical
thrombectomy should be considered (Recommendation IIa C).
To sum up the main points from the ESVS guideline: (1)
both surgical and endovascular treatments are effective but
with slightly distinctive outcomes depending on individual
patients; (2) now there are a variety of clot busting drugs and
new methods of aspirating blood clots percutaneously, without needing an operation; (3) the best outcome is achieved in
hospitals used to dealing with patients with ALI, and familiar
with all surgical and endovascular methods available, choosing the method most suitable for each individual patient.
Conclusion
Suggestive modications in the treatment of ALLI have been
proposed in recent years. While surgery represents still a signicant treatment option especially for ALLI due to embolism, endovascular techniques are acquiring a more
prominent role in case of acute on chronic ischemia.
Various mechanical endovascular systems for thrombus
removal have been investigated over the last 15 years.
Most of them have partially failed to be effectively successful or have been associated with undesirable complication rates. Newly endovascular thrombectomy devices
specically designed for peripheral intervention in this
difcult set of patients, may offer improved clinical outcomes with lower rates of major systemic and local complications. As a result, a shift of treatment recommendation
towards endovascular options may be observed in the near
future.
Case Presentation
Continued from page 225
Previous systemic heparinization (100 IU/kg), the total
endovascular rescue was performed. The pre-procedural
angiographic view conrmed a near-complete thrombosis of
the popliteal artery aneurysm and thrombosis of the proximal posterior tibial artery and chronic occlusion of the anterior tibial artery. Moreover, the anatomical setting was
characterized also by the complete thrombosis of the distal
posterior tibial artery. The revascularization procedure was
performed with Indigo/Penumbra thromboaspiration catheter CAT 6 in the distal posterior tibial artery and Indigo/
Penumbra thromboaspiration catheter CAT 3 advanced in the
plantar artery. After the thromboaspiration session and the
infusion of a bolus of the thrombolytic agent in the plantar
arch posterior tibial artery and plantar arch were assured. At
the end of the procedure, the popliteal artery aneurysm was
excluded with the implantation of a self-expanding covered
stent (Fig. 23.4).
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Part III
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Cerebrovascular Disease
Angioplasty andStenting oftheArch
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Branches
SaidAbisi, MohamedHosnySayed,
andMohamed.RagabElnemr
24
Case Presentation
A 54-year-old male patient presented with a 6.7cm aneurysm of the distal aortic arch with extensive residual type B
dissection with big infra renal fenestration. The patient
underwent aortic root, ascending aorta, and aortic valve
replacement due to type-A aortic dissection in 2014, which
was complicated by bowel ischemia for which he had right
hemicolectomy and stoma creation with residual incisional
hernia and almost complete loss of anterior abdominal wall
musculature.
After an interdisciplinary consensus, the patient was
deemed at high risk for another open surgical treatment.
Thus, totally percutaneous aortic arch repair with threeinner- branch endografts and candy plug deployment to
occlude the remaining false lumen was planned. The main
challenge in this case would be to pass the mechanical prosthesis with the wire and the tip of the sheath dilator without
damaging the leaet and without causing severe regurgitation. Our goal was to pass one leaet through the lateral side,
which would allow the second leaet to continue working,
and as such only mild valve regurgitation during the deployment of the graft should be noticed. Valve functionality
should then be reverted to normal after retrieval of the device.
It was imperative to avoid cannulation at the center of the
prosthesis between the two leaets as this may lead to
destruction of the leaets. Transesophageal echo (TOE) was
planned to conrm the location of the wire in addition to
S. Abisi (*)
Guy’s and St Thomas’ NHS Foundation Trust, London, UK
e-mail: said.abisi@gstt.nhs.uk
M. H. Sayed (*)
Guy’s and St Thomas’ NHS Foundation Trust, London, UK
Cairo University Hospitals, Cairo, Egypt
e-mail: Mohamed.Sayed@gstt.nhs.uk
M. R. Elnemr
Guy’s and St Thomas’ NHS Foundation Trust, London, UK
Cairo National Institute of Diabetes and Endocrinology,
Cairo, Egypt
multiple uoroscopic projections. The patient was informed
about the potential risk of damaging the valve in addition to
other standard risks of aortic arch branch repair and gave
written consent for all procedures.
Continued at page 246
Background
Arterial disorders of the aortic arch, including its supraaortic branches and upper extremity, are less common than
those of the lower extremity. They can present with symptoms necessitating surgical or endovascular treatments.
Different pathologies affecting the arch and its branches
can present as acute or chronic symptoms, e.g., aortic arch
aneurysm, atherosclerosis, acute aortic syndrome (dissection, penetrating aortic ulcer, and intramural hematoma
known as IMH), and less common etiologies, such as upper
extremity aneurysm and vasculitis-based disorders, e.g.,
Takayasu’s arteritis, may need revascularization.
Vascular Anatomy oftheAortic Arch
Normal Arch Development
The vascular system in humans is symmetric, with the exception of the adult aortic arch. The right common carotid and
right subclavian arteries arise from the brachiocephalic
(innominate) artery, whereas the left common carotid and
left subclavian arteries originate as separate vessels from the
aortic arch. These differences are a consequence of the
changes in the connections of the aortic arches, the dorsal
aortas, and the aortic sac. Diagrammatic representation of
these changes would suggest that the aortic arches are all
present at the same time, but in reality, the rst arches are
already regressing while the others are still developing [1].
The rst two aortic arches appear and regress quickly and
contribute very little to adult structures, whereas the fth
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
G. Geroulakos et al. (eds.), Mastering Endovascular Techniques, https://doi.org/10.1007/978-3-031-42735-0_24
239
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S. Abisi et al.
aortic arch never develops in humans. The third aortic arches
become the common carotid arteries and proximal segments
of the internal carotid arteries. The distal segments of the
internal carotid arteries are derived from the dorsal aorta
between the rst and third arches. The external carotid arteries sprout from the common carotid arteries. The dorsal aorta
on each side of the embryo between the third and fourth
arches disappears, thus directing blood through the third
aortic arch system to the head and neck regions. The fourth
aortic arches are asymmetrical with regard to their fate. The
left aortic arch forms part of the adult aortic arch between the
left common carotid and left subclavian arteries, whereas the
right aortic arch becomes the proximal segment of the right
subclavian artery. The remainder of the right subclavian
artery is derived from the right dorsal aorta and its right seventh intersegmental artery. The right dorsal aorta distal to the
seventh intersegmental artery, but proximal to the fused
common aorta, involutes. The right horn of the aortic sac,
connected to the right third and fourth aortic arches, elongates to become the brachiocephalic (innominate) artery, and
the left horn becomes the initial portion of the aortic arch.
The proximal portions of both sixth arches become the right
and left pulmonary arteries. The distal segment of the right
sixth arch disappears, but the distal segment of the left sixth
arch becomes the ductus arteriosus during fetal life and atrophies after birth to become the ligamentum arteriosum. The
ductus arteriosus in the fetus acts as a shunt between the left
pulmonary artery and the aorta to move blood away from the
immature fetal lungs to the aorta [1].
known as “Ishimaru zones” in the aortic arch as shown in
Fig.24.1.
Aortic Arch Anomalies
In light of the complexity of the arch embryological development that must occur for normal development of the aortic
arch and its branches, anomalies do occur [3]. Anomalies
result when segments of the primitive aortic arch that should
disappear persist or vice versa, when other parts that should
persist disappear. Variations in the development of vessels as
they arise from the aortic arch are relatively common. The
most common developmental pattern considered to be “normal,” as described in the preceding sections, occurs in 65%
of the population. In 22% of the population, the left common
Aortic Arch Morphology
Aortic arch morphology can be classied into three different
types, depending on the position of the take-off of the great
vessels [1]. In type I aortic arches the great vessels arise at or
above the same horizontal place as the outer curvature of the
arch. In type II aortic arches the origin of the innominate
artery lies between the horizontal planes of the inner and
outer curves of the aortic arch. In type III aortic arches the
innominate artery lies below the horizontal plane of the inner
curvature of the aortic arch. As the take-off of the supraaortic vessels moves more inferiorly (i.e., type II and type III
congurations), vessel selection and the manipulation of
sheath, balloon, and stent delivery system become more difcult because the origin of the arteries becomes more
oblique. Type III aortic arch morphologies are particularly
challenging and can lead to a higher risk of embolic events
due to repeated and/or prolonged wire and catheter manipulation leading to the disruption of aortic plaques.
The ESVS guidelines recommend the use of the denition
of attachment zones as provided by “Reporting standards for
thoracic endovascular aortic repair,” [2] which are also
Fig. 24.1 Denition of attachment zones, also known as Ishimaru
zones
24 Angioplasty andStenting oftheArch Branches
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241
carotid artery originates from the brachiocephalic trunk
rather than from the aortic arch, in what is termed a “bovine
arch.” In this case, the brachiocephalic trunk gives rise to the
right subclavian, right common carotid, and left common
carotid arteries, whereas the left subclavian artery originates
from the aortic arch as normally expected. This variant
accounts for 73% of all arch anomalies [1].
Many other variations, each occurring in less than 3% of
the population, have been described. Some of these anomalies include a short brachiocephalic trunk that bifurcates
immediately into the right subclavian and right common
carotid arteries, with the left common carotid arising from
the aortic arch at the base of the brachiocephalic trunk and a
normal origin for the left subclavian artery from the aortic
arch. The left vertebral artery can originate directly from the
aortic arch between the left common carotid and left subclavian arteries. A left brachiocephalic trunk may be present,
which bifurcates into left subclavian and left common carotid
arteries [3].
Pathology
Aortic arch pathology is very complex and may be related to
a variety of histopathologic conditions including aneurysmal
degeneration, acute aortic syndromes (aortic dissection,
intramural hematoma, and penetrating aortic ulcers), and
various forms of vasculitis (giant cell arteritis, Takayasu arteritis, and Behçet disease). Aneurysmal changes are usually
secondary to either medial degeneration or aortic dissection.
TAAAs of 6.1cm [1]. When all aneurysms of the thoracic
aorta are considered, those of the ascending aorta are the
most common (40%), followed by those of the descending
thoracic aorta (35%), aortic arch (15%), and thoracoabdominal aorta (10%) [5].
The terms saccular and fusiform should also be dened
for TAAAs because the morphology of an aneurysm will
often dictate treatment options as well as point to specic
causes (i.e., mycotic aneurysms are often saccular and at
high risk for rupture) [6]. Most TAAAs are fusiform aneurysms, which involve a chronic uniform dilatation involving
the whole circumference of the aorta. In contrast, saccular
aneurysms often represent an eccentric dilatation of the
aorta. Most authors would concur that a lower threshold is an
acceptable indication for repair of saccular aneurysms.
Etiology
About 80% of TAAAs are secondary to medial degeneration,
with approximately 15–20% caused by aortic dissection.
Patients with TAAAs secondary to aortic dissection are typically younger and involve more extensive aortic segments
than do degenerative aneurysms. The aorta in patients with
Marfan syndrome is particularly prone to aortic dissection
and subsequent TAAA formation [7]. Both systemic autoimmune disorders, such as Takayasu arteritis and chronic nonspecic aortitis, can destroy the aortic media with progressive
aneurysm formation. Aneurysms associated with arteritis are
more commonly seen in women than are degenerative aneurysms. Aneurysms of the upper thoracic aorta can also be
secondary to congenital aortic coarctations, either in unrepaired coarctations or after repair [8].
Aortic Arch Aneurysm
Denition
Aneurysms are localized dilatations in the thoracic and
abdominal aorta secondary to weakening and subsequent
expansion of the aortic wall. A TAAA by denition is a
dilatation at least 1.5 times its normal value [4]. It is critically important to dene these anatomic aortic sizes
(Table 24.1) to help identify pathologic aortic growth,
because TAAA diameter is the strongest predictor of rupture, with a reported mean aortic diameter of ruptured
Table 24.1 Normal aortic diameter by segment, as well as percentage
of aortic aneurysm total represented by each aortic segment
Mean aortic diameter
Aortic segment
Ascending 3 40
Aortic arch 2.5–3.5 15
Descending
thoracic
Thoracoabdominal 1.7–2.6 10
(cm)
2.0–2.3 35
Percentage of
aneurysms
Clinical Picture
The most common initial symptom in patients with TAAAs
is vague pain, which can occur in the chest, back, ank, or
abdomen. The differential diagnosis in a patient with a symptomatic TAAA therefore includes angina, aortic dissection,
and degenerative disease of the spine. The pain associated
with TAAAs can also be chronic, which may easily be dismissed in patients with TAAAs before the diagnosis of a
TAAA has been made. Typical of most aneurysms that are
enlarging, pain may increase in severity dramatically [9].
Symptoms may also occur in patients with TAAAs from
compression of the thoracic aorta by structures in the thoracic cavity. Hoarseness can develop in patients with TAAAs
as a result of stretching or compression of the left recurrent
laryngeal nerve. Tracheal deviation, persistent cough, or
other respiratory symptoms may also be present [10].
Dysphagia is an uncommon, nonspecic complaint due to
compression of the aneurysm by the esophagus [11]. Sudden
and catastrophic hemoptysis or hematemesis may occur as a
result of erosion of the TAAA into the bronchial and pulmonary space or the esophagus, respectively.
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Patients with TAAAs may rarely have neurologic decits,
including paraplegia. This is much more common in those
with aortic dissection. Most patients with symptoms have
TAAAs that have attained a diameter greater than 5cm.
Imaging
Accurate and precise determination of the anatomy of a
patient with a TAAA is mandatory in determining both the
need for and the details of operative repair, as well as the
prescribed follow-up in patients with TAAAs who have not
reached a diameter threshold for repair. Cross-sectional
imaging, mainly by computed tomography (CT), is the primary method to visualize the thoracic and abdominal aorta
for determining aneurysm diameter and extent. Because
most TAAAs are small when discovered, serial imaging is
required; however, level A and B evidence regarding the timing of surveillance is lacking. Serial imaging is typically performed at 6–12-month intervals, but it varies depending on
the initial diameter and extent of the aneurysm.
Acute Aortic Syndrome
Non-A–Non-B Aortic Dissection: Type B
Dissection Involving theAortic Arch
Both the Stanford and DeBakey classications do not address
the clinical scenario whereby the aortic arch, but not the
ascending aorta, is dissected. The 2010 AHA guidelines recommend that patients with descending aortic dissection and
entry within the arch be categorized as proximal type B dissection [12]. Distal type B dissection refers to descending
aortic dissection and entry distal to the LSA [12]. The evolution of the term non-A–non-B aortic dissection can be seen
more as a kind of evolution of the understanding of the
pathophysiological process, which was initially described in
1994 [13, 14].
Clinical presentation, treatment, and outcome in non-A–
non-B dissection patients are different from those commonly
reported for patients with acute type B dissection. The
involvement of the arch in the dissection process of the DTA
seems to have an important impact on clinical course and
outcome; therefore, it is reasonable not to categorize these
patients as type B, but as non-A–non-B aortic dissection [2].
Aortic Intramural Hematoma
The ESC guidelines dene aortic IMH as a circular or
crescent- shaped thickening >5mm of the aortic wall with the
absence of a dissecting membrane, intimal disruption, or
false lumen ow [15]. The ESVS guidelines dene intramural hematoma as the presence of blood within the aortic wall
without intimal disruption or an identiable entry point on
imaging [16]. Whereas current guidelines see IMH as a separate entity, distinguishing between IMH and dissection may
not always be possible in clinical practice. There is certainly
a time-dependent variable with regard to diagnosis because
patients frequently present with new intimal lesions 24–48h
after the initial imaging studies were performed. The current
denition of IMH may be challenged as more sophisticated
imaging methods will be able to identify more primary entry
tears and therefore identify more IMH as a precursor to acute
aortic dissection.
Some of the predictive factors for disease progression that
have been proposed for patients with IMH without associated ulcer or intimal erosion include involvement of the
ascending aorta, aortic diameter >50mm in initial imaging,
and persistent pain. Predictors of disease progression in
patients with IMH and an associated aortic ulcer or intimal
erosion include an increase in associated pleural effusion,
recurrent pain, an ulcer located in the ascending aorta or arch
with an initial maximum ulcer diameter >20mm or more,
and an initial maximum ulcer depth >10mm [17, 18].
Penetrating Aortic Ulcer
The current ESC guidelines on aortic disease dene PAU as
an ulceration of an aortic atherosclerotic plaque penetrating
through the internal elastic lamina into the media. It is
thought that PAU occurs in 2–7% of all patients with acute
aortic syndromes. Patients presenting with PAU frequently
have a high atherosclerotic burden. Risk factors for PAU
include advanced age, male gender, tobacco smoking, hypertension, coronary artery disease, chronic obstructive pulmonary disease, and presence of abdominal aneurysm [19].
Indications for intervention according to the current
guidelines include persistent or recurrent pain, contained
rupture, rapid growth, periaortic hematoma, and pleural
effusion. It is thought that in asymptomatic patients with
PAU, a diameter >20mm and a neck >10mm have a higher
risk of progression, and early intervention should be evaluated [2].
Atherosclerosis
Aortic arch plaque (AAP) is an established risk factor for
ischemic stroke. Large plaques (dened as ≥4mm in thickness in most studies) were proven to be strongly associated
with recurrent stroke and death [20]. In a previous study, aortic arch atherosclerosis was found to be associated with silent
brain infarctions (SBI) in patients with atrial brillation
(AF), and the authors suggested that microembolization of
small thrombi might be the mechanism for SBI [21].
Numerous case–control and prospective studies have
conrmed the role of proximal arch plaques as risk factors
for stroke and other embolic events; however, the mechanism underlying the association between AAP and white
matter hyperintensity volume (WMHV) is not immediately
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clear. The prevalence of severe AAP in stroke patients has
been reported to be between 14 and 21% [21]. With respect
to subclinical cerebrovascular disease, SBIs and WMHs are
considered to be related but somewhat different expressions of brain disease. Although SBIs are focal areas of
infarcts, presumed to result from the occlusion of a single
small perforating artery supplying the subcortical areas of
the brain, WMHs are considered areas of leukoaraiosis
(loss of white matter) because of chronic hypoperfusion of
the white matter and disruption of the blood–brain barrier,
leading to chronic leakage of plasma into the white matter
[22].
Approach toCommon Lesions
Proximal Occlusive Lesions
Chronic upper extremity ischemia due to aortic arch (i.e.,
supra-aortic trunk) lesions can be effectively treated with
angioplasty and stenting and/or a surgical bypass. For supraaortic reconstruction or extra-anatomic bypass, prosthetic
graft is preferred. Surgery is more durable and should be
considered the rst line of treatment for good surgical-risk
patients, but good outcomes have been reported using endovascular techniques [23]. For subclavian artery revascularization, both open and endovascular therapy are safe and
effective, but surgical bypass is more durable [24].
Angioplasty alone has inferior outcomes compared with
angioplasty and stenting, particularly when recanalizing
occlusive subclavian lesions. In a review of 114 patients,
assisted primary patency and freedom from recurrent symptoms were worse in patients presenting with arm ischemia
compared with those presenting with cardiac or vertebrobasilar insufciency at 5years [25]. Endovascular stent-graft
repair has been used for the repair of aneurysms and both
penetrating and blunt injuries to the axillary and distal subclavian arteries, with good results.
Aortic Arch Debranching
For patients who will undergo endovascular repair of the thoracic aorta for the management of thoracic aortic
aneurysm/dissection, coverage of the left subclavian artery
may be necessary to obtain proximal endograft xation.
Extra-anatomic upper extremity revascularization may be
performed prior to endovascular repair or only as needed
postoperatively if the patient develops symptoms. Complete
endovascular aortic arch repair using custom-made inner
branch device is one of the newly developed techniques for
the treatment of arch pathology, e.g., non A–non B dissection, aortic arch aneurysm.
Endovascular Repair
The endovascular approach has gained popularity for patients
deemed too ill for open surgery and for those with iatrogenic
catheter-induced arterial injuries.
Arterial access—Endovascular revascularization can be
accomplished from a femoral or brachial artery approach.
Arm access provides better pushability and stability, which
is crucial when recanalizing occluded upper extremity
vessels.
Femoral artery access is usually selected. Historically,
large-diameter access sheaths were required for these procedures, which necessitated open cutdown. However, latergeneration, lower-prole devices and percutaneous closure
techniques have allowed this procedure to be performed percutaneously as well.
Performance of the procedure requires the delivery of a
large-bore sheath into the aorta as well as a separate access
for arteriography. While these were previously accomplished
using a femoral artery cutdown, the comfort achieved with a
percutaneous approach for large-bore sheaths has increased,
allowing these procedures to be performed primarily percutaneously, anatomy permitting.
Up to one-fourth of patients will require alternative access
techniques due to the obligatory large sheath size for delivery of the device [26]. Passage of the sheath through a smalldiameter, tortuous, or excessively calcied external iliac
artery can lead to iliac artery disruption. Adjunctive and
alternative access techniques include balloon angioplasty/
stenting of the iliac arteries prior to sheath placement, creation of an iliac conduit, direct exposure of the common iliac
artery, direct delivery through the abdominal aorta, intravascular lithotripsy, or use of a controlled rupture technique
with a specialized device (e.g., SoloPath sheath, Terumo).
Embolic protection—With an endovascular approach,
distal embolization is possible during manipulation of the
diseased vessel. With innominate lesions, it is advisable to
place an embolic protection device (EPD) in the right internal carotid. EPDs are described elsewhere.
If EPD deployment is not possible, we prefer primary
stenting with no pre-dilatation to minimize the risk of distal
embolization. Other adjunctive procedures have been
described in addition to placing a lter protection device
[27]. One example is creating reversal of ow in the vertebral
artery by injecting vasodilator in the arm circulation.
Angioplasty/stenting—Observational studies suggest
that percutaneous transluminal angioplasty and stenting
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