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27 Introduction toTranscarotid Artery Revascularization
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carotid artery (ECA) for more support or just before the
lesion must be made based on the initial angiogram from the
micropuncture sheath.
If the origin of the external carotid artery is diseased, or if
the carotid lesion extends proximally to the carotid bifurcation, the J-wire should be maintained below this area during
arterial sheath placement, to avoid inadvertently crossing the
lesion without embolic protection.
If the external carotid artery is free of disease, the micropuncture wire and sheath should be advanced into this artery
in order to gain more wire length and support for arterial
sheath placement.
Potential Complications Specic toTCAR
Access Site Dissection
One of the most crucial steps in TCAR is obtaining safe
carotid access. The short distances and small working space
may at rst seem awkward for those accustomed to endovascular procedures with long devices and contralateral vessel
access. Therefore, careful needle placement and passage of
the microwire and sheath are paramount. If at any point it is
felt that there is poor blood return with the needle access, or
upon micro-sheath access, it is safer to remove the needle or
sheath and close the puncture site with a prolene stitch.
Trying to proceed with arterial sheath placement may result
in dissection in these cases.
In the event that a dissection does occur, frequently these
can be salvaged by endovascular means by either accessing
the vessel more proximally, before the dissection entry point,
or navigating a wire into the true lumen from the same
access. Once this is achieved, the carotid stent can be
extended proximally to cover the dissection. In the rare situation of severe carotid dissection where endovascular techniques fail, conversion to open carotid intervention may be
necessary.
ment. Branches such as the ascending pharyngeal may mimic
the course of the internal carotid artery and be inadvertently
stented.
Nerve Injury
The vagus and recurrent laryngeal nerves are most commonly encountered in the area of the common carotid dissection, and thus should be protected.
Access Site Hematoma
TCAR requires dual antiplatelets, as well as intraoperative
heparinization, both of which increase the risk of postoperative hematoma in the setting of an incision. Meticulous
hemostasis as well as reversal of heparin with protamine at
case completion are strongly recommended.
Perioperative Care
A-Line Monitoring
Patients undergoing carotid artery revascularization are
known to have acute post-operative changes in their blood
pressure. Both hypotension and hypertension can lead to
severe complications: stent thrombosis or watershed infarct,
and hyperperfusion syndrome, respectively. An arterial line
should be placed intraoperatively and maintained postoperatively for 4–6h, or longer, depending on the patient’s
blood pressure stability. Both hypotension and hypertension
should be treated proactively to prevent potential
complications.
Discharge Instructions
Pneumothorax
The location of the common carotid access is fairly proximal, and in patients with a history of pulmonary disease, the
lung apex may be directly beneath the common carotid
artery. This anatomy can be identied on pre-operative CT
scan, and in general care should be taken not to dissect
beyond the posterior wall of the common carotid artery.
Incorrect Stent Placement
Careful evaluation of the angiographic images obtained
intraoperatively should be performed prior to stent deploy-
The patient should be educated upon discharge about the
signs/symptoms of stroke, hyperperfusion syndrome, and
signs/symptoms of neck hematoma or swelling.
Additionally, it is important to emphasize the continuation of dual antiplatelet and statin therapy for at least 1month
post-operatively. Further discussion on any changes to the
regimen should be conducted between the physician and
patient.
Surveillance
The Society for Vascular Surgery published a set of guidelines for surveillance after carotid revascularization. The recommendation is for patients to undergo a baseline duplex
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A. A. Kokkosis
ultrasound after the intervention, followed by duplex ultrasound every 6months for 2years, and then annually thereafter, as long as there is no signicant restenosis or progression
of disease. Additionally, there are specic carotid duplex criteria for in-stent restenosis [7]:
• ≥50%, PSV 220cm/s, ICA/CCA≥2.7
• ≥80%, PSV 340cm/s, ICA/CCA ≥4.15
Case Presentation
Continued from page 274
After consideration of the patient’s surgically inaccessible
carotid lesion and symptomatic nature, TCAR was offered for
carotid revascularization. The patient had been previously
maintained on aspirin and a statin for her underlying comorbidities, so she was also started on clopidogrel pre- operatively.
Due to concern for possible clopidogrel resistance, she was
also sent for a blood test to assess clopidogrel response,
1week after initiating the therapy. Fortunately, she was determined to respond appropriately to the clopidogrel.
The patient was taken to the operating room and placed in
the supine position on the operating table with the head turned
to the left side. The decision was made to perform the procedure under local anesthetic and monitored sedation. A squeeze
toy was placed in her left hand, to assess her neurologic status
intraoperatively. Her right neck, chest, and bilateral groins
were prepped and draped in the usual sterile fashion. Duplex
ultrasound was used to mark the common carotid artery access
site within the triangle of the sternocleidomastoid (SCM)
muscle bellies and clavicle. Additionally, the carotid bifurcation and lesion were visualized, and color ow was noted to
pass through the stenotic area. The ultrasound was then used
to evaluate the contralateral common femoral vein (left) for
patency, and this was determined to be adequate for access.
A transverse 5 cm incision was made over the proximal
common carotid artery, about 1 ngerbreadth above the clavicle. This was deepened with cautery through the platysma.
Between the SCM muscle bellies, an avascular fatty plane was
identied, and this was dissected carefully with metsembaum
scissors. The carotid sheath was identied. The common
carotid artery was circumferentially dissected for a distance of
3cm. The vagus nerve was visualized posterior to the carotid
artery and this was protected. A silastic vessel loop was encircled at the proximal end of the carotid artery. A 5-0 prolene
Z-stitch was placed in the center of the 3cm exposure, in the
location of the access. The patient was systemically heparinized to an activated clotting time (ACT) of 250s and was given
glycopyrrolate in anticipation of a baroreceptor response to
angioplasty. Left common femoral vein access was then
obtained with a micropuncture set, and an 035″ wire was
advanced into the IVC.The venous sheath was then advanced
over the wire, and secured to the skin with a silk stitch.
Next, common carotid artery access was obtained with
the ENROUTE access kit. The needle was advanced
through the pre-placed prolene stitch, and when good
backbleeding was observed, the microwire was advanced
carefully into the common carotid artery for a distance of
5cm, noted by the silver band on the wire. The micropuncture sheath was advanced 2–3cm into the common carotid
artery, and initial contrast angiogram was performed. This
demonstrated the carotid bifurcation with a patent external
carotid artery, and the carotid lesion was located at the
proximal-mid internal carotid artery. The decision was
made to engage the ECA. The microwire was reinserted
and navigated into the ECA, and the micropuncture sheath
was advanced into the ECA.The microwire was replaced
with the 035″ J-wire and after removal of the microsheath,
the arterial sheath was advanced over the wire and sutured
to the skin. The wire and dilator were removed and the
sheath’s two ports were backbled. Next, two orthogonal
view angiograms were performed to ensure that the sheath
tip was not abutting the vessel wall (thus increasing risk
for dissection) (Fig.27.5a). The ENROUTE ow controller was connected from the arterial sheath to the venous
sheath and set on HIGH ow. At this point, prior to clamping of the carotid artery, angioplasty balloon and stent
availability, a target systolic blood pressure of 140–
160mmHg, a target heart rate of 70, and target ACT of 250
were conrmed. The carotid artery was clamped, and thus
ow reversal was now employed. The patient’s neuro status was assessed by asking the patient to squeeze the toy.
A 5×30mm balloon had been selected based on the CT
measurement of the normal distal ICA at 5 mm, and a
10 × 40 mm ENROUTE stent was selected based on a
common carotid artery measuring 8mm.
The lesion was traversed with the 014” ENROUTE wire,
and the balloon was advanced to the lesion. Angioplasty
was performed (Fig.27.5b). Again the patient’s neuro status was assessed and noted to be intact. Next, the ENROUTE
stent was advanced to the lesion and deployed (Fig.27.5c).
After waiting 2min for washout of any particles through
the ow reversal during the lesion manipulation, completion angiogram was performed (Fig.27.5d). This demonstrated good stent expansion with no residual stenosis, and
in general any residual stenosis <30% is acceptable. The
carotid artery was unclamped, the ow reversal system was
disconnected, and the arterial sheath was removed with the
prolene stitch tied for hemostasis. The venous sheath was
then removed and manual pressure was held. The heparin
was reversed with protamine, and the neck incision was
closed in standard fashion. The patient was taken to the
recovery room with continuous arterial line monitoring.
After an uneventful post-operative course, she was discharged the next day and instructed to maintain the dual
antiplatelet and statin therapy, and was counseled on signs/
27 Introduction toTranscarotid Artery Revascularization
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a bc d
279
Fig. 27.5 Intraoperative angiographic images. (a) Initial angiogram. (b) Angioplasty with 5×30mm balloon. (c) Stenting with 10×40mm stent.
(d) Completion angiogram
3. Chang DW.A new approach to carotid angioplasty and stenting with
symptoms of stroke, TIA, hyperperfusion syndrome, and
wound complications. She was scheduled for a post-operative visit in 2weeks, where a baseline duplex would be performed of the stent.
References
1. Macdonald S, Lee R, Williams R, Stansby G.Towards safer carotid
artery stenting: a scoring system for anatomic suitability. Stroke.
2009;40(5):1698–703.
2. Brott TG, Hobson RW 2nd, Howard G, Roubin GS, Clark WM,
Brooks W, etal. Stenting versus endarterectomy for treatment of
carotid-artery stenosis. N Engl J Med. 2010;363:11–23.
transcervical occlusion and protective shunting: why it may be a better carotid artery intervention. J Vasc Surg. 2004;39(5):994–1002.
4. Criado E, etal. Transcervical carotid stenting with internal carotid
artery ow reversal: feasibility and preliminary results. J Vasc Surg.
2004;40:476–83.
5. Kwolek CJ, Jaff MR, Leal JI, Hopkins LN, Shah RM, Hanover TM,
et al. Results of the ROADSTER multicenter trial of transcarotid
stenting with dynamic ow reversal Presented at the Late Breaking
Clinical Trials Session at Vascular Interventional Advances (VIVA)
2014, November 4–7, 2014. J Vasc Surg. 2015;62(5):1227–34.e1.
6. Kokkosis AA, Macdonald S, Jim J, Shah R, Schneider PA.Assessing
the suitability of the carotid bifurcation for stenting: anatomic and
morphologic considerations. J Vasc Surg. 2021;74(6):2087–95.
7. Zierler RE, Jordan WD, Lal BK, Mussa F, Leers S, Fulton J, etal.
The SVS practice guidelines on follow up after vascular surgery
arterial procedures. J Vasc Surg. 2018;68:256–84.
Intracranial Atheromatous Stenosis
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QuentinHolay, WilliamBoisseau, GregoryWalker,
JulienBoucherit, andRaphaëlBlanc
28
Illustrative Case
A 71-year-old right-handed female was rst admitted in July
2013 to the neurology intensive care unit for an acute left
sylvian stroke causing an aphasia and a right hemiparesis.
Her medical history included a poorly balanced type II
diabetes, high blood pressure, and overweight. The rst brain
MRI shown an acute stroke on DWI-weighted imaging in
left corona radiata and a severe stenosis of the distal M1 segment of the left middle cerebral artery (Fig. 28.1a). The
patient was put on an intensive medical treatment with dual
antiplatelet therapy (DAPT) and a statin.
Despite this medical therapy, the patient had a recurrent
stroke 2 months later with even worse aphasia and right
hemiparesis (NIHSS score of 7). The MRI found a new
ischemic stroke in the left posterior junctional territory and
the persistence of the severe stenosis of M1 segment
(Fig.28.1b). An efcacy test with the double antiplatelet
therapy was also performed and showed a good response to
both drugs.
Q. Holay · W. Boisseau · J. Boucherit · R. Blanc (*)
Departement of Interventional Neuroradiology,
Hopital Fondation Rothschild, Paris, France
G. Walker
Division of Neurology, Department of Medicine, Royal Columbian
Hospital, New Westminster, BC, Canada
© 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_28
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ab c
Q. Holay et al.
de
Fig. 28.1 Patient with ICAS and recurrent stroke despite optimal medical treatment. First diffusion weighted imaging (DWI) (a) shows an
acute stroke in left corona radiata. Second DWI (b) shows a recurrent
stroke in the same territory. Digital subtraction angiography (DSA) (c)
shows a 5-mm-long tight M1 stenosis, with a clear downstream circula-
Background
tory slowing. A balloon angioplasty was rst performed with a
2×12mm Gateway balloon (d), and then a 2.5 ×15mm Wingspan
stent was placed along the stenosis (e) allowing a satisfying angiographic result without residual stenosis (f)
stenosis (more than 70% of the diameter of a major intracranial artery). According to recent trials, recurrence rates can
Intracranial atherosclerotic stenosis (ICAS) is one of the
most common causes of stroke worldwide [1], with wide
variations in prevalence between ethnic groups. ICAS is
reported to be highly prevalent in Asian [2], Black, and
Hispanic [3], while it remains an uncommon cause of stroke
in Caucasian populations [3, 4]. The most common sites of
ICAS in descending order are the middle cerebral artery, the
internal carotid artery distal to the petrous segment, the midbasilar trunk, the intracranial vertebral (V4 segment) arteries, and the posterior and anterior cerebral arteries [5, 6].
Symptomatic (i.e., causing stroke or transient ischemic
attack (TIA)) ICAS is associated with a high risk of recurrent
cerebrovascular ischemia [5–7], especially in cases of severe
reach as high as 7% in the rst year [8, 9], even despite
aggressive optimal medical treatment (i.e., combination of
antiplatelet medication and vascular risk factor control).
Alternatives therapies are therefore still needed for these
patients.
Interventional treatments (percutaneous transluminal
angioplasty with or without stenting (PTAS)) exist to attempt
rapid restoration of normal arterial caliber and prevent shortand long-term morbidity and mortality. These techniques
have been used in hyperacute and subacute settings. However,
over the past two decades, randomized trials have generally
shown harm and lack of benet even when combined with
the best medical therapy [5–7, 9].
f
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Here, we discuss three objectives: (1) current indications
of PTAS for symptomatic and severe ICAS, (2) a description
of the devices and PTAS techniques, and (3) a discussion of
the forthcoming improvements in PTAS.
Indication forIntervention
The 2021 Guidelines for the prevention of stroke in patients
with stroke and transient ischemic attack statement is “angioplasty and stenting should not be performed as an initial
treatment, even for patients who were taking an antithrombotic agent at the time of the stroke or TIA.” [10] This recommendation is based on data from three randomized trials
that showed harm or lack of benet of PTAS (with either
self-expanding or balloon-expandable stents) when compared with medical therapy [6, 7, 9].
The SAMMPRIS (Stenting versus Aggressive Medical
Management Therapy for Preventing Recurrent Stroke in
Intracranial Stenosis) [6] and VISSIT (Vitesse Intracranial
Stent Study for Ischemic Therapy) [7] trials compared intensive medical therapy alone with intracranial stent placement
plus intensive medical therapy in patients with 70–99%
intracranial stenosis who had a TIA or stroke within 30days
before enrollment. The SAMMPRIS trial used the selfexpanding Wingspan stent, while the VISSIT trial tested the
PHAROS Vitesse balloon-expandable neurovascular stent
system (Codman Neurovascular, Raynham, MA).
SAMMPRIS trial was halted early because of increased
30-day stroke or death rate events in the stenting arm compared with aggressive medical management (14.7% versus
5.7%, P=0.002) [6]. The enrollment in VISSIT was halted
after these negative results and because of futility after 112
patients out of a planned 250 were enrolled. At 1year, 36.2%
of patients in the stent group had a recurrent stroke or TIA,
versus 15.1% in the medical group [10]. The recently published CASSISS (China Angioplasty and Stenting for
Symptomatic Intracranial Severe Stenosis) trial [9] had similar entry criteria except excluded patients with perforator
ischemic stroke (i.e., brainstem or basal ganglia territory
infarct). This trial randomized 360 patients to PTAS plus
optimal medical management (n=176) versus optimal medical management alone (n=182). The 1-year rate of the primary endpoint (a composite of stroke or death within 30days
or stroke in the qualifying artery territory beyond 30days
through 1year) was similar between the two groups (8.0%
for PTAS plus medical therapy versus 7.2% for medical therapy alone, p=0.82) [9].
The only indication for PTAS remains for patients with
ICAS and recurrent cerebrovascular ischemic event despite
optimal medical treatement [11]. Currently, only the
Wingspan system is approved (as a Humanitarian Device
exception) for patients between 22 and 80years of age with
≥2 cerebrovascular ischemic events localizable to the stenotic vessel despite medical treatment with a recovery to a
modied Rankin Scale (mRS) score≤3. The patient must
have had experienced the most recent stroke >7days before
the planned treatment with Wingspan and have 70–99% stenosis due to ICAD [11]. Using this FDA on-label indication,
the WEAVE registry (Wingspan Stent System Post Market
Surveillance) included 152 patients. There was a lower-thanexpected (2.6%) periprocedural stroke, intracranial hemorrhage, or death rate for the interim analysis [12]. However,
no additional information was provided from this trial, especially on longer-term stroke and death event rates.
Preoperative Preparation
Imaging
Several imaging modalities, such as transcranial Doppler
(TCD), magnetic resonance angiography (MRA, with Timeof- Flight (TOF) and Contrast-Enhanced (CE) MRA), computed tomographic angiography (CTA), and digital
subtraction angiography (DSA), are used commonly in routine clinical practice to detect intracranial artery stenosis.
However, consensus about the optimal imaging strategy has
not been established so far. While anatomic diagnosis of
arterial narrowing is made with reasonable accuracy with
these imaging techniques [13–15], identifying the underlying cause of the stenosis remains challenging in clinical
practice [16]. There are several diseases including brain vasculitis, moyamoya disease, radiation-induced vasculopathy,
reversible cerebral vasoconstriction syndrome, or intracranial dissection that may mimic ICAS [16].
DSA remains the gold standard and was mandatory for
the diagnosis of ICAS in all aforementioned trials [6, 7, 9].
DSA provides excellent visualization of vessel contour, anatomic localization, and assessment of the degree and length
of stenosis and collateral circulation. However, DSA may
not adequately assess vessel wall pathology and can be of
limited value in differentiating between causes of intracranial vasculopathies [17].High-resolution magnetic resonance
with vessel wall imaging (VWI) is currently the subject of
extensive research [18]. Although further validation is
needed, VWI might be a promising technique for the diagnosis of ICAS [18]. Patterns and intensity of postgadolinium
enhancement of vascular lesions with MRI T1 postcontrast
VMI could help differentiate between intracranial atherosclerosis and other vasculopathies [18]. ICAD typically
shows eccentric thickening and asymmetric enhancement,
while vasculitis shows smooth, intense, and homogeneous
enhancement [18].
In summary, our current diagnostic strategy includes the
use of MRA and VWI as screening tools for ICAS diagnosis
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and then DSA for conrmation and preparation of
treatment.
Timing ofIntervention
The optimal timing between the qualifying cerebrovascular
ischemic events and the PTAS procedure is unknown.
Recurrent cerebrovascular ischemic events due to ICAS can
often occur in the early period after the index event [19]. In a
post-hoc analysis of the WASID (the Warfarin-Aspirin
Symptomatic Intracranial Disease) trial, among patients who
had recurrent cerebrovascular ischemic events, almost half
experienced recurrent cerebrovascular ischemic event within
30 days [19]. On the other hand, early stenting has been
reported to increase the periprocedural risk [20, 21]. As one
example, the periprocedural stroke risk in SAMMPRIS was
more than ve times that seen in the WEAVE registry, with
median enrollment times of 7 and 22days from index event,
respectively [6, 12]. Several speculative explanations have
been suggested for this nding. First, intracranial stenting on
recently symptomatic, still vulnerable plaques may increase
the risk of procedural stroke (the “snowplowing” effect)
[22]. Second, delaying the stenting could give time for the
blood brain barrier healing and then reduce the risk of hemorrhage and hyperperfusion syndrome [20]. Finally, delayed
stenting may also enable the patients a better antiplatelet and
medical preparation for the procedure possibly rendering the
plaque more “stable” and the stent environment less prothrombotic [20].
The recently published CASSISS trial limited enrollment
of patients to beyond 3weeks after their index event [9]. As
mentioned above, this trial found no difference in stroke
recurrence between PTAS and medically treated patients.
However, both groups had signicantly lower rates of stroke
recurrence compared to historical controls [6, 7], likely in
part due to later enrollment [9]. This timeline of delaying the
procedure to more than 3weeks post index event may underestimate or not capture the upfront stroke risk in both endovascular and medically managed groups.
In summary, although delayed PTAS seems to be more
efcient and safer, it also exposes the patient to a signicant
risk of early recurrence. The proper cut-off point of timing is
yet to be determined.
for up to 90days post-ICAS [6, 7, 9, 23]. Yet, some issues
remain. Previous trials have used various dose of aspirin,
from 75 to 325mg [6, 7, 9, 23]. The optimal antiplatelet regi-
ment remains unknown. Few studies have compared clopidogrel, ticagrelor, and cilostazol in the context of PTAS.Only
one trial (the TOSS II trial [24]) has compared the efcacy of
dual antiplatelet therapy (DAPT) with aspirin plus cilostazol
versus aspirin plus clopidogrel. No signicant differences
were seen in total cardiovascular events (nonfatal stroke,
nonfatal myocardial infarction, and vascular death) and the
frequency of new ischemic lesions on brain MRI follow-up
[24]. Individual responses to clopidogrel vary [25]. Low
response to clopidogrel is commonly reported [25] and might
be associated with recurrent cerebrovascular ischemic
events, especially in patients with symptomatic ICAS [26].
Ticagrelor is considered to have no resistance and could be
an alternative. Although some retrospective studies have suggested that ticagrelor might be as effective and safe as clopidogrel in neurointerventional procedures [27, 28],
randomized data are still needed. The TIC-TAC trial [29],
comparing Ticagrelor and Clopidogrel in stenting cerebral
aneurysm, is already completed with nal results still
pending.
Finally, preoperative timing of antiplatelet initiation is yet
to be determined. While early DAPT reduces the risk of
recurrent cerebrovascular ischemic events, it also carries the
risk of hemorrhagic transformation. In contrast, a potential
delay in the initiation of DAPT could lead to an increase
early recurrence risk. This dilemma between ischemic and
hemorrhagic risks could explain the large number of proposed treatment regimens. Clopidogrel is a good example of
this variability with various timing (from one [6] to several
[7, 9, 12] days before the surgery) and dose (with [6] or with-
out [7, 9, 12] a loading dose varying from 300 to 600mg)
initiation. Intravenous P2Y12 inhibitors (Cangrelor) might
be the ideal treatment in this context, given its interesting
pharmacologic properties (rapid and complete platelet inhibition, quick platelet function recovery after treatment interruption, and easy transition to oral antiplatelet therapy) [30].
Again, although Cangrelor seems to be a valuable therapeutic option [31], there is currently no evidence that this treatment leads to better outcome and comparable safety during
PTAS. Clearly, larger studies exploring these agents and
regimen are certainly needed.
Medical Treatment
Dual Antiplatelet Therapy (DAPT)
There exists a signicant amount of heterogeneity in data
and practice for the timing, regimen, and antiplatelet agents
used for pre- and post-PTAS. The current consensus, based
on several previous trials, is to use aspirin plus clopidogrel
Management ofModiable Risk Factors
In association with DAPT, American [10] and European
[32] guidelines recommend, in patients with a TIA or stroke
attributable to 50–99% stenosis of a major intracranial
artery, maintenance of systolic blood pressure below
140mmHg, high-intensity statin therapy, and at least moderate physical activity to prevent recurrent stroke and vascular events.
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Historically, blood pressure was intentionally left high to
mitigate the presumed effects of stenosis. The paradigm
slowly shifted in part due to a post-hoc analysis from the
WASID trial [33] showing that long-term higher blood pressure was associated with an increased risk of stroke and other
vascular event. On the other hand, a recent randomized controlled trial has shown that intensive blood pressure control
(under 120mmHg) in patients with symptomatic ICAS may
increase ischemic lesion volume in the subacute stage compared to modest BP treatment (under 140mmHg). This data
has served as the framework for the current guidelines, recommending targeting a systolic blood pressure of around
140mmHg [10, 32].
Endovascular Strategy andTechnique
Stent Devices
The Wingspan system is currently the only stent approved by
the FDA and the CE.
Over the last two decades, several stents have come on the
market. These products and characteristics are summarized
in Table28.1. It is important to note that few of these new
devices have been compared to the Wingspan stent. The efcacy and safety of most devices are based on noncontrolled
observational studies. Data are lacking to justify the use of
one device over another. Main results are summarized in
Table28.2.
Percutaneous Transluminal Angioplasty
withStenting (PTAS) Procedure
Anesthetic Techniques
This question remains unanswered as no clinical trials have
compared general anesthesia and conscious sedation in this
context. Proponents of general anesthesia will argue that
minimizing the patient movement will reduce the risk of iatrogenic complication. On the other hand, awake procedure
has been proven feasible [41], allowing per-procedural monitoring and quick response in case a neurological decit.
Procedural Description: Tips andTricks
In the next paragraph, we delineate a step-by-step description of PTAS techniques based on our experience and techniques reported in the literature.
After arterial puncture (femoral or radial), intravenous
heparin is given to maintain the activated clotting time (ACT)
between 200 and 300s throughout the procedure.
A guiding catheter (a long introducer sheath or a balloon
guide catheter (BGC) for proximal ow arrest) is navigated
into the target proximal cervical vessel (carotid or vertebral
Table 28.1 List and characteristics of available stent for ICAS
treatment
Stent
diameter
Product name
Self-expanding stent
WINGSPAN D: 2.5–4.5
ATLAS D: 3–4.5
SOLITAIRE D: 3–6
ENTERPRISE D: 4.5
Balloon-mounted stent
Apollo
(MicroPort
Medical,
Shanghai, China)
R-Onyx DES
ZotarolimusEluting Coronary
stent system
(Medtronic)
Acclino ex stent
(Acandis GmbH,
Pforzheim,
Germany)
Drug-eluting stent
NOVA
intracranial
sirolimus-eluting
stent system;
SINOMED
CE European conformity; FDA US Food and Drug administration; ID
internal diameter
and length
(mm)
L: 9, 15,
20
L: 15, 21,
24, 30
L:15, 20,
30, 40
L: 14, 22,
28, 37
Unspecied
D: 2.25–5
L:
8–38mm
D: 3–8
L: 15–60
Unspecied
Minimum
microcatheter
ID (inch)
Own delivery
system
0.0165 No No
0.021 or 0.027
(5 to 6 ∅)
0.021 No No
Own delivery
system
0.017 except
0.021 for 6.5
∅ and 0.027
for 8 ∅
FDA
approved
Yes Yes
No No
No No
No No
CE
approved
artery). Three-dimensional volume images and multi-planar
sectional images of the target artery are obtained and are
critical for the rest of the procedure. These images help
determine the most optimal projection for the procedure or
“working projections.” The length of the stenosis, the diameter of the healthy segments of the target vessel, as well as
the diameter of the stenosis are used to select the appropriate
devices and sizes. These images will serve as data points for
comparison and reference with future images from the procedure as well as for follow-up or retreatments.
Working projections using road maps or smart masks
allow for endovascular navigation. It is of paramount importance to always keep the tip of the guiding catheter visible on
at least one of the projections to provide feedback on access
stability throughout the procedure.
There are no randomized control trials to dictate the exact
microwire an operator should use; however, key features
286
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Table 28.2 Noncontrolled studies evaluating efciency and safety of new stents
Early outcome 1-year rates
(72h)
(72h)
(72h)
References Device Study period
Kang etal. (JNIS,
2021) [34]
Hassan etal. (Front
neurol, 2020) [35]
Mohammaden etal.
(JNIS 2022) [36]
WEAVE registry
(Stroke, 2019) [12]
Duan etal. (JNIS,
2016) [37]
Buonomo etal.
(Heliyon, 2021) [38]
Cui etal. (Front neurol,
2021) [39]
Jia etal. (JAMA
neurol, 2022) [40]
Apollo NS 159 0 0 6.3 0.6 23.4 3.1
R-Onyx October
2019–January
2020
Acclino 2010–2020 232 5.6
Wingspan 2012–2018 152 1.3
Solitaire 2010–2014 44 9.09 0 4.55 (mean
Atlas 2019–2020 10 0 0 NA NA NS NS
Enterprise 2015–2019 130 1.5
N O VA 2015–2018 263 2.3 0.8 0.8 0.8 9.5 0
Number of
patients
18 NS NS 0 0 0 0
%
Restenosis
0.9
3.7 (6month) 1.6 24.8 11.3
(72h)
1.3 NA NA NA NA
0 11.36 4.55
follow-up 25m)
0.8 4.8 0.8 14.4 3.4
Symptomatic
restenosisStroke Death Stroke Death
Q. Holay et al.
should include a soft distal tip to minimize the risk of distal
vessel perforation. Perfect visualization of distal vessels by
the operating team and a keen eye on the distal part of the
guidewire at all times are very important. The guidewire
must be adequately supportive, navigable, and compatible
with the balloon and stent one will use. An 014’ Synchro 14
(Stryker, California, USA) or Traxcess (MicroVention,
California, USA) are commonly used given its soft tip, support, and pushability. At some point, the microwire should be
exchangeable length namely 300cm.
Variations in technique for crossing the stenosis exist.
One can attempt to preload the balloon on the microwire in
the event support from a microcatheter is not needed to get
the microwire past the stenosis. If the wire crosses the stenosis with ease, you are then ready to position the wire distally
before plasty. Ideal placement is in a healthy segment of the
largest vessel in that territory. For example, if you are treating an ophthalmic segment stenosis, placing the microwire
in the M1 segment of the ipsilateral MCA would be sufcient. If you are treating an M1 stenosis, the wire would
ideally be placed in a straight segment of the larger of the
two M2 divisions. This is done in order to minimize perforation risk. Keeping the wire tip still and in the same place of
“pinning” is a skill that must be taught and learned with
great care.
In the event a microcatheter is needed for support to cross
the stenosis, the microcatheter should be used to gently cross
the stenosis once as well as a type of low-prole modied
Dotter angiocatheter plasty. If a microcatheter is used, then
an exchange maneuver is performed to exchange the microcatheter and add the balloon. Communication and teamwork
to keeping the distal wire tip in place and the system straight
are key.
Table 28.3 List and characteristics of available balloon for ICAS
treatment
Stent
diameter
and length
Product name
Gateway or
Maverick
(Stryker/Boston
Scientic)
Neuro Elutax
SV (Aachen
Resonance,
Luxembourg)
CE European conformity; FDA US Food and Drug administration; ID
internal diameter
(mm)
D: 1.5–4
L: 9, 15,
20
D: 1.5–6
L: 10–250
Minimum
microcatheter
ID (inch)
0.064 Yes Ye s
Own delivery
catheter
FDA
approved
No No
CE
approved
Pre-stenting balloon angioplasty is commonly needed.
Predilatation allows stent delivery systems to be advanced
through the stenosis without being constrained or trapped.
We generally used non-compliant angioplasty balloons varying in size from 1.5 to 2.5mm diameter. These products and
characteristics are summarized in Table28.3.
Several features need to be considered here:
– Balloons are deliberately undersized by 0.5mm diameter
to reduce the risk of arterial damage or rupture by using
angiographically obtained measurements.
– The shortest available length to fully cross the lesion was
chosen to improve balloon tracking and minimize unnec-
essary coverage of adjacent perforators when inated.
– Slow ination times were used to minimize rupture and
dissection. Balloon is generally inated until the range of
6 atmospheres, ex 1atm per 15–30s while an operator
pins the microwire in place.
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In case of satisfactory result, the balloon catheter is then
slowly withdrawn after control angiogram via an exchange
maneuver. If the wire moves forward or back, then exchange
maneuver should be halted, and the cause should be identied. Review of angiographic runs should be immediately
performed as to not miss any complication such as distal
spasm, inadvertent embolization, or vessel perforation.
(a) Stent Selection and Deployment
The stent must be of sufcient size to allow complete
apposition to the vessel lumen. In most instances we use:
– 2.5–3.5-mm-diameter stent for ICA, vertebral, and
basilar trunk stenosis.
– 2–3-mm-diameter stent for MCA stenosis.
– Once the stent is deployed, follow-up angiographic
runs are performed to assess complications and deter-
mine if post-stenting balloon angioplasty is needed.
(b) Post-stenting Balloon Angioplasty
We generally postdilate the most stenotic portion of
the stented area with a 2–3.5 mm diameter, short balloon, depending on the size of the causal vessel. A mild
residual stenosis of the target lesion (<20%) is acceptable to avoid generating excessive embolic debris and
avoid potentially severe embolic or hemorrhagic
complications.
Surgical Procedure
Based on the results of the EC/IC Bypass study (International
Cooperative Study of Extracranial/Intracranial Arterial
Anastomosis), current guidelines do not recommend
extracranial- intracranial bypass surgery in patients with
symptomatic ICAS [10, 32]. In this study, in the Bypass
group had an higher risk of stroke recurrence (44% versus
23.7%) [44].
Encephaloduroarteriosynangiosis is another surgical
procedure currently under evaluation. A phase II trial has
suggested safety and efcacy of encephaloduroarteriosynangiosis plus intensive medical management in patients
with symptomatic ICAS [45]. A phase III trial is
pending.
Follow-Up
There is no consensus regarding the optimal follow-up imaging protocol. In our current protocol, patients are seen in
clinic at approximately 3months and 1year after PTAS as
part of routine follow-up care. A modied Rankin Scale and
NIHSS scores are determined, and vascular risk factors are
managed. A brain magnetic resonance imaging and DSA are
generally performed at 3months.
Post-procedural Management
After PTAS procedure, a close monitoring of blood pressure
is done in intensive care. If the blood pressure is greater than
140mmHg systolic, intravenous antihypertensive treatment
is required to lower the risk of reperfusion injury once PTAS
has been performed.
DAPT is usually continued during 90days, and then aspi-
rin is continued alone over the long term.
Alternatives Interventional Options
Angioplasty Alone
In light of safety issues related to PTAS, balloon angioplasty
alone (i.e., without placement of an intracranial stent) has
been considered a possible alternative for endovascular therapy [42]. However, no RCTs have compared angioplasty
alone with medical therapy for stroke prevention in patients
with symptomatic ICAS. A systematic review and metaanalysis of 25 studies of angioplasty alone compared event
rates in patients treated with angioplasty to events in the
SAMMPRIS medical group and found no benet of angioplasty due to high periprocedural morbidity and mortality
[43]. Further investigations are warranted to clarify the efcacy and safety of angioplasty alone in patients with symptomatic ICAS.
Other Situations
ICAS-Related LVO
ICAD could be revealed by a large vessel occlusion (LVO).
Several criteria have been proposed to identify patients with
ICAS-related LVO: (1) absence of atrial brillation, (2) existence of stenosis in other cerebral arteries, (3) absence of CT
hyperdense sign or MRI susceptibility, (4) watershed infarction, (5) residual stenosis on DSA after several passes, or (6)
early reocclusion [32].
Acute management of this group of patients can be chal-
lenging, with the common failure of conventional mechanical thrombectomy, and commonly requires rescue therapy
with antiplatelet therapy (such as anti-GPIIBIIIA [46–48]
or cangrelor [49]), angioplasty, stenting, or a combination
of treatment modalities [50, 51]. A framework has been
proposed with antiplatelet therapy as rst-line treatment
and, in case of persistent occlusion, additional angioplasty
with or without stenting [52]. However, the safety and efcacy of these rescue treatments have not yet been established, and current evidence is largely driven by small
retrospective case series [46–51]. Again, proper validation
of the best pharmacological and mechanical strategies
through prospective randomized clinical trials is
warranted.
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