Acs0610 Carotid Angioplasty And Stenting

© 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice
6 VASCULAR SYSTEM 10 CAROTID ANGIOPLASTY AND STENTING — 1

10 CAROTID ANGIOPLASTY AND
STENTING
Timothy M. Sullivan, M.D., F.A.C.S.

Choice between Carotid Endarterectomy and Carotid who were determined to be good operative risks on the basis of
Angioplasty and Stenting reasonable life expectancy (so that they would be available for fol-
low-up) and the absence of other potential causes of stroke (e.g.,
OPERATIVE RISK AND PATIENT SELECTION atrial fibrillation) [see Table 1].
For most patients with high-grade carotid lesions, whether A number of investigators have examined the results of CEA
symptomatic or asymptomatic, surgical endarterectomy [see 6:9 in high-risk subsets, albeit using several different ways of defining
Treatment Carotid Artery], rather than best medical therapy (i.e., high risk [see Tables 2 and 3].4-8 In one study, involving 776 con-
risk factor reduction and antiplatelet agents), is the treatment of secutive CEAs performed at the Mayo Clinic in Rochester,
choice for stroke prophylaxis, as the North American Sympto- Minnesota, procedures were categorized as high risk according to
matic Carotid Endarterectomy Trial (NASCET) and the Asymp- the patient inclusion and exclusion criteria employed by the
tomatic Carotid Atherosclerosis Study (ACAS) have shown.1,2 In Stenting and Angioplasty with Protection in Patients at HIgh Risk
NASCET, the risk of disabling stroke or death after carotid for Endarterectomy (SAPPHIRE) trial of CAS with cerebral
endarterectomy (CEA) was 1.9%, and the risk of minor stroke embolic protection.4 Of the 776 CEAs, 323 (42%) were consid-
was 3.9%. In ACAS, the risk of major stroke or death was 0.6% ered high risk. The clinical presentation was similar in the high-
when the 1.2% risk of stroke caused by diagnostic arteriography risk and low-risk groups.The overall postoperative stroke rate was
was excluded.These findings have led to the performance of CEA 1.4% (symptomatic, 2.9%; asymptomatic, 0.9%), and there was
in increasing numbers of patients. no statistical difference in stroke rate between the high-risk group
In the past few years, however, despite the proven efficacy of and the low-risk group. Patients at significantly increased stroke
CEA in preventing ischemic stroke, great interest has been gener- risk were those who underwent cervical radiation therapy, those
ated in carotid angioplasty and stenting (CAS) as an alternative to who had class III or IV angina, those who were symptomatic at
surgical therapy, and CEA has again come under attack.3 Pro- presentation, and those who were 60 years of age or younger.
ponents of CAS have suggested that the results of NASCET and Overall mortality was 0.3% (symptomatic, 0.5%; asymptomatic,
ACAS are not achievable in general practice outside selected cen- 0.2%), and there was no significant difference between the high-
ters of excellence. Both ACAS and NASCET included patients risk group (0.6%) and the low-risk group (0.0%). Myocardial

Table 1 High-Risk Carotid Endarterectomy as Defined by Major Exclusion Criteria for NASCET and ACAS

Exclusion Criteria

Study Comorbidities
Age History Anatomic Criteria
Cardiac Pulmonary Renal Other

Unstable angina
Uncontrolled hypertension
Contralateral CEA < 4 mo Atrial fibrillation Previous ipsilateral CEA
Renal Uncontrolled diabetes
Major surgical procedure Valvular heart mellitus Tandem lesion > target
> 79 yr Pulmonary failure failure
NASCET1 < 1 mo disease stenosis
Hepatic failure
Stroke in evolution Symptomatic
CHF Cancer with < 50%
chance of 5-yr survival
MI < 6 mo

> 180 mm Hg systolic
BP, > 115 mm Hg
Unstable angina diastolic BP Previous ipsilateral
Atrial fibrillation Fasting glucose > 400 CEA
Major surgical procedure Pulmonary failure
ACAS2 > 79 yr < 1 mo Valvular heart with impact on 5-yr SCr > 3 mg/dl Tandem lesion > target
disease survival mg/dl Hepatic failure stenosis
Stroke in evolution
Symptomatic Cancer with < 50% Cervical radiation
CHF chance of 5-yr survival treatment
Active ulcer disease
Warfarin anticoagulation

ACAS—Asymptomatic Carotid Atherosclerosis Study BP—blood pressure CEA—carotid endarterectomy CHF—chronic heart failure MI—myocardial infarction NASCET—North
American Symptomatic Carotid Endarterectomy Trial SCr—serum creatinine concentration

1


Table 2 High-Risk Carotid Endarterectomy as Defined by Major Inclusion Criteria for Selected Studies

Inclusion Criteria

Study Comorbidities
Age History Anatomic Criteria
Cardiac Pulmonary Renal Other

Ouriel (2001)5 PTCA or CABG < 6 mo Severe COPD SCr > 3
History of CHF mg/dl

Coronary procedure < 1 mo Previous ipsilateral CEA
CABG < 6 wk Cervical radiation treatment
Jordan (2002)6 Major vascular proce- FEV1 < 1 L
Angina NYHA class III or IV Contralateral carotid occlusion
dure < 1 mo Home oxygen
EF < 30% High cervical lesion
MI < 4 wk Lesion below clavicle

NYHA functional class III or IV Previous ipsilateral CEA
Heart failure Canadian class Steroid dependence SCr > 3 Cervical radiation treatment
Gasparis (2003)7 ≥ 80 yr mg/dl
III or IV Oxygen dependence Contralateral carotid occlusion
CABG < 6 mo High cervical lesion

Open heart surgery < 6 wk Previous ipsilateral CEA
MI < 4 wk Severe tandem lesion
Angina CCS class III or IV Cervical radiation treatment
SAPPHIRE8 > 80 yr CHF class III or IV Contralateral carotid occlusion
EF < 30% High cervical lesion (at least C2)
Abnormal cardiac stress test Lesion below clavicle
result Contralateral laryngeal palsy

CABG—coronary artery bypass graft CCS—Canadian Cardiovascular Society CEA—carotid endarterectomy CHF—congestive heart failure COPD—chronic obstructive pulmonary
disease EF—ejection fraction FEV1—forced expiratory volume in 1 sec MI—myocardial infarction NYHA—New York Heart Association PTCA—percutaneous transluminal coronary
angioplasty SAPPHIRE—Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy SCr—serum creatinine concentration

infarction (MI) was more frequent in the high-risk group (3.1%) tive pulmonary disease (COPD), or the development of renal
than in the low-risk group (0.9%); notably, all of the MIs report- insufficiency [see Table 2]. For the composite end point of stroke,
ed in this series were nontransmural (non-Q). A composite cluster death, and MI, the rate was 3.8% in the group as a whole (stroke,
of adverse clinical events (death, stroke, and MI) was more fre- 2.1%; MI, 1.2%; death, 1.1%); however, the rate was 7.4% in
quent in the symptomatic high-risk group (9.3% versus 1.6%), high-risk patients, compared with only 2.9% in low-risk patients.
but not in the asymptomatic cohort. There was a trend toward a High-risk patients were further subdivided into those who under-
higher incidence of major cranial nerve injuries in patients with went CEA alone and those who underwent CEA combined with
local risk factors (e.g., high carotid bifurcation, reoperation, and coronary artery bypass grafting (CABG). Not surprisingly, the
cervical radiation therapy) (4.6% versus 1.7%). In 121 patients incidence of the composite end point was greater in the latter sub-
who were excluded on the basis of synchronous or immediate subgroup than in the former. Among patients who underwent CEA
sequent operations (and who would also have been excluded from
SAPPHIRE), the overall rates of stroke (1.65%), death (1.65%),
and MI (0.83%) were not significantly different from those in the
study population. The authors concluded that SAPPHIRE-eligi-
Table 3—SAPPHIRE Exclusion Criteria for
ble high-risk patients could undergo CEA with stroke and death Defining High-Risk Carotid Endarterectomy8
rates that were well within accepted standards and that patients Acute stroke (≤ 48 hr)
with local risk factors were at higher risk for cranial nerve injuries Staged elective procedure (within 30 days after CEA)
but not necessarily for stroke.These conclusions call into question Elective percutaneous intervention
the application of CAS as an alternative to CEA, even in high-risk Contralateral CEA
patients. Other elective operation
Although these studies do not support the premise that opera- Synchronous operation
CCA angioplasty/stenting or bypass
tive risk is higher in patients who would be excluded by NASCET
Cardiac operation
and ACAS criteria, there may in fact be categories of patients for
Noncardiac operation
whom CEA is not optimal therapy.A 2001 study from the Cleveland Intracranial pathology
Clinic attempted to identify a subgroup of patients who, on retro- Intracranial mass
spective analysis, were at increased risk for CEA and therefore Aneurysm > 9 mm
might be better served by CAS.5 A total of 3,061 carotid endar- Arteriovenous malformation
terectomies were examined from a prospective database covering Ventriculoperitoneal shunt
a 10-year period. A high-risk cohort was identified on the basis of
CCA—common carotid artery CEA—carotid endarterectomy
the presence of severe coronary artery disease, a history of conges-
tive heart failure (CHF), the presence of severe chronic obstruc-


Reasonable criteria for patients at increased risk for CEA have
Table 4—Indications for Carotid Angioplasty been developed, and these criteria may serve as a general guide for
and Stenting in High-Risk Patients those embarking on a program of carotid stenting [see Table 4].
Relative contraindications to CAS have also been determined [see
Severe cardiac disease Table 5]. CAS should be performed by physicians with a thorough
Requirement for PTCA or CABG knowledge of the pathophysiology and natural history of carotid
History of CHF disease and by those with current expertise in peripheral, cardiac,
Severe chronic obstructive pulmonary disease or neurointerventional procedures. If a physician is unable to par-
Requirement for home oxygen
ticipate in FDA-approved trials, the procedure should be per-
FEV1 < 20% of predicted
Severe chronic renal insufficiency
formed as part of a local Institutional Review Board (IRB)–approved
Serum creatinine concentration > 3.0 mg/dl protocol with dispassionate oversight, independent preprocedural
Patient currently on dialysis and postprocedural neurologic examination, and prospective case
Previous CEA (restenosis) review. In addition, development of a carotid stenting program
Contralateral vocal cord paralysis may facilitate cooperation among the various specialists who may
Surgically inaccessible lesions desire to participate in this high-profile arena. A team of experi-
Lesion at or above C2 enced personnel should be assembled (including one or two physi-
Lesion inferior to clavicle cians and a technician) to ensure patient safety, maximize expo-
Radiation-induced carotid stenosis sure within a small cadre of operators, and avoid duplication of
Previous ipsilateral radical neck dissection
effort. All patients considered for CAS should have provided in-
formed consent, should receive counseling regarding the risks and
benefits vis-à-vis CEA and best medical therapy, and should pos-
alone, the risk of death was significantly greater in the high-risk sess a clear understanding of the investigational nature of the pro-
group. Notably, although the risk of the combined end point was cedure. In addition, patients must agree to regular and careful fol-
greater in the high-risk group, the difference was not statistically low-up examinations.
significant. In addition, the rates of the individual end points of MI
and stroke did not differ statistically between the high-risk group
and the low-risk group. Anatomic Considerations
These data appear to support the notion that the patients A solid grasp of the anatomy of the cerebral circulation is cru-
enrolled in the multicenter trials of CEA (i.e., NASCET and cial for the planning of CAS. Several anatomic considerations are
ACAS) were probably similar to the Cleveland Clinic’s low-risk particularly germane. The first important anatomic issue to ad-
group and that the patients in the Clinic’s high-risk group might not dress is the configuration of the aortic arch. With advancing age,
have had such stellar outcomes if they had been included in those the apex of the arch tends to become displaced further distally.
multicenter endarterectomy trials. Subsequent clinical investiga- This displacement makes selective catheterization of the brachio-
tions have therefore focused on medically compromised, high-risk cephalic vessels more challenging and influences the choice of a
patients who may benefit from alternatives to CEA (e.g., CAS). catheter.The interventionalist should become familiar with a vari-
ety of selective catheters; I prefer the Simmons II catheter, which
INDICATIONS FOR CAROTID ANGIOPLASTY AND STENTING
allows deep cannulation of the common carotid artery (CCA) and
The basic indications for CAS are essentially the same as those thus facilitates eventual passage of a guide wire for delivery of a
for standard open CEA: sheath. As the level of the vessel’s origin becomes farther from the
dome of the arch, the task of obtaining guide-wire and sheath access
1. Asymptomatic lesions that fall within the high-grade steno-
becomes more difficult. Cannulation of a left CCA arising from a
sis (typically, 80% to 99%) range on duplex ultrasonography,
common brachiocephalic trunk (bovine arch) may be particularly
which correlates with a stenosis of at least 60% on angiogra-
phy [see 6:2Asymptomatic Carotid Bruit]. Most clinical trials
of CAS in asymptomatic patients require an angiographic
stenosis of at least 80% for study inclusion.
2. Symptomatic lesions (e.g., hemispheric transient ischemic Table 5—Limitations of and Contraindications
attack [TIA], amaurosis fugax, or stroke with minimal resid-
to Carotid Angioplasty and Stenting
ua) with a stenosis of at least 70% on angiography [see 6:1
Stroke and Transient Ischemic Attack]. Symptomatic patients Inability to obtain femoral artery access
who have greater than 50% stenoses with ulceration may Unfavorable aortic arch anatomy
benefit from endarterectomy; however, this finding has not Severe tortuosity of CCA or ICA
yet been extrapolated to carotid intervention. Severely calcified or undilatable stenoses
Lesions containing fresh thrombus
At present, there is a paucity of data on the safety and efficacy Large amount of laminated thrombus at site of patch angioplasty
of CAS from well-controlled studies. Accordingly, my use of CAS (previous CEA) on duplex ultrasonography
to date has been limited to treatment of patients judged to be at Extensive stenoses (> 2 cm)
high risk for CEA. Such patients account for 10% to 20% of all Critical (≥ 99%) stenoses
Lesions adjacent to carotid artery aneurysms
patients undergoing intervention (open or endovascular) for
Contrast-related issues
carotid disease in the Division of Vascular Surgery at the Mayo
Chronic renal insufficiency
Clinic. Symptomatic patients with greater than 50% angiograph- Previous life-threatening contrast reaction
ic stenosis and asymptomatic patients with greater than 80% Preload-dependent states (e.g., severe aortic valvular stenosis)
angiographic stenosis are considered for intervention, either surgi-
cal or percutaneous.


difficult to accomplish. Problematic arch configurations should be and more efficient, thereby serving the main goals of therapy—
identified on preprocedural contrast studies or magnetic reso- patient safety and exemplary results.
nance angiography (MRA) of the aorta. Especially at the begin- In all cases, a thorough history should be taken and a careful
ning of an operator’s experience with these interventions, a com- physical examination performed, with close attention paid to
plete study that includes the aortic arch and the origins of the bra- comorbid medical conditions and femoral pulses. A complete neu-
chiocephalic trunks is essential. rologic examination should be performed by a certified neurolo-
Another important issue is the presence of any tandem lesions gist. In addition to preprocedural arteriography or MRA, duplex
along the course of the cerebral circulation. If a proximal CCA ultrasonography should be performed in an accredited vascular
lesion is present, intervention may be required before revascular- laboratory—ideally, the same laboratory where the follow-up
ization of the internal carotid artery (ICA) to provide safe access examinations will be performed. In my practice, patients receive
to the ICA. A third concern is the tortuosity of the ICA. Fortun- aspirin, 325 mg daily for at least 1 week before the procedure, and
ately, most ICAs are relatively straight; however, some patients do clopidogrel, 75 mg daily for at least 3 days beforehand. All patients
have extremely tortuous ICAs, which may preclude safe passage of receive antibiotics (typically cefazolin, 1 g I.V.) immediately before
a guide wire or protection device and thus render safe intervention the procedure.
impossible. The anatomic configuration of the external carotid
artery (ECA) typically is not an important consideration in carotid
intervention, even when this vessel is affected by stenosis of iatro- Operative Planning
genic origin or is covered with a bare stent. Regardless of the exact physical location at which the procedure
Finally, the collateral circulation (or lack thereof) through the is performed, access to high-quality imaging equipment is manda-
circle of Willis is an important consideration that may profound- tory; portable C-arms are less than ideal for this purpose. I per-
ly influence procedural strategy. The status of the contralateral form CAS in a neuroradiology suite, which has the advantage of
ICA, the vertebral-basilar system, and the intracranial collaterals offering biplane imaging. With this arrangement, duplication of
may affect the type of embolic protection to be used. Anatomic effort and equipment is avoided, and the room is staffed by knowl-
variations in the circle of Willis are actually the rule rather than edgeable personnel, including a certified registered nurse anes-
the exception: a complete circle is present in fewer than 50% of thetist (CRNA), who monitors the patient with continuous electro-
all cases. Common variations include a hypoplastic (10%) or cardiography, blood pressure, and pulse oximetry readings. Patients
absent A1 segment of the anterior cerebral artery and a plexi- are placed in a supine position, and both groins are prepared.The
form (10% to 33%) or duplicated (18%) anterior communicat- head is placed in a cradle and gently secured to minimize patient
ing artery. Anomalies of the posterior portion of the circle of motion during critical portions of the procedure.The procedure is
Willis, including a hypoplastic (33%) or absent posterior com- generally performed with the patient awake, though minimal seda-
municating artery, occur in about 50% of all cases. During pre- tion is acceptable if the patient is particularly anxious.
procedural angiography or intracranial MRA, careful attention
should be paid to the anterior and posterior communicating
arteries. Patients with limited collateral circulation may exhibit Operative Technique
reversible neurologic symptoms during inflation of a protective The technique of CAS has evolved over time. In its current iter-
balloon or angioplasty of the target lesion. They may also be ation, the procedure is performed in the following steps, with few
at higher risk for permanent neurologic deficits because their exceptions. Although it is, of course, essential to be able to adjust
limited collateral blood supply is less likely to be able to com- the technical approach to deal with unanticipated situations, it is
pensate for any iatrogenic arterial occlusions that may compli- nonetheless desirable to standardize the procedure as much as
cate the procedure. possible.
Basic principles of endovascular surgery are discussed more
fully elsewhere [see 6:8 Fundamentals of Endovascular Surgery]; the
Preoperative Evaluation following steps focus primarily on the procedural elements specif-
For those with limited experience in carotid intervention, ic to CAS.
diagnostic angiography of the arch, the carotid arteries, and the
STEP 1: SECURING OF ARTERIAL ACCESS
cerebral arteries (done well in advance of the proposed interven-
tion) is suggested; high-quality MRA that includes the aortic Retrograde femoral access is obtained, and a 5 French sheath is
arch is an acceptable substitute. This measure allows the inter- inserted. Full heparin anticoagulation (typically 100 mg/kg body
ventionalist to make a careful, unhurried evaluation of the aortic mass) is instituted after arterial access is secured and before mani-
arch and the brachiocephalic origins, which is essential for pulation of catheters in the aortic arch and the brachiocephalic
determining the ease or difficulty of sheath or guide access to the vessels.
CCAs—an issue that has a direct bearing on the success of the
STEP 2: SELECTIVE CAROTID CATHETERIZATION
procedure. If the brachiocephalic trunk (i.e., the innominate
AND ARTERIOGRAPHY
artery) or the left CCA originates in a location more than two
CCA diameters (approximately 2 cm) below the dome of the After selective catheterization of the midportion of the ipsilater-
aortic arch, some difficulty with access should be anticipated. In al CCA (typically with a Simmons II catheter), a selective arterio-
addition, the length of the lesion, the maximum degree of steno- gram of the carotid bifurcation is obtained, with care taken to choose
sis, and the diameters of the CCA and the ICA can be deter- a view that yields minimal overlapping of the ICA and the ECA
mined by placing a radiopaque marker of known diameter in the and maximal visualization of the target lesion. A complete cerebral
field of view; ball bearings of progressively increasing diameter (2 arteriogram, if not previously obtained, is obtained at this point to
through 7 mm) are ideal for this purpose. These measurements serve as a baseline and to identify any intracranial pathologic con-
facilitate preprocedural selection of appropriately sized balloons ditions (e.g., aneurysms and arteriovenous communications) that
and stents and make performance of the procedure smoother may be present.


STEP 3: ADVANCEMENT OF SHEATH AND DILATOR INTO The second technique is to use a variable-diameter wire (0.018
COMMON CAROTID ARTERY in. at the tip, enlarging to 0.035 in. more proximally) to cross the
Two techniques have been employed to advance a sheath into internal carotid lesion, providing additional guide-wire support to
the CCA. The first technique—which I prefer—is to place an ex- facilitate sheath advancement. This approach is a reasonable
change-length guide wire into the terminal branches of the ECA. option, but it ultimately necessitates crossing the target lesion
I generally use a stiff, angled glide wire (keeping in mind that twice.
sheath exchange over this highly slippery wire can be tricky). The STEP 4: REMOVAL OF GUIDE WIRE AND DILATOR AND
diagnostic catheter and the 5 French sheath are removed (with SELECTIVE ARTERIOGRAPHY OF CAROTID BIFURCATION
constant visualization of the guide wire in the ECA maintained all
the while). A long (70 to 90 cm, depending on patient body habi- Once the sheath is in place, the guide wire and the dilator are
tus) 6 French sheath is then advanced, along with its dilator, into removed.The sheath sidearm may be attached to a slow, continu-
the CCA. If larger (> 8 mm in diameter) stents are required, a 7 ous infusion of heparin-saline solution to keep blood from stag-
French sheath may be necessary to allow contrast injection around nating in the sheath. Selective angiography of the carotid bifurca-
the stent delivery system. Care must be taken to identify the tip of tion is then performed through the sheath, again demonstrating
the dilator (which is not radiopaque) because it may extend a sig- the area of maximal stenosis, the extent of the lesion, and the nor-
mal ICA and CCA above and below the lesion. Roadmapping, if
nificant distance from the end of the sheath, depending on the
available, is helpful in crossing the lesion with an embolic protec-
brand of sheath used. Obviously, inadvertently advancing the dila-
tion device or guide wire [see Step 6, below]. The overwhelming
tor into the carotid bulb may have disastrous consequences. In
majority of procedures are now performed with the aid of an
patients with short CCAs or low bifurcations, the sheath can be
embolic protection device, typically a filter [see Figure 1].
advanced over the dilator once the sheath edge (a radiopaque
marker) is past the origin of the CCA. STEP 5: MEASUREMENT OF ACTIVATED CLOTTING TIME
The second technique is to advance the long sheath into the
It is advisable to measure the activated clotting time (ACT)
transverse arch over a guide wire. The dilator is removed, and an
before crossing the lesion and performing CAS. If balloon occlu-
appropriate selective diagnostic catheter is advanced into the
sion of the ICA is being used for embolic protection, an ACT
CCA. This catheter must be substantially longer than the sheath,
longer than 300 seconds is desirable. If a filter-type device or a
typically more than 100 cm long. A stiff guide wire is then
standard guide wire is being used, an ACT longer than 250 sec-
advanced into the ECA. Both the wire and the catheter are pinned onds is probably sufficient. The interventional team should dis-
at the groin to provide support, and the sheath (without the dila- cuss, in detail, all the subsequent steps to be performed so that all
tor) is advanced into the CCA. This technique may be advanta- members are on the same page. Balloons are flushed and pre-
geous in so-called hostile arches, in that the catheter and the wire pared, and special care should be taken to remove all air from the
provide more support than a wire alone would; however, without system as a protective measure against the unlikely event of bal-
the protection of the sheath dilator, there is a risk of “snowplow- loon rupture.The stent is opened and placed on the table, and the
ing” the edge of the sheath at the junction of the aortic arch and crossing guide wire or embolic protection device is prepared. For
the innominate artery or the left CCA, which can cause dissection de novo lesions, I typically administer atropine (0.5 to 1.0 mg I.V.)
or distal embolization. as prophylaxis against bradycardia during balloon inflation in the
The importance of gaining and maintaining sheath access to the carotid bulb; for restenoses after CEA, this measure may not be
distal CCA should not be underestimated: once the 0.035 in. necessary.The monitoring nurse or CRNA should be alerted that
guide wire is removed (and, eventually, exchanged for a 0.014 in. balloon inflation may cause significant hemodynamic instability.
wire), support for angioplasty and stent placement is provided
solely by the sheath. If the sheath backs up into the aortic arch STEP 6: ADVANCEMENT OF GUIDE WIRE ACROSS LESION
during the interventional procedure, it is virtually impossible to The guide wire or embolic protection device (0.014 in.) is
advance it into the CCA over a 0.014 in. guide wire or protection advanced across the lesion with the aid of roadmapping (if avail-
device. Appropriate patient selection and accurate recognition of able). Care should be taken when the device is inserted through
which arches to avoid are essential for success. In particularly dif- the sheath valve because the tip can be damaged at this juncture.
ficult arches, deep inspiration or expiration may facilitate sheath If a protection device is being used, it should be deployed into the
advancement by subtly changing the configuration of the brachio- distal extracranial ICA, just before the horizontal petrous segment.
cephalic origins once guide-wire access has been obtained. Alter- For balloon-occlusion devices, absence of flow in the ICA must be
natively, when a sheath cannot be advanced into the CCA, a pre- demonstrated. For filter devices, apposition of the device to the
shaped guide catheter can be seated in the proximal CCA. Al- ICA must be documented, along with flow in the ICA through the
though this maneuver may facilitate an otherwise impossible inter- device; these should also be documented after each subsequent
vention, it should be kept in mind that guide catheters provide a step of the intervention to detect possible occlusion of the filter by
less stable support platform than sheaths do and should be used debris.
only if there is no other reasonable alternative.
STEP 7: PREDILATION OF LESION
Troubleshooting
The lesion is predilated with a 5.0 mm angioplasty balloon, typ-
In patients with an occluded ECA, sheath access to the CCA ically on a monorail or rapid-exchange platform.To save time, the
may be difficult to obtain. Two techniques may be employed to balloon can be advanced into the distal CCA before the lesion is
overcome this difficulty. The first is to place a stiff 0.035 in. wire crossed with the guide wire or protection device. In most cases, the
with a preshaped J into the distal CCA, taking care to avoid the desired balloon profile can be achieved with relatively low inflation
bulb and the bifurcation.The J configuration keeps the guide wire pressures (4 to 6 mm Hg). After the predilation balloon is re-
from crossing the lesion. A stiff wire with a shapable tip can be moved, another bifurcation angiogram is performed through the
used to the same end. sheath (unless distal balloon occlusion is employed, in which case


a b c

d e

Figure 1 Carotid angioplasty and stenting. In this example, a filter device is used
for cerebral protection. (a) MRA shows aortic arch and cervical carotid and vertebral
arteries. (b) MRA shows recurrent (postendarterectomy) high-grade stenosis of right
ICA. (c) Selective angiogram shows right carotid bifurcation. (d) FilterWire EX (Boston
Scientific, Natick, Massachusetts) is deployed within ICA; angiographic assessment is
performed in two planes (left, right) to confirm adequate apposition of filter to vessel wall
(arrows). (e) Shown is vessel after angioplasty and placement of self-expanding nitinol
stent. Sheath is properly positioned in distal CCA (star). Spasm may be seen at site of
filter (arrow).

the ICA will not be visualized and the distal stent must be placed operator to miss the target lesion.To counter this tendency, I typ-
according to predetermined bony landmarks and the location of ically expose and deploy two or three stent rings, then wait for 5
the CCA bifurcation). to 7 seconds, allowing the distal stent to become fully expanded,
well apposed to the ICA, and attached to the vessel wall above the
STEP 8: DEPLOYMENT OF STENT
lesion. I can then deploy the remainder of the stent more rapidly,
Once correct positioning has been confirmed, the stent is with little worry that it will migrate.
deployed. Currently, I prefer to use nitinol stents, most common- The diameter of the stent is determined by the diameter of the
ly extending an 8 to 10 mm × 30 mm stent from the ICA into the largest portion of the vessel, which is typically the distal CCA (not
CCA and covering the origin of the ECA. Nitinol stents exhibit a the ICA). It is important that there be no unapposed stent in the
tendency to “jump” distally when deployed rapidly (despite man- CCA: any part of the stent that is not apposed to the vessel wall
ufacturers’ claims to the contrary), and this jump may cause the may become a nidus for thrombus formation.The diameter of the


unconstrained stent should be at least 10% (approximately 1 to 2 been described, but the majority of strokes are attributable to cere-
mm) larger than the maximum diameter of the CCA. On occasion, bral embolization of atheromatous debris or thrombus. Even when
the lesion is limited to the ICA well above the carotid bifurcation; cerebral emboli do not produce a major stroke, they may cause
in such cases, a shorter stent confined to the ICA may be used. substantial cognitive impairment. A prospective study of 100
patients monitored with transcranial Doppler ultrasonography
STEP 9: POSTDILATION OF LESION
(TCD) during CEA found that microemboli were detected dur-
If necessary, the lesion is postdilated with a 5 or 5.5 mm bal- ing 92% of procedures.9 Although most of the emboli were air
loon; larger balloons are rarely necessary. As noted [see Step 7, emboli (and were not associated with adverse clinical events),
above], I currently prefer to use a relatively large balloon (5 mm) there were more than 10 particulate emboli whose presence was
for predilation so as to obviate postdilation if possible. A residual correlated with significant deterioration of postoperative cognitive
stenosis of 10% or so is completely acceptable; the goal of the function.
intervention is protection from embolic stroke, not necessarily a A subsequent study evaluated 70 patients who underwent car-
perfect angiographic result. diac surgery with cardiopulmonary bypass, measuring cognitive
function at 1 week, 2 months, and 6 months after operation; elder-
STEP 10: COMPLETION ARTERIOGRAPHY
ly patients who underwent urologic surgery served as the control
A completion angiogram of the carotid bulb and bifurcation group.10 TCD detected more than 200 emboli in 40 patients, prin-
and the distal extracranial ICA is obtained before wire removal to cipally during aortic clamping and release, when bypass was initi-
verify that no dissection or occlusion has occurred. Severe vaso- ated, and during defibrillation. Emboli were associated with sig-
spasm may be encountered (sometimes mimicking dissection); nificant memory loss. In addition, cognitive function deteriorated
watchful waiting, coupled on occasion with administration of more in the study group than in the control group, though it
vasodilators through the sheath (e.g., nitroglycerin in 100 µg recovered by 2 months after operation.
aliquots), usually resolves this problem. Sometimes, the wire must A study using a rat model examined the effect of atheroemboli
be removed before vasospasm will resolve completely, but this of varying sizes on neuronal cell death.11 The animals exposed to
should be done only after dissection is excluded. After the wire is particles less than 200 µm in diameter showed no evidence of
removed, completion angiography of the carotid and intracranial brain injury at 1 and 3 days, whereas those exposed to particles
circulation is performed in two views. between 200 and 500 µm showed a scattered pattern of neuronal
cell death at necropsy. At 7 days after embolization, however, both
STEP 11: ACCESS-SITE HEMOSTASIS
groups showed evidence of cell death.These findings suggest that
Heparin anticoagulation typically is not reversed. Access-site whereas the brain may have a substantial tolerance for small
hemostasis is achieved with a percutaneous closure device. emboli in the acute setting, even particles smaller than 200 µm
may cause neuronal ischemia at a later point.
Postoperative Care Angioplasty and Carotid Embolization
After the procedure, the patient is monitored in the recovery Various studies have assessed the embolic potential of carotid
area for approximately 30 minutes, then transferred to a moni- plaques in ex vivo models. One such study, which used specimens
tored floor; admission to an intensive care unit generally is not of human atherosclerotic plaque in a flow chamber to model CAS,
necessary. In 2 to 3 hours, patients are allowed to ambulate if a clo- found that substantial numbers of particles were released from the
sure device was used and are allowed to resume a regular diet. lesions during angioplasty and that most of these particles were
Some patients experience prolonged hypotension from carotid captured by an experimental filter device.12 The filter device itself
sinus stimulation; this problem can be managed with judicious produced very few particles, thanks to its low crossing profile.
fluid administration, pharmacologic treatment of bradycardia, A subsequent study also addressed the embolic potential of
and, occasionally, I.V. infusion of a vasopressor (e.g., dopamine). human carotid plaques during experimental angioplasty.13 An
Rarely, a patient experiences prolonged hypotension that must be average of 133 emboli per angioplasty were measured, and there
treated with an oral agent (e.g., phenylephrine or midodrine). was a positive correlation between lesion severity and the maxi-
A duplex ultrasonogram is obtained before hospital discharge mum size of the embolic particles. A notable finding was that
as a baseline study; the criteria for stenosis and restenosis change patients who had been placed on statin therapy more than 4 weeks
after placement of a metal stent in the carotid artery. Subsequent before operation had significantly fewer and smaller emboli.
ultrasound examinations are performed at 6 weeks, 6 months, and A clinical study that employed a distal balloon-occlusion system
1 year, then yearly thereafter. Neurologic evaluation is performed during CAS found that the median number of particles, their
according to the same schedule as the duplex studies. Patients are maximum diameter, and their maximum area were all significant-
treated with aspirin for life and with clopidogrel for 4 to 6 weeks. ly higher in patients with periprocedural neurologic complica-
As with carotid endarterectomy, proper patient selection, pro- tions.14 Three procedural steps are associated with an increased
cedural standardization, and meticulous attention to detail are risk of embolization: predilation, stent deployment, and postdila-
mandatory for a successful procedure, regardless of the exact tech- tion [see Operative Technique, Steps 7, 8, and 9, above].15
nique used for CAS.
Devices for Cerebral Embolic Protection
The use of embolic protection in large numbers of patients has
Special Considerations been described with respect to the coronary vascular bed, where
interventional procedures performed on diseased aortocoronary
CEREBRAL PROTECTION
saphenous vein grafts carry a 20% risk of periprocedural compli-
Ischemic stroke remains the most devastating complication of cations, largely related to distal embolization of atheromatous
procedures directed at the extracranial carotid artery, whether debris. The Saphenous vein graft Angioplasty Free of Emboli
open or endovascular. A number of different causes of stroke have Randomized (SAFER) trial was the first multicenter randomized


a b c

d e

Figure 2 Carotid angioplasty
and stenting. In this example, a
balloon occlusion device is used
for cerebral protection. (a) MRA
shows aortic arch and cervical
carotid and vertebral arteries.
(b) MRA shows de novo athero-
sclerotic stenosis of right ICA.
(c) Diagnostic arteriogram of
right carotid bifurcation in a
symptomatic patient shows tan-
dem ulcerated stenoses. (d) Right
ICA is occluded with PercuSurge
GuardWire device. (e) Shown is
vessel after angioplasty and place-
ment of nitinol stent.

study to evaluate the use of distal embolic protection during Three types of embolic protection—distal balloon occlusion,
saphenous vein graft interventions.16 Of the 801 eligible patients, distal filter protection, and reversal of ICA flow—are currently
406 were randomly assigned to angioplasty and stenting with dis- available for use in the carotid artery, either as part of an FDA-
tal balloon protection and 395 to angioplasty and stenting over a approved clinical trial or as an “off-label” application of a device
conventional guide wire.The composite primary end point (death, approved for noncarotid use. A 1987 study was the first to report
MI, emergency coronary bypass, target lesion revascularization) on the use of an angioplasty technique involving temporary occlu-
was reached in 16.5% of the control group and 9.6% of the study sion of the internal carotid artery during manipulation of ulcerat-
group; the differences between the two groups were largely driven ed plaques.18 The same investigators subsequently reported on the
by decreases in MI and distal embolization.These dramatic results use of a triple-coaxial catheter system for angioplasty with cerebral
suggest that patients with lesions of high embolic potential (e.g., protection in 13 patients19; cholesterol crystals ranging in size from
those at the carotid bifurcation) may benefit from some type of 600 to 1,200 µm were aspirated at the time of intervention. The
embolic protection. A 2000 study using an ex vivo model of angio- PercuSurge GuardWire (Medtronic AVE, Santa Rosa, California),
plasty confirmed the findings of other investigators that emboli which is approved for aortocoronary saphenous vein graft inter-
occur at several stages of carotid intervention and stressed that vention, has been used in the MAVERIC trial of carotid interven-
cerebral protection techniques should be effective from the earli- tion and has been employed extensively for off-label carotid inter-
est stages of the procedure.17 vention outside FDA-approved clinical trials [see Figure 2]. The


advantages of this device include its low profile (which allows it to The evidence accumulated to date suggests that most, if not
cross the target lesion easily), its procedural simplicity, and its abil- all, CAS procedures should be performed with a cerebral embol-
ity to aspirate large debris particles after intervention. The disad- ic protection device. In time, more such devices will be approved
vantages include the potential for incomplete occlusion of the ICA by the FDA and will be available outside the setting of clinical
in patients with particularly large arteries (because the device can trials.
be inflated only from 3 mm to 6 mm in diameter) and the device’s
inability to aspirate exceptionally large particles into the suction
catheter after intervention.14 In addition, as flow is diverted into Outcome Evaluation
the ECA, emboli may travel by this route and into the ipsilateral The short-term results of CAS depend largely on the presence
middle cerebral artery via periorbital and ophthalmic artery col- or absence of cerebral embolization. It is therefore not surprising
laterals.20 Finally, a small percentage of patients with an incom- that the addition of cerebral protection to CAS appears to have
plete circle of Willis and an isolated cerebral hemisphere may be reduced the stroke risk associated with the procedure. Admittedly,
intolerant of even temporary ICA occlusion. A 2002 study that however, ongoing technological developments have created some-
evaluated the PercuSurge device in 75 CAS procedures found that thing of a moving target, making evaluation of the results of CAS
four patients (5%) experienced transient neurologic symptoms difficult at best. Nevertheless, the available literature is sufficient
during balloon occlusion that resolved with deflation and restora-
tion of internal carotid flow.21 Embolic material was aspirated
from the ICA in all patients; no patients had suffered major or
minor stroke at 30 days after the intervention.
Table 6 Results of Carotid Angioplasty and Stenting
Filter protection devices have been the object of a great deal of
Combined
interest in the past few years. Such devices are designed to be able Study Arteries (N) Symptomatic Cerebral Stroke-Death
to trap large particulate debris while maintaining flow in the ICA, Vessels (%) Protection
Rate (%)
thereby not only providing continued cerebral perfusion during
intervention but also allowing angiography of the target vessel Diethrich (1996)28 117 28 No 7.3
during various phases of the procedure. All of the currently avail- Yadav (1997)29 126 59 No 7.9
able filters have pores larger than 100 µm, which means that they Henry (1998)30 174 35 Mixed 2.9
allow passage of smaller particles that may not cause clinically sig- Teitelbaum (1998)31 25 68 No 27.3
nificant neurologic events but may nonetheless cause silent neu- Bergeron (1999)32 99 44 No 2
ronal injury. These filters also have higher physical profiles than Shawl (2000)33 192 61 No 2.9
balloon occlusion devices and thus may be difficult to pass across Malek (2000)34 28 100 No 3.6
particularly severe stenoses. Filters that are not completely Roubin (2001)26 604 52 Mixed 7.4
apposed to the vessel wall may allow emboli to pass around the Ahmadi (2001)35 298 38 Mixed 3.0
device and into the distal cerebral circulation. A 2001 study CAVATAS (2001)36 251 96 No 10
described CAS performed in 86 lesions with three different filter Brooks (2001)37 53 100 No 0
devices.22 In three cases, the filter could not be advanced across d’Audiffret (2001)38 68 30 Mixed 5.8
Chakhtoura (2001)39 50 39 No 2.2
the lesion. However, more than half of the successfully deployed
Leger (2001)40 8 38 No 0
filters contained macroscopic embolic material, and only one
Dietz (2001)41 43 100 Yes 5
patient (1.2%) experienced a neurologic complication (a minor
Baudier (2001)42 50 98 Mixed 6
stroke).
Reimers (2001)22 88 36 Yes 2.3
Finally, a device has been developed that induces reversal of Pappada (2001)43 27 93 Mixed 3.7
flow in the ICA through balloon occlusion of the CCA and the Paniagua (2001)44 69 16 No 5.6
ECA and creation of a temporary arteriovenous shunt between Criado (2002)27 135 40 Mixed 2
the ICA and the femoral vein.23 This device, though potentially Guimaraens (2002)45 194 92 Yes 2.6
more cumbersome than other protection devices, may produce Al-Mubarak (2002)46 164 48 Yes 2
virtually complete protection by preventing any emboli from trav- Bonaldi (2002)47 71 100 Mixed 5.6
eling to the intracranial circulation. Kao (2002)48 118 75 No 4.2
A 2004 report summarized one group of operators’ experience Whitlow (2002)21 75 56 Yes 0
with 1,202 CAS procedures between 1994 and 2002.24 In 33% of Qureshi (2002)49 73 37 Mixed 4.1
the patients studied, a cerebral protection device was used during Macdonald (2002)50 50 84 Yes 6
the procedure.The overall stroke rate was 4.4%; the risk of stroke Stankovic (2002)51 102 37 Mixed 0
reached its height (9.1%) during the period extending from Kastrup (2003)52 100 63 Mixed 5
September 1996 to September 1997 and reached its nadir (0.6%) Cremonesi (2003)53 442 57 Yes 1.1
during the final year of the study. The authors concluded that Terada (2003)54 87 80 Yes 2.3
improvements in technique, equipment, and pharmacotherapy, as Bowser (2003)55 52 60 No 5.7
well as the use of neuroprotection, contributed significantly to Wholey (2003)56 12,392 53 Mixed 4.75
improvements in results. In an earlier series, 46 patients were Becquemin (2003)57 114 33 Mixed 7.0
Dabrowski (2003)58 73 Not stated Mixed 5.5
treated with CAS, of whom 25 received cerebral protection.25 Two
Cernetti (2003)59 104 26 Yes 4
neurologic events (9.5%) occurred in the unprotected cohort; no
Bush (2003)60 51 29 No 2
events occurred in the protected group. Although the small num-
Gable (2003)61 31 69 No 3
bers of patients prevented meaningful statistical analysis, the
Lal (2003)62 122 45 Mixed 3.3
authors concluded that cerebral protection was technically feasi- SAPPHIRE (2004)8 167 30 Yes 5.5
ble and effective in preventing neurologic complications during Total 17,087 4.7
CAS.


to provide a reasonably accurate picture of the current status of adverse events (stroke, death, and MI). Inclusion and exclusion
the procedure [see Table 6].8,21,22,26-62 criteria for the study are listed more fully elsewhere [see Tables 2
In a study from the University of Alabama at Birmingham and and 3]. Patients were independently evaluated by a certified neu-
Lenox Hill Hospital in New York,26 a total of 604 arteries were rologist before and after the procedure. The majority of the ran-
treated in 528 consecutive patients over a 5-year period. CAS was domized patients were asymptomatic: in the CAS group, only
performed both with balloon-expandable stents and with self- 30% were symptomatic, and in the CEA group, only 28% were
expanding stents and both with and without cerebral protection symptomatic. A key point to keep in mind is that this trial was
devices.The overall 30-day combined stroke-death rate was 8.1% designed to test the idea that CAS was not inferior to CEA, not to
(minor stroke, 5.5%; major stroke, 1.6%; nonneurologic death, establish that CAS was superior to CEA or CEA to CAS. At 30
1%). On a year-by-year basis, the risk of stroke and death reached days, the risk of stroke was not significantly different in the two
its maximum (12.5%) in the period ending in September 1997 groups (CAS, 3.6%; CEA 3.1%).Two patients in the CAS group
and fell to its minimum (3.2%) the following year.This rather dra- (1.2%) and four patients in the CEA group (2.5%) died within 30
matic change in results from one year to the next probably is attri- days; this difference did not reach statistical significance (P =
butable to technical advances (e.g., in protection devices, stents, 0.39). More patients experienced periprocedural MI in the CEA
and guide wires), as well as to improvements in the investigators’ group (6.1%) than in the CAS group (2.4%), a difference that did
ability to select appropriate patients for intervention. not reach statistical significance on the basis of intent to treat.
A subsequent report describes the authors’ experience with Notably, most of the MIs were non-Q MIs, identified by routine
CAS in a vascular surgery practice.27 During a 40-month period postprocedural laboratory studies.The incidence of the combined
from 1997 to 2001, 135 procedures were performed in 132 pa- end point (stroke-death-MI) was higher in the CEA group (9.8%)
tients, most (60%) of whom were asymptomatic.The rate of com- than in the CAS group (4.8%), but this difference was statistical-
plications was acceptable (2%), and only one patient had a signif- ly insignificant as well. These results have been used to support
icant restenosis at follow-up (mean follow-up interval, 16 months). FDA approval of the stent and filter protection device used in this
Perhaps more important, these 132 patients represented 41% of important study.
all patients being treated for carotid disease in this practice. This Lesions of the proximal CCA are relatively uncommon in
percentage seems extraordinarily high, but it may simply be a bell- comparison with lesions of the carotid bifurcation, but they can
wether of things to come in the practice of vascular surgery, and it also be effectively treated with CAS. In my experience, most are
underscores the importance of multispecialty involvement in this treated with common carotid cutdown, retrograde angioplasty,
new technology. and placement of a balloon-expandable stent. Of 14 consecutive
The results of the SAPPHIRE trial of CAS in high-risk patients CCA interventions performed at the Cleveland Clinic,63 one
were published in 2004.8 To date, this trial, which included 334 was converted to carotid-subclavian transposition after iatro-
patients randomly assigned to either CAS (N = 167) or CEA genic dissection, and two resulted in stroke secondary to ICA
(N = 167), is the only industry-sponsored FDA-approved trial thrombosis. In both of the interventions resulting in stroke,
that was actually randomized. A separate registry of nonrandom- which were performed in conjunction with redo bifurcation
ized patients was compiled that included those who were felt to endarterectomies, the CCA was patent at the time of surgical
be at unacceptably high risk for CEA and therefore underwent reexploration and ICA thrombectomy. Although the carotid
CAS (N = 406), as well as those who were not suitable candidates stent procedure is unlikely to have played a role in causing these
for CAS and therefore underwent CEA (N = 7). The goal of the strokes, it is nonetheless advisable to exercise caution when per-
SAPPHIRE trial was to evaluate the combined end point of major forming these combined procedures.

References

1. North American Symptomatic Carotid Endarterec- 7. Gasparis AP, Ricotta L, Cuadra SA, et al: High-risk 13. Bicknell CD, Cowling MG, Clark MW, et al: Carotid
tomy Trial Collaborators: Beneficial effect of carotid carotid endarterectomy: fact or fiction. J Vasc Surg angioplasty in a pulsatile flow model: factors affecting
endarterectomy in symptomatic patients with high- 37:40, 2003 embolic potential. Eur J Vasc Endovasc Surg 26:22,
grade carotid stenosis. N Engl J Med 325:445, 1991 8. Yadav JS,Wholey MH, Kuntz RE, et al: Stenting and 2003
2. Executive Committee for the Asymptomatic Carotid Angioplasty with Protection in Patients at High Risk 14. Tübler T, Schlüter M, Dirsch O, et al: Balloon-pro-
Atherosclerosis Study: Endarterectomy for asympto- for Endarterectomy Investigators. Protected carotid- tected carotid artery stenting: relationship of peripro-
matic carotid artery stenosis. JAMA 273:1421, 1995 artery stenting versus endarterectomy in high-risk cedural neurological complications with the size of
patients. N Engl J Med 351:1493, 2004 particulate debris. Circulation 104:2791, 2001
3. Menzoian JO: Presidential address: carotid end-
arterectomy, under attack again! J Vasc Surg 37:1137, 9. Gaunt ME, Martin PJ, Smith JL, et al: Clinical rele- 15. Al-Mubarak N, Roubin GS, Vitek JJ, et al: Effect of
2003 vance of intraoperative embolization detected by the distal-balloon protection system on macroem-
transcranial Doppler ultrasonography during carotid bolization during carotid stenting. Circulation 104:
4. Mozes G, Sullivan T, Torres-Russotto D, et al: endarterectomy: a prospective study of 100 patients. 1999, 2001
Carotid endarterectomy in SAPPHIRE-eligible Br J Surg 81:1435, 1994 16. Baim DS,Wahr D, George B, et al: Randomized trial
‘high-risk’ patients: implications for selecting patients 10. Fearn SJ, Pole R,Wesnes K, et al: Cardiopulmonary of a distal embolic protection device during percuta-
for carotid angioplasty and stenting. J Vasc Surg support and physiology. J Thorac Cardiovasc Surg neous intervention of saphenous vein aorto-coronary
39:958, 2004 121:1150, 2001 bypass grafts. Circulation 105:1285, 2002
5. Ouriel K, Hertzer NR, Beven EG, et al: Preproce- 11. Rapp JH, Pan XM, Sharp FR, et al: Atheroemboli to 17. Coggia M, Goëau-Brissonière, Duval J-L, et al: Em-
dural risk stratification: identifying an appropriate the brain: size threshold for causing acute neuronal bolic risk of the different stages of carotid bifurcation
population for carotid stenting. J Vasc Surg 33:728, cell death. J Vasc Surg 32:68, 2000 balloon angioplasty: an experimental study. J Vasc
2001 Surg 31:550, 2000
12. Ohki T, Marin ML, Lyon RT, et al: Ex vivo human
6. Jordan WD Jr, Alcocer F,Wirthlin DJ, et al: High-risk carotid artery bifurcation stenting: correlation of le- 18. Theron J, Raymond J, Casasco A, et al: Percutaneous
carotid endarterectomy: challenges for carotid stent sion characteristics with embolic potential. J Vasc angioplasty of atherosclerotic and postsurgical steno-
protocols. J Vasc Surg 325:16, 2002 Surg 27:463, 1998 sis of carotid arteries. Am J Neuroradiol 8:495, 1987


19. Theron J, Courtheoux P, Alachkar F, et al: New in high-risk symptomatic NASCET-ineligible pa- 49. Qureshi AI, Suri MF, New G, et al: Multicenter
triple coaxial catheter system for carotid angioplasty tients. Stroke 31:3029, 2000 study of the feasibility and safety of using the memo-
with cerebral protection. Am J Neuroradiol 11:869, 35. Ahmadi R,Willfort A, Lang W, et al: Carotid artery therm carotid arterial stent for extracranial carotid
1990 stenting: effect of learning curve and intermediate- artery stenosis. J Neurosurg 96:830, 2002
20. Al-Mubarak N, Vitek JJ, Iyer S, et al: Embolization term morphological outcome. J Endovasc Ther 8: 50. Macdonald S,Venables GS, Cleveland TJ, et al: Pro-
via collateral circulation during carotid stenting with 539, 2001 tected carotid stenting: safety and efficacy of the
the distal balloon protection system. J Endovasc 36. Endovascular versus surgical treatment in patients MedNova NeuroShield filter. J Vasc Surg 35:966,
Ther 8:354, 2001 with carotid stenosis in the Carotid and Vertebral 2002
21. Whitlow PL, Lylyk P, Londero H, et al: Carotid Artery Transluminal Angioplasty Study (CAVATAS): 51. Stankovic G, Liistro F, Moshiri S, et al: Carotid
artery stenting protected with an emboli contain- a randomised trial. Lancet 357:1729, 2001 artery stenting in the first 100 consecutive patients:
ment system. Stroke 22:1308, 2002 results and follow up. Heart 88:381, 2002
37. Brooks WH, McClure RR, Jones MR, et al: Carotid
22. Reimers B, Corvaja N, Moshiri S, et al: Cerebral angioplasty and stenting versus carotid endarterecto- 52. Kastrup A, Skalej M, Krapf H, et al: Early outcome
protection with filter devices during carotid artery my: randomized trial in a community hospital. J Am of carotid angioplasty and stenting versus carotid end-
stenting. Circulation 104:12, 2001 Coll Cardiol 38:1589, 2001 arterectomy in a single academic center. Cerebrovasc
23. Ohki T, Parodi J, Veith FJ, et al: Efficacy of a proxi- 38. d’Audiffret A, Desgranges P, Kobeiter H, et al:Tech- Dis 15:84, 2003
mal occlusion catheter with reversal of flow in the nical aspects and current results of carotid stenting. J 53. Cremonesi A, Manetti R, Setacci F, et al: Protected
prevention of embolic events during carotid artery Vasc Surg 33:1001, 2001 carotid stenting: clinical advantages and complica-
stenting: an experimental analysis. J Vasc Surg
39. Chakhtoura EY, Hobson RW 2nd, Goldstein J, et al: tions of embolic protection devices in 442 consecu-
33:504, 2001
In-stent restenosis after carotid angioplasty-stenting: tive patients. Stroke 34:1936, 2003
24. New G, Roubin GS, Iyer SS, et al: Outcomes from incidence and management. J Vasc Surg 33:220, 54. Terada T,Tsuura M, Matsumoto H, et al: Results of
carotid artery stenting in over 1,000 cases from a sin- 2001 endovascular treatment of internal carotid artery
gle group of operators. J Am Coll Cardiol 41(suppl
40. Leger AR, Neale M, Harris JP: Poor durability of stenoses with a newly developed balloon protection
A):868, 2003
carotid angioplasty and stenting for treatment of re- catheter. Neurosurgery 53:617, 2003
25. Parodi JC, LaMura R, Ferriera LM, et al: Initial current artery stenosis after carotid endarterectomy:
evaluation of carotid angioplasty and stenting with 55. Bowser AN, Bandyk DF, Evans A, et al: Outcome of
an institutional experience. J Vasc Surg 33:1008,
three different cerebral protection devices. J Vasc carotid stent-assisted angioplasty versus open surgi-
2001
Surg 32:1127, 2000 cal repair of recurrent carotid stenosis. J Vasc Surg
41. Dietz A, Berkefeld J,Theron JG, et al: Endovascular 38:432, 2003
26. Roubin GS, New G, Iyer SS, et al: Immediate and treatment of symptomatic carotid stenosis using
late clinical outcomes of carotid artery stenting in 56. Wholey MH, Al-Mubarek N,Wholey MH: Updated
stent placement: long-term follow-up of patients
patients with symptomatic and asymptomatic carotid review of the global carotid artery stent registry.
with a balanced surgical risk/benefit ratio. Stroke
artery stenosis: a 5-year prospective analysis. Circu- Catheter Cardiovasc Interv 60:259, 2003
32:1855, 2001
lation 103:532, 2001 57. Becquemin JP, Ben El Kadi H, Desgranges P, et al:
42. Baudier JF, Licht PB, Roder O, et al: Endovascular
27. Criado FJ, Lingelbach JM, Ledesma DF, et al: treatment of severe symptomatic stenosis of the in- Carotid stenting versus carotid surgery: a prospective
Carotid artery stenting in a vascular surgery practice. ternal carotid artery: early and late outcome. Eur J cohort study. J Endovasc Ther 10:687, 2003
J Vasc Surg 35:430, 2002 Vasc Endovasc Surg 22:205, 2001 58. Dabrowski M, Bielecki D, Golebiewski P, et al: Per-
28. Diethrich EB, Ndiaye M, Reid DB: Stenting in the 43. Pappada G, Marina R, Fiori L, et al: Stenting of ath- cutaneous internal carotid artery angioplasty with
carotid artery: initial experience in 110 patients. J erosclerotic stenoses of the extracranial carotid artery. stenting: early and long-term results. Kardiol Pol
Endovasc Surg 3:42, 1996 Acta Neurochir (Wien) 143:1005, 2001 58:469, 2003
29. Yadav JS, Roubin GS, Iyer S, et al: Elective stenting 44. Paniagua D, Howell M, Strickman N, et al: Out- 59. Cernetti C, Reimers B, Picciolo A, et al: Carotid
of the extracranial carotid arteries. Circulation 95: comes following extracranial carotid artery stenting artery stenting with cerebral protection in 100 con-
376, 1997 in high-risk patients. J Invasive Cardiol 13:375, 2001 secutive patients: immediate and two-year follow-up
30. Henry M, Amor M, Masson I, et al: Angioplasty and results. Ital Heart J 4:695, 2003
45. Guimaraens L, Sola MT, Matali A, et al: Carotid an-
stenting of the extracranial carotid arteries. J En- gioplasty with cerebral protection and stenting: re- 60. Bush RL, Lin PH, Bianco CC, et al: Carotid artery
dovasc Surg 5:293, 1998 port of 164 patients (194 carotid percutaneous stenting in a community setting: experience outside
31. Teitelbaum GP, Lefkowitz MA, Giannotta SL: Carotid transluminal angioplasties). Cerebrovasc Dis 13:114, of a clinical trial. Ann Vasc Surg 17:629, 2003
angioplasty and stenting in high-risk patients. Surg 2002 61. Gable DR, Bergamini T, Garrett WV, et al: Interme-
Neurol 50:300, 1998 46. Al-Mubarak N, Colombo A, Gaines PA, et al: Multi- diate follow-up of carotid artery stent placement.
32. Bergeron P, Becquemin JP, Jausseran JM, et al: Per- center evaluation of carotid artery stenting with a fil- Am J Surg 185:183, 2003
cutaneous stenting of the internal carotid artery: the ter protection system. J Am Coll Cardiol 39:841, 62. Lal BK, Hobson RW 2nd, Goldstein J, et al: In-stent
European CAST I Study. Carotid Artery Stent Trial. 2002 recurrent stenosis after carotid artery stenting: life
J Endovasc Surg 6:155, 1999 47. Bonaldi G: Angioplasty and stenting of the cervical table analysis and clinical relevance. J Vasc Surg
33. Shawl F, Kadro W, Domanski MJ, et al: Safety and carotid bifurcation: report of a 4-year series. Neuro- 38:1162, 2003
efficacy of elective carotid artery stenting in high-risk radiology 44:164, 2002 63. Sullivan TM, Gray BH, Bacharach JM, et al: Angio-
patients. J Am Coll Cardiol 35:1721, 2000 48. Kao HL, Lin LY, Lu CJ, et al: Long-term results of plasty and primary stenting of the subclavian, in-
34. Malek AM, Higashida RT, Phatouros CC, et al: elective stenting for severe carotid artery stenosis in nominate, and common carotid arteries in 83 pa-
Stent angioplasty for cervical carotid artery stenosis Taiwan. Cardiology 97:89, 2002 tients. J Vasc Surg 28:1059, 1998

Acs0610 Carotid Angioplasty And Stenting

Recomendados

Recomendados

Más contenido relacionado

La actualidad más candente

La actualidad más candente (19)

Destacado

Destacado (17)

Similar a Acs0610 Carotid Angioplasty And Stenting

Similar a Acs0610 Carotid Angioplasty And Stenting (20)

Más de medbookonline

Más de medbookonline (20)

Acs0610 Carotid Angioplasty And Stenting