carotid artery stenting: update
TRANSCRIPT
REVIEW ARTICLE
Carotid Artery Stenting: Update
ROBERT S. DIETER & JOHN R. LAIRD
Washington Hospital Center/Georgtown University
Abstract‘‘Extracranial carotid artery stenosis is responsible for approximately 20–30% of ischemic strokes. Traditionally, carotidartery stenosis has been treated with carotid endarterectomy. However, the low periprocedural complication rate and themid term durability of carotid artery stenting has made it a competitive alternative treatment strategy. This update reviewsthe technical aspects of carotid artery stenting, clinical data supporting carotid artery stenting-particularly in high riskpatients, and the complications associated with carotid artery stenting.’’
Key Words: Carotid artery, stent, complication, procedure, trials
Introduction
Strokes represent the third leading cause of death in
the USA and the leading cause of disability in the
elderly. At five years, the mortality rate is roughly
50% with an excess of 50 billion dollars expended
annually on patients who have suffered a stroke (1).
Eighty percent of strokes are ischemic, with the
extracranial carotid artery contributing to twenty
percent of these (1). The risk of sentinel stroke
increases with stenosis severity and plaque morphol-
ogy. Symptomatic patients are at significantly higher
risk of a subsequent event than their asymptomatic
counterparts. Despite medical therapy, the risk of a
recurrent event for symptomatic patients approaches
26% at two years and 11% at five years for asympto-
matic patients (1,3). For the past five decades,
carotid endarterectomy (CEA) has been effectively
employed to reduce the risk of stroke associated with
carotid artery stenosis (4). Despite annual absolute
risk reductions of approximately 1% for asympto-
matic patients and 8% for symptomatic patients,
trials evaluating carotid endarterectomy have sys-
tematically excluded patients considered to be high
risk surgical candidates.
Multiple studies have demonstrated that ‘real-
world’ practice of stroke prevention involves patients
who would have been excluded from the major CEA
trials and are at considerable operative risk. Owing
to the co-morbidities associated with these high-risk
patients, an endovascular approach to the carotid
artery was developed in an attempt to reduce the
morbidity and mortality of the procedure. Based
upon several clinical trials in these high-risk patients,
carotid artery stenting (CAS) for the treatment of
both asymptomatic and symptomatic extracranial
carotid artery stenosis became FDA approved in the
fourth quarter of 2004.
Procedural overview of carotid artery stenting
The carotid artery is generally approached percuta-
neously from the common femoral artery. Initial
anatomic evaluation includes an aortic arch angio-
gram. This aortogram will define the atherosclerotic
burden of the aortic arch as well as the proximal arch
vessels. Furthermore, an assessment of the suitability
for cannulation of the arch vessels can be made as
well as definition of anatomic variants such as the
bovine arch. Selective extracranial carotid angiogra-
phy is performed with an emphasis on the carotid
artery bifurcation. Particular attention is given to the
internal carotid artery with regards to the potential
for positioning an embolic protection device. An
intracranial evaluation of at least the anterior
circulation should be standard both pre-intervention
and post intervention.
Patients undergoing CAS receive systemic anti-
coagulation with a goal ACT of 250 seconds or
greater. All patients should be pre-treated with dual
anti-platelet therapy (aspirin and a thienopyridine
derivative) that is continued for at least two to four
weeks post-procedure and aspirin indefinitely.
Correspondence: Robert S. Dieter, Director of Vascular Medicine, Section of Cardiovascular Medicine, Medical College of Wisconsin, 8701 Watertown Plank
Road, Milwaukee, WI 53226, USA. E-mail: [email protected]
International Journal of Cardiovascular Interventions. 2005; 7: 126–133
ISSN 1462-8848 print/ISSN 1471-1796 online # 2005 Taylor & Francis
DOI: 10.1080/14628840510039559
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Sedation is generally withheld so that accurate
neurological status can be evaluated throughout
the procedure. The use of a ‘squeeze-toy’ in the
contra-lateral hand allows for periodic neurological
assessment.
Various strategies have been employed to access
the common carotid artery with either a guiding
sheath or guide catheter. Generally, most involve the
selective wiring of the external carotid artery to
provide support while the catheter is advanced into
the common carotid artery. With stable access to the
common carotid artery, the lesion is crossed with a
distal/embolization protection device. Upon crossing
the lesion, the patient is generally pre-medicated
with atropine to help prevent the carotid baro-
receptor activation during the procedure. Lesions
are typically pre-dilated with a 4mm balloon, stented
with a self-expanding stent, and then gently post-
dilated with a 5 mm balloon. Some degree of residual
stenosis is acceptable after post dilation and overly
aggressive post-dilation is associated with increased
complications. Continuous invasive hemodynamic
monitoring during the procedure is mandatory and
significant alterations should be acutely corrected.
Finally, the embolization protection device is
removed and completion extracranial and intracra-
nial angiograms are performed.
Results from clinical trials
Randomized trials
There are four randomized clinical trials comparing
CEA to CAS. The first trial was published in
1998 and consisted of only seventeen patients.
Symptomatic patients with w70% stenosis were
prospectively enrolled and randomized to either
CEA with patching or to carotid artery stenting.
The expected enrollment was 300, but the study
was terminated early by the data safety and moni-
toring board (5). Primary stenting of the carotid
was attempted with the Wallstent (Schneider,
Minneapolis, MN) and if unsuccessful, the lesion
was pre-dilated. Of the 10 patients who underwent
CEA, none had a periprocedural TIA or CVA or
thirty day disabling CVA whereas, five of the seven
CAS patients had a periprocedural TIA/CVA and
three had a disabling CVA at 30 days. Although the
interventionalist performing the CAS was experi-
enced in the peripheral circulation, only eight prior
CAS had been performed. Furthermore, no distal
protection devices were employed.
The Wallstent trial was a multi-center, equiva-
lency trial of CEA and CAS. Two hundred and nine
symptomatic patients with 60–99% stenosis were
enrolled, 107 to CAS and 112 to CEA. The patients
were treated with the Wallstent, without distal
protection (6). The primary endpoint (ipsilateral
CVA, procedure related death, or vascular death at
one year) was reached by 12.1 and 3.6% of those
randomized to CAS and CEA, respectively
(P50.022). The rate of major CVA was 3.7 and
0.9%, respectively. The 30-day periprocedural com-
plication rate (any stroke or death) occurred in
12.1% of CAS patients and 4.5% of CEA patients
(P50.049). This study was terminated prior to the
planned 700 patient enrollment due to the inferiority
of CAS. The interventionalists in this study were
relatively inexperienced and no distal protection
devices were used.
The Carotid and Vertebral Artery Transluminal
Angioplasty Study (CAVATAS) was published in
2001. This multi-center (Europe, Australia, and
Canada) trial randomized 504 patients (principally
symptomatic) to either CEA (253) or CAS (251)
(7). Lesions had to be amenable to either CEA or
CAS; patients with significant co-morbidities (recent
myocardial infarction, poorly controlled hyper-
tension or diabetes, significant renal or pulmonary
disease) were excluded. Only 26% of patients
received a stent—either the Wallstent, Palmaz stent
(Johnson & Johnson), or the Strecker stent and no
embolic protection devices were used. The results
were essentially equivalent between the CAS and
CEA groups at thirty days (death or any CVA 10%
versus 10%, death 3% versus 2%, disabling CVA 4%
versus 4%, respectively). At one year the restenosis
rate (w70%) was 14% with 4% occlusions in the
CAS group and 4 and 1% in the CEA arm,
respectively. Although equivalency was demon-
strated, this trial is criticized for high event rates
compared to the standard NASCET and ECST
trials; furthermore, this was principally a carotid
artery, angioplasty study—since only 26% received a
stent.
The SAPPHIRE study, published in 2004, was a
randomized, multi-center non-inferiority trial of
high risk patients. Patients with high risk anatomic
or co-morbid conditions, with either symptomaticw
50% or asymptomaticw80% stenosis were rando-
mized to either CAS (n5167) or to CEA (n5167)
(8). The CAS procedure utilized the Smart or
Precise stent (Cordis) and the Angioguard or
Angioguard XP (Cordis) distal protection device.
The prespecified primary endpoint (death, CVA, or
myocardial infarction at 30 days, and death plus
ipsilateral CVA from day 31 to one year) of non-
inferiority of CAS versus CEA was reached in 12.2%
of those assigned to CAS and 20.1% assigned to
CEA, P50.004. The 30-day stroke, myocardial
infarction, or death rate was 4.8% in the CAS arm
and 9.8% in the CEA arm. In symptomatic patients,
the primary outcome was seen in 16.8 and 16.5% of
the CAS and CEA groups, respectively. In asympto-
matic patients, the rates were 9.9 and 21.5%,
respectively. The trial demonstrated both the non-
inferiority of CAS to CEA, but also that this high
risk cohort has significant event rates.
Carotid artery stenting 127
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Randomized trials underway include the National
Institute of Health sponsored Carotid Revas-
cularization Endarterectomy versus Stent Trial
(CREST). This is an on-going prospective, rando-
mized study of conventional risk patients with
symptomaticw50% carotid stenosis. All interven-
tionalists are required to have performed at least 20
procedures with the Acculink and Accunet systems
(Guidant). The Stent Protected Angioplasty versus
Carotid Endarterectomy (SPACE) trial is underway
in Germany and CAVATAS II is underway in
Europe.
Registries
Despite a limited number of prospective, rando-
mized trials there over ten carotid artery stent
registries, primarily in high-risk patients, in various
stages of completion.
There are three Acculink for Revascularization of
Carotids in High Risk Patients (ARCHeR) trials
sponsored by Guidant. ARCHeR 1 and 2 used the
over the wire Acculink and Accunet platforms
(ARCHeR 1 did not use distal protection.
ARCHeR 3 used rapid exchange systems). The
three studies involved patients with high-risk ana-
tomic or co-morbid conditions and symptomatic>
50% stenosis or asymptomatic>80% stenosis.
ARCHeR 1, 2, 3 enrolled 158, 278, and 145 patients
respectively. The 30-day combined endpoint of
death, CVA, or myocardial infarction was reached
in 7.6, 8.6, and 8.3% of patients; death 2.5, 2.2, and
1.4%; CVA 4.4, 5.8, and 6.2% in ARCHeR 1, 2,
and 3 respectively. From day 31 to one year, there
was one major and four minor strokes in ARCHeR 1
and 2. The composite endpoint of death, CVA, and
myocardial infarction within 30 days and ipsilateral
CVA to one year was 8.3% in ARCHeR 1 and 10.2%
in ARCHeR 2. A weighted historical control was
calculated based upon a similar cohort of patients if
they had undergone CEA. Based upon the risk
profile, the weighted historical control event rate if
patients underwent CEA was 14.5% (9). These
findings helped Guidant be the first company to gain
FDA approval for their carotid stent platform.
SECuRITY is a registry Study to Evaluate the
NeuroShield Bare Wire Cerebral Protection System
and Xact Stent in Patients at High Risk for Carotid
EndarTerectomY sponsored by Abbott. Patients in
this registry had symptomatic>50% or asympto-
matic>80% angiographic carotid stenosis and high
risk anatomic or co-morbid conditions. The primary
endpoint was death, all stroke, and myocardial
infarction at 30 days and any ipsilateral stroke to
one year. A total of 305 patients were enrolled after
93 lead-in patients (not included in the final
analysis) and the study was completed in February
2004. The lesion procedural success rate was 96.7%
(stent delivery—94.1% and EmboShield delivery
and retrieval—96.7%). The 30-day major adverse
event rate was 7.5%: myocardial infarction- 0.3%,
minor stroke—4.2%, major stroke 2.0%, and
death—1%. From days 31 to 365, the ipsilateral
stroke rate was 2.0% and the primary endpoint was
seen in 9.5% of the patients. The ultrasound
restenosis rate at one year was 4.1% with a 12-
month target lesion revascularization rate of 0.6%.
Although not sponsored by a device manufacturer,
nor under the same rigorous criteria and follow-up
as other registries, The Global Carotid Artery Stent
Registry provides insight into the ‘real-world’ prac-
tice of carotid artery stenting around the world. First
initiated in 1997 with 24 surveys in Europe, South
America, North America, and Asia, the Global
Carotid Artery Stent Registry, now has 53 centers
and was required in September 2002.(10) A total of
11 243 patients and 12 392 lesions are included in
the registry. The technical success was very high at
98.9%. Aproximately half of the patients were
symptomatic (53.2%). As the learning curve of
stenting progressed, there was a shift away from
balloon expandable stents to the use of self-
expanding stents with the Wallstent (Boston
Scientific, Natick, MA) and the Cordis Smart and
Precise stents (Cordis, Johnson & Johnson, Warren,
NJ) being the most commonly deployed. The 30-day
complication rates were 3.07% TIAs, 2.14% minor
strokes, 1.20% major strokes, and 0.64% deaths (per
lesion analysis) with a combined stroke and death
rate of 4.75% (of which 0.77% were not procedure
related deaths). The 30-day rate in asymptomatic
patients was 2.95% and 4.94% in symptomatic
patients.
The preliminary results from a number of other
carotid artery stenting registries have been reported
with 30-day major adverse event rates usually
between 5 and 8%. (See Table 1.)
Embolic protection devices
There will likely never be a prospective, randomized
trial comparing carotid artery stenting with and
without distal embolization protection devices
(EPDs). Studies have demonstrated that cerebral
embolization occurs during all stages of carotid
artery stenting. Analysis of the Global Carotid Artery
Stent Registry suggests that EPDs reduce the stroke
risk involved with CAS. Among the 6753 lesions that
underwent treatment without EPD, the stroke and
death rate was 6.15% whereas among the 4221
patients in which an EPD was used, the stroke and
death rate was 2.85%. This protection is seen in
the asymptomatic patients (without—4.78% death/
stroke rate, with—2.51%) and the symptomatic
patient subgroups (without—6.93% death/stroke
rate, with—3.22%). The most commonly used
EPDs in the Global Carotid Artery Stent Registry
were the PercuSurge (Medtronic, Sunnyvale, CA),
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Table 1. Summary of carotid artery stenting trials and registries (courtesy of Endovascular Today).C
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the Angioguard (Cordis) and the EPI Filterwire
(Boston Scientific).
There are essentially three types of EPDs—those
that arrest antegrade ICA flow, those that reverse
ICA flow, and the filters. (See Table 2.) The
PercuSurge GuardWire is representative of the
EPD which arrests antegrade flow. The GuardWire
has an inflatable balloon approximately 3.5 cm
proximal to the guide-wire tip that can be inflated
to 6 mm to arrest antegrade flow. The column of
blood and any debris that is dislodged during the
procedure is then aspirated and the balloon is then
deflated. With the PercuSurge inflated and the
cessation of antegrade flow, contrast injections
cannot be performed for vessel visualization. The
second class of EPD involves reversing the flow in
the ICA. Occlusive balloons are placed in the
proximal ICA as well as the ECA, blood flow is
then reversed and auto-transfused after being passed
through a filter. This is the only type of EPD that
allows crossing of the stenosis under protection. The
final category of EPDs is filters. A variety of filters
have been developed (e.g. Accunet, EmboShield, EZ
Filter, AngioGuard, Spider). There have been
several iterations of the filters to allow for easier
delivery and recovery with varying porosity of the
filter. The filters are perhaps the easiest to use and
allow for contrast injections for lesion and arterial
visualization during the procedure.
There have been no trials directly comparing the
various EPD, although there have been retrospective
studies evaluating the clinical efficacy of different
EPDs. In ex-vivo models of carotid tortuosity, the
Angioguard protection system performed the worst
while the FilterWire EX demonstrated no reduction
in efficacy in tortuous arteries (11). Clinically,
however, there has been no difference in the
outcomes when comparing various filters and
balloon occlusion devices (12). We compared the
clinical outcomes in 151 patients undergoing carotid
artery stenting at our institution—77 utilizing the
FilterWire and 74 with the PercuSurge GuardWire.
We found no difference in the periprocedural stroke
rate, in-hospital, 30-day, or six-month mortality
rate.
Although designed to minimize complications
during CAS, all EPDs have the potential for com-
plications. The PercuSurge system of arresting
antegrade flow is generally well tolerated, however,
intolerance to balloon occlusion occurs in 5–15% of
patients (13,14). Intolerance to cessation of ante-
grade flow with the balloon occlusion EPDs has a
bimodal presentation. An immediate intolerance is
usually manifested by the loss of consciousness or
seizure activity. Patients with severe contralateral
carotid, concomitant vertebral artery, or intracranial
disease may be at higher risk of this complication.
A later intolerance develops in some within a few
minutes of the procedure. This intolerance is usually
manifested by more localized neurological signs-
such as a transient neurological deficit, temporary
loss of consciousness, or agitation (13,14). Other
major complications of EPDs include arterial dis-
section and filter entrapment (14). Not uncom-
monly, EPDs result in arterial spasm. Finally, it is
important to recognize that all EPDs have the
potential of causing embolization- either while
crossing the lesion or during device deployment in
the more proximal vessel.
Complications of carotid artery stenting
Stimulation of the carotid sinus, which is located at
the carotid bifurcation, can lead to an increased vagal
tone and reduction in sympathetic tone. Clinically,
this results in bradycardia and hypotension. Variably,
between 13 and 38% of patients develop bradycardia
and 5–26% will develop hypotension (15). Sustained
hypotension and bradycardia can be seen in up to a
third of patients undergoing CAS. Hypertension in
the periprocedural period is seen in up to 40% of
patients. Patients at particular risk of complications
from the hemodynamic alterations include those with
a cardiomyopathy, severe coronary artery disease,
valvular heart disease, preload dependent states,
and those with critical contralateral or intracranial
stenosis.
Cerebral reperfusion hemorrhage can be a devas-
tating consequence to the loss of intracerebral
autoregulation and blood flow being directly propor-
tionate to mean arterial pressure. Patients thought to
be at increased risk include those with significant
contralateral carotid stenosis, history of contralateral
endarterectomy, those with significant asymmetry in
hemispheric cerebral blood flow, and those with
periprocedural hypertension (16,17). Patients may
present with a headache with or without neurological
alterations such as seizures, focal symptoms, or a
depressed level of consciousness. Rarely, contrast
encephalopathy can mimic diffuse intraparenchymal
hemorrhage.
As already discussed, although CAS is directed at
the reduction of future strokes, the procedure itself
can lead to both intracranial embolization and
hemorrhage. Intracranial hemorrhage, particularly
in the aged population that undergoes CAS, is not
only more common with the systemic anticoagula-
tion that is necessary for the procedure, but also
frequently fatal. In part because of the potential of
increased hemorrhagic complications and the lack of
proven efficacy in CAS, intravenous glycoprotein
IIb/IIIa antagonists are not routinely advised for
CAS (18). Embolization can occur during nearly any
stage of the carotid artery stenting procedure—even
diagnostic angiography carries approximately a 1%
risk of stroke. Meticulous technique is mandatory
throughout the CAS procedure and the use of distal
embolization devices should be standard.
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Table 2. Carotid artery stent device overview (courtesy of Endovascular Today).C
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The aging process can elongate the aortic arch
resulting in the great vessels originating from the
ascending aorta. Such arch types are more difficult
to engage and to perform the CAS procedure.
Proximal arch vessel disease can increase the risk
of embolization as well as vessel injury and dissec-
tion. Not uncommonly, the ICA is tortuous or has
distinct kinks or coils. Such anatomic variations or
changes with aging can make the safe landing of an
EPD difficult and the distal landing zone of the stent
can lead to distortion and translation of the kinks
cephalad with the creation of pseudolesions.
Ulcerated lesions or those filled with thrombus are
at particular risk for embolization and the approach
to these must be done with great care. Accordingly,
echolucent plaques and by inference less stable
plaques, have increased neurological complications
following CAS (19). Significant lesion calcification,
increases the risk for periprocedural complications,
(especially in the patient with renal insufficiency
who is independently at increased risk of contrast
induced nephropathy), particularly if there is a
concentric arc of calcium.
Post-intervention follow-up
Prior to initiating the CAS procedure, all patients
should be on dual antiplatelet therapy consisting of
aspirin and a thienopyridine derivative, preferably
clopidogrel due to fewer side effects compared to
ticlopidine. Although there have been no rando-
mized, placebo controlled trials of clopidogrel after
carotid artery stenting, most trials have prescribed
clopidogrel for two to four weeks after the procedure
(8). Arguably, however and neither based upon firm
clinical data nor FDA approval, dual antiplatelet
therapy should be continued indefinitely in this
high-risk cohort. Every patient requires aggressive
attention to his or her cardiovascular risk factors
(20).
As with patients who have undergone CEA, CAS
require surveillance imaging to evaluate patency and
possibly to follow a contralateral carotid artery
stenosis. A duplex evaluation should be done prior
to the patient being discharged, at six months, one
year, and then yearly thereafter. If any duplex
demonstrates lesion progression or clinical symp-
toms dictate, then more frequent carotid duplex
evaluations are recommended. There is a consider-
able amount of interest in how CAS affects the
biomechanical properties of the carotid artery.
Stenting likely changes the compliance of the carotid
artery thereby affecting the detected velocities by
ultrasound duplex examination (21). Studies corre-
lating the velocities in the carotid artery immediately
after stenting to the final angiogram and existing
duplex criteria have found that existing criteria
overestimate the stenosis severity (21). Our practice
is to downgrade the stenosis severity, based upon
duplex findings, one-grade on the side that has
undergone CAS as well as integrate the velocity
criteria with the B-mode imaging. Post CAS
intracranial evaluation with MRI or CT may be
necessary if the neurological status of the patient
changes, but otherwise routine post CAS intracra-
nial imaging is not required.
The carotid arteries are elastic (conductance)
arteries, and therefore the in-stent restenosis rate
should be low. Systematic review of 34 studies
involving 4185 patients found that the restenosis
rates (>50–70%) at one and two years were
approximately 6 and 7.5%, respectively (22).
Criteria for restenosis were heterogeneous, but these
rates are consistent with the individual CAS studies.
In the SECuRITY trial, the one year ultrasound
restenosis rate was 4.15% with a target vessel
revascularization rate of 0.6%. In the SAPPHIRE
trial, the target vessel revascularization rate was
0.7% after CAS and 4.6% after CEA. The ARCHeR
1 and 2 trials had target lesion revascularization rates
of 2.2 and 2.8%, respectively; the weighted historical
control rate was 4–7%. Risk factors for in-stent
restenosis include female gender, advanced age
(unlike after CEA), treatment for CEA restenosis
or after radiation therapy, and possibly the number
of stents implanted (23).
Training and credentialing
Most new procedures do not generate such enthu-
siastic forums regarding training and credentialing,
as has CAS. The discussion of training and
credentialing for CAS is particularly involved
because complications in the territory at risk can
be devastating. Furthermore, several disciplines with
catheter-based skills would like to perform CAS. In
an effort to form a consensus regarding training,
the Society for Vascular Medicine and Biology,
the Society for Cardiovascular Angiography and
Intervention, the Society for Vascular Surgery, the
Society for Clinical Vascular Surgery, and the
American College of Cardiology Foundation either
approved or endorsed a document outlining creden-
tialing and training processes for CAS in 2004 (24).
Since neither neuroradiology nor radiology societies
endorsed this statement, the American Heart
Association because of its policy on unanimity was
unable to as well. A complete discussion of
credentialing and reimbursement is well beyond
the scope of this review.
Conclusions
The development of CAS is a significant advance-
ment in the treatment of carotid artery stenosis.
Patients who otherwise underwent CEA with a high
surgical morbidity rate can now have the option of a
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potentially safer treatment modality for stroke
prevention. Although technically, the procedure
may be similar to others that are performed by
interventional cardiologists, the carotid artery dis-
ease and the complications of treatment are likely
somewhat unfamiliar. It is crucial that for this
procedure to move forward with continued success,
interventionalists undergo proper education into the
pathophysiology and treatment of carotid artery
disease and stroke. CAS also is an opportunity for
the development of a collaborative and multi-
disciplinary approach to patient care.
References
1. Heart Disease and Stroke Statistics—2004 Update. Dallas, Texas:
American Heart Association; 2004. #2004, American Heart
Association.
2. North American Symptomatic Carotid Endarterectomy Trial
Collaborators. Beneficial effect of carotid endarterectomy in
symptomatic patients with high-grade carotid stenosis.
N Engl J Med. 1991;325:445–53.
3. Executive Committee for the Asymptomatic Carotid
Atherosclerosis Study. Endarterectomy for asymptomatic
carotid stenosis. JAMA. 1995;273:1421–8.
4. Gray WA. A cardiologist in the carotids. J Am Coll Cardiol.
2004;43:1602–5.
5. Naylor AR, Bolia A, Abbott RJ, et al. Randomized study of
carotid angioplasty and stenting versus carotid endarterect-
omy: a stopped trial. J Vasc Surg. 1998;28:326–34.
6. Marks MJ for the publications committee of WALLSTENT.
Results of a multicenter prospective randomized trial of
carotid artery stenting vs carotid endarterectomy. Stroke.
2001;32:325.
7. CAVATAS Investigators. Endovascular versus surgical
treatment in patients with carotid stenosis in the Carotid
and Vertebral Artery Transuluminal Angioplasty Study
(CAVATAS): a randomized trial. Lancet. 2001;357:1729–37.
8. Yadav JS, Wholey MH, Kuntz RE, et al. Stenting and
Angioplasty with Protection in Patients at High Risk for
Endarterectomy Investigators. Related Articles, Links
Abstract Protected carotid-artery stenting versus endarter-
ectomy in high-risk patients. N Engl J Med. 2004;
351:1493–501.
9. Guidant Corporation. Prospective Clinical Trials for Carotid
Stenting with Embolic Protection in High Surgical Risk
Patients: The Acculink for Revascularization of Carotids in
High Risk Patients, 2004.
10. Wholey MH, Al-Mubarek N, Wholey MH. Updated review
of the global carotid artery stent registry. Catheter Cardiovasc
Interv. 2003;60:259–66.
11. Order BM, Glass C, Liess C, Heller M, Muller-Hulsbeck S.
Comparison of 4 cerebral protection filters for carotid
angioplasty: an in vitro experiment focusing on carotid
anatomy. J Endvasc Ther. 2004;11:211–18.
12. Schmidt A, Diederich KW, Scheinert S, et al. Effect of two
different neuroprotection systems on microembolization
during carotid artery stenting. J Am Coll Cardiol.
2004;44:1966–9.
13. Henry M, Henry I, Polydorou A, Polydorou A, Le Borgne E,
Hugel M. Carotid angioplasty and stenting under cerebral
protection with PercuSurge Guardwire system. J Interven
Cardiol. 2004;17:233–43.
14. Cremonesi A, Manetti R, Setacci F, Setacci C, Castriota F.
Protected carotid stenting clinical advantages and complica-
tions of embolic protection devices in 442 consecutive
patients. Stroke. 2003;34:1936–43.
15. Dieter RS, Laird JR. Defining and minimizing the risk of
complications during carotid artery interventions. In:
Henry M, et al., editors. Angioplasty and Stenting of the
Carotid and Supra-Aortic Trunks, Martin-Dunitz; 2004.
Chapter 45. London & New York.
16. Kaku Y, Yoshimura S, Kokuzawa J. Factors predictive of
cerebral hyperperfusion after carotid angioplasty and stent
placement. Am J Neuroradiol. 2004;25:1403–8.
17. Abou-Chebl A, Yadav JS, Reginelli JP, Bajzer C, Bhatt D,
Krieger DW. Intracranial hemorrhage and hyperperfusion
syndrome following carotid artery stenting: risk factors,
prevention, and treatment. J Am Coll Cardiol.
2004;43:1596–601.
18. Hofmann R, Kerschner K, Steinwender C, et al. Abciximab
bolus injection does not reduce cerebral ischemic complica-
tions of elective carotid artery stenting: a randomized study.
Stroke. 2002;33:725–7.
19. Biasi GM, Froio A, Diethrich EB, et al. Carotid plaque
echolucency increases the risk of stroke in carotid stenting:
the Imaging in Carotid Angioplasty and Risk of Stroke
(ICAROS) study. Circ. 2004;110:756–62.
20. Creager MA, Jones DW, Easton JD, et al. American Heart
Association. Atherosclerotic Vascular Disease Conference:
Writing Group V: medical decision making and therapy. Circ.
2004;109:2634–42.
21. Lal BK, Hobson RW 2nd, Goldstein J, Chakhtoura EY,
Duran WN. Carotid arteryvstenting: is there a need to revise
ultrasound velocity criteria? J Vasc Surg. 2004;39:58–66.
22. Groschel K, Riecker A, Schulz JB, Ernemann U, Kastrup A.
Systematic review of early recurrent stenosis after carotid
angioplasty and stenting. Stroke. 2005;36:367–73.
23. Dieter RS, Laird JR. General overview of restenosis in
peripheral arterial interventions. Endovascular Today.
2004;Oct:36–38.
24. Rosenfield K, Cowley MJ, Jaff MR, et al. SCAI/SVMB/SVS
Clinical competence statement on carotid stenting: training
and credentialing for carotid stenting—multispecialty con-
sensus recommendations a report of the SCAI/SVMB/SVS
writing committee to develop a clinical competence statement
on carotid interventions. Cathet Cardiovasc Interven.
2005;64:1–11.
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