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C. Karkos and T. Kalogirou
is recommended during these maneuvers to assure that the
stent is not displaced or deformed. Finally, if all these fail,
open surgical removal may be necessary (Fig.26.4).
Retrieval ofEPD
Occasionally, this phase can be the most challenging part of
the entire intervention. When there has been massive distal
embolization, the risk of losing the captured material during
lter retrieval and causing a cerebral embolic event is signicant. Therefore, following stent placement and postdilatation, the operator must routinely evaluate the EPD for
trapped embolic material before it can be recaptured. In the
majority of cases, the embolic load will be minimal
(Fig.26.5).
Most lters are removed using a dedicated retrieval catheter. Occasionally, navigating these retrieval catheters
through a stent can be difcult, particularly when there are
tortuous vessels or underexpansion of the proximal edge of
the stent. Simple tricks, such as breath holding, neck turning,
swallowing, or applying manual external compression to the
stented area, may facilitate passage. Other possibilities are
(1) advancing the guiding catheter/sheath over the lter wire
until its tip is within the stent or even until it abuts the lter
device, (2) additional balloon angioplasty, or (3) replacing
the retrieval catheter with a 125cm-long angulated 5F diagnostic catheter, such as a Headhunter or multipurpose catheter, and advancing its tip up to the lter [6, 7].
Once the EPD is recaptured, careful manipulation and
removal under uoroscopic observation are crucial.
Entrapment of the lter within the stent struts and, sometimes, detachment of the lter can be due to abrupt manipu-
lations. Maneuvers like turning the patient’s head or asking
the patient to cough or the Valsalva maneuver may solve the
problem. Failing this, replacement of the retrieval catheter
with an angled 5F catheter will allow the EPD to be retrieved
in most cases. In the unlikely event of a lter fracture, “jailing” of the retained lter part against the arterial wall is a
useful bailout option [21].
At this very late stage of the procedure, troublesome
situations, such as vasospasm, dissection, or a full lter
basket, may occasionally occur and can be difcult to differentiate between them. The radiopaque wall-opposing
markers on lter elements allow differentiation between
procedural ow arrest owing to ow-limiting spasm or distal ICA dissection (the markers are drawn together) and a
full lter (the markers remain unchanged compared with
initial postdeployment images). This is clearly an important distinction as the management differs depending on
the underlying problem [22]. When vasospasm interferes
with the removal of the distal EPD, the vasospasm usually
improves following an intra- arterial injection of 50–200μg
of nitroglycerine. If there is an underlying dissection
which has been induced by the EPD, placement of a second self-expanding stent may be necessary. Small, nonow-limiting dissections may be left untreated and
observed. Finally, a full lter with complete or partial
occlusion of the ICA is a difcult problem. In such cases,
an aspiration catheter can be used to clear enough material
from the lter to allow safe removal through the guiding
catheter. If the risk of removing the full lter percutaneously
seems prohibitive, the nal option may be open surgical
removal.
a bc
Fig. 26.4 Accidental proximal “watermelon seeding” of an Xact
carotid stent with the upper edges of the stent being constrained by the
tight, irregular carotid stenosis (a). The stent delivery system got stuck
to the deployed stent, and despite adjunctive maneuvers, we were
unable to remove it. Open conversion was necessary along with longitudinal carotid arteriotomy, removal of the stent and the lter (b), endarterectomy, and primary closure (c)
26 Technique andComplications ofTransfemoral Stenting
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a
267
Fig. 26.5 Intraprocedural photographs of trapped embolic material in lters retrieved from several different patients undergoing lter-protected
transfemoral CAS (a, b)
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C. Karkos and T. Kalogirou
b
Fig. 26.5 (continued)
Other Post-procedural Complications
Adverse Hemodynamic Events (Bradycardia
andHypotension)
In clinical practice, bradycardia and hypotension are wellknown physiological responses during CAS and in most
cases are transient and self-limiting. Only occasionally these
hemodynamic responses are severe enough to cause
periprocedural cardiac or neurological adverse effects. While
the bradycardia usually resolves within seconds, the hypotension may persist for hours or even days [7]. In the absence
of symptoms in such patients, no special treatments are necessary unless systolic blood pressure drops below 80mmHg.
Withholding the patient’s routine antihypertensive medications, administering intravenous uids, and encouraging
early mobilization are all that are needed to solve the problem
and avoid prolonged hospitalization. If it is necessary to raise
the blood pressure, a dopamine infusion is usually adequate.
Certain high-risk patients, such as those with severe stenosis
of both carotid arteries, contralateral carotid occlusion,
severe aortic stenosis, left ventricular systolic dysfunction,
or signicant coronary artery disease, may tolerate less well
a period of sustained hypotension, and in these cases, it may
be advantageous to maintain a systolic blood pressure of
>90 mmHg. Although hypotension usually resolves within
24h, it is essential not to be reassured and miss other important causes of post-procedural hypotension, such as retroperitoneal hemorrhage or myocardial infarction [23].
Thromboembolic Events
Cerebrovascular ischemic complications due to thromboembolism may occur both during and after CAS and may jeop-
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269
ardize the success of the intervention. Faced with an
alteration in the patient’s neurological status, one must consider the differential diagnosis of hypoperfusion, embolism,
hemorrhage, or hypotension. If an intraprocedural intracranial arterial occlusion is noted, it is advisable to seek the help
of a neuro-interventionist who can perform “acute stroke”
cerebrovascular interventions [7].
Cerebral Hyperperfusion Syndrome
andIntracranial Hemorrhage
The cerebral hyperperfusion syndrome (CHS) post-CAS
may clinically manifest as ipsilateral headache, nausea,
vomiting, focal seizures, altered mental status, focal neurological decit, and ipsilateral intracerebral edema or fatal
intracranial hemorrhage (ICH). It is accompanied by a markedly elevated post-intervention blood pressure in the majority of patients [1, 7, 24].
The exact incidence of CHS varies in the literature, and
the pooled rate in meta-analyses ranges from 1.16 to 4.6%,
depending on the studies included, research design, and disease denition [25–27]. A recent Spanish national prospective multicenter study reported that CHS occurred in 2.9%
of 757 patients after CAS [28]. With respect to the
hyperperfusion- induced ICH, the incidence also differs
from series to series, and representative gures from relatively recent publications are 0.85% in a Canadian
population- based cohort study (16,688 patients, 14% CAS,
province of Ontario, 2002–2015) [29], 0.7% in the Spanish
national prospective multicenter study [28], and as high as
3.14% in a Chinese series (of 446 patients with symptomatic severe carotid stenosis, 2011–2018) [30]. The above
differences, in both CHS and ICH rates, may be partially
explained by the differences in the included patient populations [24].
Likely risk factors for CHS and hyperperfusion-induced
ICH after CAS include:
• Older age
• Female gender
• Chronic kidney disease
• Longstanding preexisting hypertension
• Critical intracranial atherosclerotic stenosis ≥90%
• Severe contralateral intracranial atherosclerotic disease
• Left-sided carotid disease
• Progressive neurological decit
• Frequent transient ischemic attack
• Prior stroke due to hemodynamic insufciency
• Preexisting brain lesions
• Recurrent hemorrhage
• Reduced cerebral vascular reserve and microvascular
disease
• Severe unilateral carotid stenosis
• The presence of near total occlusion
• Incomplete circle of Willis
Identication of patients at risk of developing CHS postCAS is the rst important step to preventing this complication. Further on, the management of CHS consists of careful
monitoring, early recognition, and aggressive blood pressure
control to prevent the situation from escalating into cerebral
edema and hemorrhage. Ideally, such patients should be
monitored in a high-dependency or intensive care unit. The
prognosis following ICH is dismal, and the mortality exceeds
50%. In contrast, the prognosis is much better if patients
with CHS are identied early post-CAS and treated prior to
developing cerebral edema or ICH [1, 7, 24–30].
Postoperative Care andSurveillance
Most patients would be able to be discharged home on the
rst postoperative day. If hypotensive, we advise them to
withhold antihypertensive agents until blood pressure comes
up, which usually occurs 2–3days later. Our preference is to
continue a dual antiplatelet therapy for the rst 6 months
and, after that, to carry on with a single antiplatelet drug for
life. Patients are followed up in the outpatient clinic in
6-monthly intervals with clinical assessment and carotid colorow duplex scan.
Case Presentation
Continued from page 259
The patient clearly understood the benets and risks of
carotid intervention and opted for CAS as she considered this
less invasive than endarterectomy. Clopidogrel 75 mg was
added to her medications a week prior to the scheduled date of
the procedure. Under local anesthesia and a transfemoral
approach, a 7F-11cm sheath was introduced, and 5000units
of heparin were given intravenously. A 7F-100cm JR4 guiding catheter was advanced over a 0.035″ stiff hydrophilic
guidewire to the aortic arch, and the innominate and the right
CCA were selectively catheterized. After advancing the guidewire in the ECA, the catheter was positioned in the distal CCA
proximal to the carotid lesion. The 0.035″ wire was removed,
and the Emboshield NAV6 (Abbott Cardiovascular) lter was
gently advanced through the lesion and deployed in the distal
extracranial ICA.A 7mm×40mm carotid Wallstent (Boston
Scientic) was deployed, and this was postdilated with a
5mm×20mm RX balloon. Atropine 1mg was given prior to
balloon ination to avoid bradycardia. Post-stenting angiography was satisfactory, and the lter was retrieved using the
dedicated retrieval system. Completion angiography, includ-
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C. Karkos and T. Kalogirou
a
bcd
ef gh
Fig. 26.6 Transfemoral lter-protected CAS. Selective right carotid
DSA runs through the guiding catheter showed >90% stenosis at the
origin of the right ICA (a–c). An Emboshield NAV6 lter was deployed
ing intracranial views, showed a satisfactory result (Fig.26.6).
She had been asymptomatic with no neurological decits
throughout the entire procedure. At the end, the femoral sheath
was removed, and puncture site hemostasis was achieved with
manual compression. The patient was transferred to the highdependency unit for overnight monitoring. Post-procedure,
she developed persistent hypotension (systolic blood pressure
in the distal ICA, and a 7mm×40mm carotid Wallstent was implanted
with satisfactory angiographic result prior to (d–g) and after lter
retrieval (h–j)
of 90mmHg). As she was asymptomatic, this required no specic action other than adequate intravenous hydration and
withholding the antihypertensive agents. She had an otherwise
uneventful recovery and was discharged home the following
day. She was advised to continue dual antiplatelet therapy for
6months and, following this, to carry on with a single antiplatelet for life.
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Introduction toTranscarotid Artery
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Revascularization
AngelaA.Kokkosis
27
Case Presentation
An 80-year-old female presented to the ofce with an episode of right-sided amaurosis fugax. The patient stated that
this occurred 2weeks ago for the rst time, and for about
1min she could not see through her right eye. She went to
her ophthalmologist for evaluation, and upon further examination he referred her for a vascular consult. Her past medical history was remarkable for hypertension, type 2 diabetes,
and hyperlipidemia. She denied any prior history of stroke or
transient ischemic attack.
On physical exam she had palpable upper and lower
extremity pulses, and no neurologic decits. Duplex exam
demonstrated a peak diastolic velocity/end diastolic velocity
(PSV/EDV) of 627/227cm/s in the mid-right internal carotid
artery (Fig.27.1), and CTA conrmed a 90% stenosis of the
mid-right internal carotid artery at the level of C2. Her left
Fig. 27.1 Right carotid artery duplex demonstrating the 70–99% stenotic lesion
A. A. Kokkosis (*)
Vascular Surgery, Stony Brook University Medical Center,
Stony Brook, NY, USA
e-mail: Angela.kokkosis@stonybrookmedicine.edu
© 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_27
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A. A. Kokkosis
carotid artery and bilateral vertebral arteries were patent
without signicant disease.
Surgical options for carotid revascularization were discussed, including carotid endarterectomy, transfemoral
carotid artery stenting, and transcarotid artery
revascularization.
Continued at page 278
Background
For many years the gold standard for carotid revascularization has been carotid endarterectomy (CEA). With the advent
of endovascular interventions, transfemoral carotid artery
stenting (TF-CAS) came to light. However, after extensive
research and numerous trials, perioperative stroke risk could
not equal or surpass that of CEA.Several features of TF-CAS
were thought to contribute to this elevated perioperative
stroke risk, such as aortic arch manipulation with wires and
catheters, need for crossing the lesion to deploy an embolic
protection device, and inadequate particle capture of the distal embolic protection devices [1, 2]. In 2004, a new concept
for carotid stenting was introduced to avoid aortic arch navigation and crossing the lesion prior to employing embolic
protection—delivery of the stent via a transcervical approach
and with ow reversal as the embolic protection [3, 4]. After
the pivotal ROADSTER trial, which demonstrated the lowest
30-day stroke and combined stroke/death rates for transcarotid artery revascularization (TCAR) [5], this concept
became an FDA-approved intervention in the United States
in 2016. Currently, TCAR is commercially available as a
carotid revascularization option for both high-risk and
standard- risk patients.
Pre-operative Considerations
Suitable Patients forTCAR
Medications
As with any patient undergoing carotid stent placement, dual
antiplatelet therapy is essential during the perioperative
period and for at least 1month post-procedure. Typically this
consists of aspirin and clopidogrel. However, in instances of
clopidogrel resistance, other antiplatelet agents may be considered. Statins should also be part of the patient’s regimen
as they have been shown to promote plaque stabilization.
Anticoagulation is not a necessary maintenance medication for carotid stents; however, many patients undergoing
TCAR may be on anticoagulation for a cardiac or hypercoagulable indication. In these situations, careful discussion
should be undertaken with the patient and their specialists to
determine the best way to manage the dual antiplatelets and
anticoagulation.
Imaging
Both duplex ultrasound and computed tomography angiography (CTA) or magnetic resonance angiography (MRA) are
recommended in patients being considered for TCAR.
Duplex ultrasound is valuable for its ability to provide
dynamic information on ow, velocities and plaque characteristics, and to assess the potential access site at the common carotid artery. Axial imaging of the head and neck via
CTA or MRA demonstrates the anatomy of the lesion, exact
location of the lesion, and any potential kinks or turns in the
artery which may affect stent placement, and it offers the
ability to measure artery diameters, and intracranial circulation and assessment of the circle of Willis. CTA is preferable
to MRA, especially in instances of calcied lesions, since
MRA shows signal dropout in areas of calcium. However,
CTA may overestimate calcium burden. Additionally, MRA
offers the ability to obtain non-contrast ow imaging (“time
of ight”) for those patients who have a contraindication to
contrast use.
Patients being considered for TCAR must meet specic anatomic criteria in order for the procedure to be performed
safely and successfully. They must have a common carotid
artery that measures at least 6mm, a length from the access
site to the lesion of at least 5cm, and an access site at the
common carotid artery that is free of signicant atherosclerotic disease.
Lesion characteristics should also be carefully evaluated
for successful stent deployment. Severe calcication, vessel
tortuosity, acute thrombus, mobile plaque, long-segment disease, and carotid artery diameters outside the range of commercially available stents may not be good candidates for
TCAR [6].
Anesthetic Technique
TCAR is a less invasive carotid revascularization approach,
and thus it offers the possibility of performing the intervention under general anesthesia, regional nerve block, or local
anesthesia with monitored sedation. Currently, there is no
data to suggest that one technique is superior to the other,
and thus careful discussion with the patient as well as consideration of available anesthetic capabilities at one’s institution are important. For those vascular specialists who are
early in their TCAR experience, general anesthesia may be
preferable for the rst few cases.
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Intraoperative Considerations
Patient Positioning andDraping
The patient should be placed in the supine position on the
operating table with the head turned to the contralateral side.
The neck and chest should be prepped and draped, as with a
standard CEA, as well as bilateral groins for venous access.
Consider a shoulder roll to facilitate further extension of the
neck; however, this is not always necessary since the carotid
exposure site is low on the neck.
abc
e
fg
Endovascular Devices
The Silk Road ENROUTE® system is the only commercially
available device for TCAR. This system includes the neuroprotection system, the stent device, the access kit, and the
0.014″ guidewire (Fig.27.2).
Other endovascular equipment that should be available
includes:
• 0.014″ monorail platform angioplasty balloon (sizes
4–6mm×20 or 30mm)
d
h
Fig. 27.2 Silk Road ENROUTE® Devices. (a) Arterial sheath. (b) Venous sheath. (c) Flow reversal controller. (d) 035″ J-wire. (e) ENROUTE®
Stent system. (f) Micropuncture access set. (g) 014” Wire. (h) Full assembly of the ENROUTE system
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• Angioplasty balloon insufator
• Directional catheter
• Additional 0.014″ wire
• 10cc syringes for injection
• Separate micropuncture access kit for femoral vein access
• 0.035″ wire for venous sheath placement
Open Surgical Instruments
Standard instruments used for CEA are more than enough
for common carotid artery exposure and vessel control.
Duplex Ultrasound
A. A. Kokkosis
With the patient on the surgical table and in the operative
position, duplex ultrasound should be performed to mark the
desired access site, the location of lesion, and the borders of
the sternocleidomastoid. Additionally, the ultrasound should
be draped in a sterile manner for later use in the venous
access. In rare situations, a critical carotid stenosis may
occlude asymptomatically prior to the intervention, and thus
carotid duplex with color ow assessment prior to incision
may be prudent.
TCAR Technique
Incision Choice
Either a vertical or transverse incision may be employed
for common carotid artery exposure. The vertical incision
affords the ability to extend more distally in the rare event
of conversion to carotid endarterectomy, while the transverse incision tends to be more cosmetic. Regardless of the
incision choice, the location of the incision should be
within the borders of the superior edge of the clavicle, the
lateral border of the sternal head of the sternocleidomastoid, and the medial border of the clavicular head
(Fig.27.3).
Stent andBalloon Selection
Fig. 27.3 Example of transverse incision within the triangle of the
sternocleidomastoid muscle bellies and the clavicle
Fig. 27.4 Example of using a Gregory profunda clamp
Vessel Clamping Choice
Control of the common carotid artery is usually obtained
with a silastic vessel loop or umbilical tape. The actual
clamping of the vessel may be achieved either with a vascular clamp (such as a Gregory profunda or PVD) or with doubling of the vessel loop (Fig.27.4).
Stent sizing is typically 1–2 mm larger than the common
carotid artery diameter when the ENROUTE stent is used,
and pre-dilatation balloon sizing should be based on the normal distal internal carotid artery.
Stop Short or Engage External Carotid Artery
Upon initial access of the common carotid artery, the decision of whether to advance the 0.035″ J-wire into the external
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