Carotid Artery Stenting

Updated: May 31, 2022
Author: Faisal Aziz, MD; Chief Editor: Karlheinz Peter, MD, PhD 



Carotid artery stenting (CAS) is a minimally invasive technique for treating carotid artery disease. Carotid endarterectomy (CEA) has been shown to reduce the incidence of stroke in patients with symptomatic and asymptomatic carotid stenosis.[1, 2, 3, 4] With ongoing advances in endovascular technology, growing experience with CAS on the part of interventionalists, and an increasing focus on training and credentialing,[5] CAS has become an alternative to CEA for treatment of patients with carotid artery disease, though it has not supplanted CEA.[6]


Indications for CAS include the following:

  • Inability to tolerate general anesthesia for CEA
  • History of damage to the contralateral vocal cord (previous CEA or neck surgery)
  • Previous neck surgery on the ipsilateral side
  • Neck irradiation
  • Restenosis after CEA


Contraindications for CAS include the following:

  • History of allergic reaction to intravenous (IV) contrast material
  • Unfavorable anatomy
  • Unstable carotid plaque
  • Unstable aortic arch plaque

Technical Considerations


The principal arteries supplying the head and neck are the two common carotid arteries (CCAs). These vessels ascend in the neck, where each divides into two branches, the external carotid artery (ECA; supplying the exterior of the head, the face, and the greater part of the neck) and the internal carotid artery (ICA; supplying to a great extent the parts within the cranial and orbital cavities).

For more information about the relevant anatomy, see Arterial Supply Anatomy and Arteries to the Brain and Meninges.

Best practices

In February 2016, the Society for Cardiovascular Angiography and Interventions (SCAI) and the Society for Vascular Medicine (SVM) published an expert consensus statement aimed at providing guidance on physician training and credentialing for CAS so as to facilitate the incorporation of this procedure into clinical practice within cardiovascular medicine programs focused on preventing stroke.[5]


Naylor et al, in a prospective, randomized trial of CEA versus CAS for symptomatic patients with greater than 70% internal carotid artery stenosis, found that all 10 of the CEA patients proceeded without any complications, whereas five of the seven CAS patients had an ischemic stroke within 30 days of the procedure.[7] The trial was stopped because of the dramatically bad outcome in the endovascular group.

Brooks et al, in a randomized study of 104 patients presenting with cerebrovascular ischemia related to internal carotid artery stenosis who underwent either CEA (n = 51) or CAS (n = 53), reported one death in the CEA group and one transient ischemic attack in the CAS group.[8] CAS was equivalent to CEA and did not carry an increased risk of major complications (ie, death or stroke).

These authors subsequently published 10-year outcomes for 173 patients. Half of the patients had died from other conditions in this period. They did not find any difference in long-term protection against ipsilateral stroke in either group. Overall, the risk of heart attack was high among patients randomized to CEA.[9]

In the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS), a multicenter clinical trial in which 504 patients with carotid stenosis were randomly assigned to undergo either CEA (n = 253) or CAS (n = 251), there was no substantial difference in the rate of ipsilateral stroke over a 3-year follow-up period.[10] However, the results of surgery were worse as compared to surgical standards for CEA; moreover, cerebral protection devices (CPDs) were used in only 27% of the patients who underwent CAS.

The Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial, an industry-sponsored randomized, controlled trial that included 334 high-risk surgical patients who underwent either CAS or CEA, concluded that CAS was superior to CEA among high-risk surgical patients.[11] The primary end points were combined death, stroke, and myocardial infarction (MI). An asymptomatic rise in troponin levels was regarded as MI, and the higher rate of MI among patients who underwent CEA shifted the balance in favor of CAS.

In the Carotid Revascularization Endarterectomy versus Stenting Trial (CREST), which included 2502 patients who were randomly assigned to undergo either CEA or CAS, the combined risk of death, MI, or stroke (the primary end points) was comparable for the two procedures (6.8% for CEA vs 7.2% for CAS).[12] However, the incidence of stroke was 2.3% for CEA versus 4.1% for CAS. The incidence of MI was 2.3% for CEA versus 1.1% for CAS. Stroke is a disabling event, and extreme caution should be observed in interpreting the results from CREST.

A subsequently published subanalysis of the CREST trial[13] showed that restenosis and occlusion rates were similar up to 2 years after CEA and CAS.

In the multicenter randomized CASWEP (Carotid Artery Stenting Without Embolic Protection) trial (N = 279), Gorgulu et al compared the clinical outcomes in selected symptomatic and asymptomatic patients with significant carotid artery stenosis who underwent either CAS without CPD (n = 140) or CAS combined with CPD (n = 139).[14] They found no significant differences with respect to periprocedural in-hospital TIAs, ipsilateral stroke, death, or new ischemic brain lesions on postprocedural diffusion-weighted magnetic resonance imaging (DW-MRI).


Periprocedural Care

Preprocedural Planning

Carotid ultrasonography (US) and transcranial Doppler or transcranial color-coded US may be useful for diagnosis, risk stratification, peri-interventional monitoring, and follow-up of patients with carotid artery disease who undergo carotid artery stenting (CAS).[15]  There is growing interest in the application of optical coherence tomography (OCT) to CAS.[16, 17]


Listed below are the standard equipment and materials needed for CAS. All interventionalists who are performing percutaneous carotid interventions should choose their equipment in accordance with their personal preferences and with the local availability of specific materials and devices.

Access kit

Access can be obtained using a micropuncture kit (Cook, Inc). This kit consists of a 21-gauge needle for obtaining access to the vessel, Torq-Flex® wire, and a coaxial catheter.

Guide wires

The following two wires can be used:

  • 0.035-in. hydrophilic guide wire (Terumo) to access the aortic arch
  • 0.014-in. hydrophilic guide wire (Spartacore) to cross the lesion

Introducer sheaths

A 6-French access sheath can be used initially, followed by a 6-French long guiding sheath system.


To gain access to the aortic arch and advance the guide wire through the carotid lesion, complex catheter manipulations may be required, especially if the patient has a tortuous anatomy. Catheters with varying degrees of angulation assist in minimally traumatic catheter passage. Available catheters include the following:

  • JB-2 catheter (Cook, Inc)
  • SIM 1 catheter (Cook, Inc)
  • SIM 2 catheter (Cook, Inc)
  • H1 catheter (Cook, Inc)
  • VTK catheter (Terumo)
  • Glide vertebral catheter
  • Simmons catheter
  • Mani catheter

Balloon systems

There are two main types of balloon systems: coaxial and monorail. For carotid interventions, monorail balloons can be used, with predilation of the lesion with a 2- or 3-mm balloon.

The balloon length is chosen according to the length of the stenotic lesion. To reduce the risk of atheroembolization, poststent dilation is generally avoided. If such dilation is required, a 5- or 6-mm balloon is used, depending on the diameter of the stent and the diameter of the stenotic lesion.

Stents (balloon-expandable and self-expanding)

There are two basic types of stents: balloon-expandable and self-expanding.

Balloon-expandable stents are mounted on a balloon catheter and passively enlarged to the desired diameter at the implantation site by dilating the balloon. They are better suited for proximal carotid artery and innominate artery lesions and offer greater precision during CAS. Their collapsed diameter is slightly larger than that of self-expanding stents; therefore, it is often difficult to cross a lesion with them unless the stenosis is predilated. The Express® stent (Boston Scientific) is the available balloon-mounted stent for carotid artery lesions.

Self-expanding carotid stents are used as a minimally invasive alternative to carotid endarterectomy (CEA). They open actively after being released from the delivery system. Their self-expanding character depends either on the braiding structure or on the type of alloy (usually nitinol or stainless steel). Commercially available self-expanding stents include the following:

  • Carotid WALLSTENT ® (Boston Scientific)
  • Nexstent ® (Boston Scientific)
  • Precise ® (Cordis)
  • Protege ® (ev3)
  • Xact ® (Abbott)

Cerebral protection devices

The purpose of cerebral protection devices (CPDs) is to capture atherosclerotic emboli during catheter manipulation, angioplasty, and stenting. The risk of atheroembolization is greatest during balloon angioplasty of the stenosis and when the lesion is crossed by a wire. Different types of CPDs are commercially available, as follows:

  • GuardWire ® temporary occlusion and aspiration system (Medtronic) - This is available in two balloon sizes, 2.5-5 mm and 3-6 mm, on a 0.014-in. wire system
  • GORE Neuro Protection System (W. L. Gore & Associates; previously called Parodi Anti-Embolic System) - This system, based on the hemodynamic principle of reversal of internal carotid artery (ICA) blood flow with common carotid artery (CCA) occlusion, comes with a set of two balloons, one placed in the external carotid artery (ECA) and the other in the CCA; when both balloons are inflated, backbleeding generally occurs from the ICA
  • Filterwire EZ ® embolic protection system (Boston Scientific) - The basic mechanism is filter-based; it is based on a 0.014-in. wire system
  • Angioguard RX ® emboli capture guide wire system (Cordis)
  • RX Accunet ® embolic protection system (Abbott)
  • Emboshield NAV6 ® embolic protection system (Abbott)
  • Spider FX ® embolic protection device (ev3)

Patient Preparation


Conscious sedation and local anesthesia are preferred so as to permit continuous monitoring of the patient’s neurologic status. During balloon inflation, bradycardia and hypotension may occur; therefore, continuous cardiac monitoring and intra-arterial blood pressure monitoring are performed in all patients who undergo CAS.


Carotid stenting procedures are performed in a hybrid, fixed C-arm operating room where multiplanar views are easily obtained. The patient is supine, with the head turned toward the opposite side. The operating surgeon usually stands on the patient's right side. Extra table length is added at the foot of the table to ensure that all wire lengths can be handled easily in a sterile field.

Monitoring & Follow-up

The 2018 guidelines from the Society for Vascular Surgery (SVS) recommended that after CAS, surveillance with duplex US should be carried out at baseline and every 6 months for 2 years and annually thereafter until the patient is stable (ie, until no restenosis or in-stent restenosis [ISR] is observed in two consecutive annual scans).​[18] The first duplex study should be done soon after the procedure (preferably ≤ 3 months) to establish a posttreatment baseline. Surveillance should be maintained at some regular interval (eg, every 2 years) for the life of the patient.

For patients undergoing CAS who are diabetic, have aggressive (type IV) ISR patterns, have previously been treated for ISR, have previously undergone cervical irradiation, or have heavy calcification, the SVS recommended, in addition to the baseline duplex US, surveillance with duplex US every 6 months until a stable clinical pattern is established, and then annually afterward.[18]

The SVS recommended that post-CAS duplex US include at least the following assessments[18] :

  • Doppler measurement of peak systolic velocity and end diastolic velocity in the native CCA; in the proximal, middle, and distal stent; and in the distal native ICA; modified threshold velocity criteria should be used to interpret the significance of these measurements after CAS
  • B-mode imaging should be used to supplement and to enhance the accuracy of velocity criteria to estimate the severity of luminal narrowing


Approach Considerations

Access for carotid artery stenting (CAS) can be obtained through a variety of approaches, as follows:

  • Femoral - This is the approach preferred by most interventionalists; it avoids technique-related angulation and offers improved guide-wire and catheter maneuverability
  • Brachial/radial - A brachial approach is associated with a risk of damaging the median nerve; moreover, owing to the extreme angulation, manipulation of the catheter is difficult with this approach
  • Carotid - Both percutaneous and direct open exposures have been reported, and both have been associated with the risk of causing inadvertent dissection and inadvertent crossing of the stenotic lesion; however, newer techniques of transcervical CAS with flow reversal [19] have been associated with high technical success, almost zero mortality, and very low rates of major or minor stroke, myocardial infarction (MI), and complications

Carotid Stent Insertion

Before and for a minimum of 30 days after CAS, dual-antiplatelet therapy (DAPT) with aspirin (81-325 mg/day) plus clopidogrel (75 mg/day) has been recommended.[20] For patients intolerant of clopidogrel, ticlopidine (250 mg q12hr) may be substituted. 

The 2018 guidelines on carotid and vertebral artery disease from the European Society for Vascular Surgery (ESVS) suggested that preintervention statin therapy may reduce procedural complications.[21] The guidelines recommended starting DAPT with aspirin (300 mg initially for up to 14 days followed by 75 mg/day if the patient is not already taking aspirin) and clopidogrel (75 mg/day) 3 days prior to CAS. Aspirin and clopidogrel should be continued for at least 1 month, followed by clopidogrel thereafter, unless the treating physician opts for an alternative long-term antiplatelet regimen.

The standard technique for CAS is described below. Certain steps may vary, depending on the patient’s anatomy and the surgeon's preferences (see the image below).

Key steps in carotid stenting. Image courtesy of K Key steps in carotid stenting. Image courtesy of Kurt Mansor, Jobst Vascular Institute.

The patient is placed in a supine position. Both femoral regions are prepared and draped in a standard fashion. Anatomic landmarks are marked on the patient (ie, the anterior superior iliac spine and pubic tubercle).

The femoral pulsation is palpated, and a micropuncture needle is inserted one fingerbreadth below the inguinal ligament. Upon entry into the artery, a hydrophilic wire is inserted through the needle by means of the Seldinger technique. The needle is removed and is replaced by a 4-French sheath. The sheath is upsized to 6 French.

A guide wire is advanced into the aorta under direct fluoroscopy. An H1 catheter is placed over the guide wire and positioned in the aortic arch. Heparin 80 IU/kg is administered. An aortogram is obtained in the left anterior oblique position at 45° of angulation. The aortic arch, innominate artery, left common carotid artery (CCA), and left subclavian artery are identified. Selective catheterization of the left or right common artery is performed.

The guide wire is placed in the external carotid artery (ECA), and the H1 catheter is then placed in the ECA. The guide wire is replaced with a stiffer wire (Amplatz/Lunderquist wire). A shuttle sheath is advanced to the CCA. A carotid arteriogram is obtained (in anteroposterior, lateral, and intracerebral views).

The lesion is crossed with 0.014-in. wire. A cerebral protection device (CPD) is positioned with a monorail system. Predilatation is performed with a 2- to 3-mm balloon. The stent is placed across the lesion and deployed.

A repeat arteriogram is performed (see the image below). Any residual stenosis exceeding 30% is treated with balloon angioplasty. Sheaths and wires are removed, and an access site closure device is deployed.

Images show vessel before and after carotid artery Images show vessel before and after carotid artery stenting. Image courtesy of Cheong Lee, MD.


Potential complications of CAS include the following:

  • Stent fracture or deformation [22]
  • Stroke [23, 24]
  • MI [23, 24]
  • Silent new ischemic cerebral lesions [25]

Long-term outcomes of CAS remain to be fully defined. One study reviewed records for 219 patients who underwent CAS to assess the risk of carotid stent fractures or deformations following the procedure. Results showed a 15% rate of fracture or deformation at 2 years and a 50% rate at 4 years. Open-cell stents led to deformation more frequently than closed-cell stents did, and stent fractures were significantly associated with heavy calcification. These are potentially important early observations that should be recorded for all CAS patients to determine future clinical implications.[22]

In a 2018 meta-analysis of randomized controlled trials aimed at assessing the safety of CAS vs CEA for asymptomatic carotid stenosis with average risk, Cui et al found that as compared with CEA, CAS had a higher rate of periprocedural stroke and periprocedural minor stroke and a similar rate of periprocedural major stroke, periprocedural ipsilateral stroke, or MI.[23] They were not able to reach any robust conclusions about midterm to long-term complications.

A meta-analysis by Yuan et al that assessed CAS against CEA in the setting of asymptomatic carotid stenosis found that CEA was associated with a lower risk of perioperative stroke and a higher risk of MI but that CEA and CAS appeared to be essentially equivalent with regard to the risk of death.[24]

Hemodynamic instability—as defined by hypertension (systolic blood pressure >160 mm Hg), hypotension (systolic blood pressure < 90 mm Hg), bradycardia (heart rate < 60 beats/min), or a combination thereof—has been reported to occur after CAS.[26] Patients with prolonged hemodynamic instability after the procedure are at increased risk for TIA and stroke.



Medication Summary

Medications are routinely used before, during, and after carotid artery stenting.

Anticoagulants, Cardiovascular

Class Summary

Anticoagulants prevent recurrent or ongoing thromboembolic occlusion of the vertebrobasilar circulation.


Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents recurrence of a clot after spontaneous fibrinolysis.

Antiplatelet Agents, Cardiovascular

Class Summary

Antiplatelets inhibit the activation of factors involved in platelet aggregation. This class of drugs has been shown to reduce mortality by reducing the risk of fatal strokes, fatal myocardial infarctions, and vascular death in patients with a history of TIAs.

Aspirin (Ascriptin Maximum Strength, Bayer Aspirin Extra Strength, Bufferin, Ecotrin)

Odorless white powdery substance available in 81 mg, 325 mg, and 500 mg for oral use. When exposed to moisture, aspirin hydrolyzes into salicylic acid and acetic acids.

Stronger inhibitor of both prostaglandin synthesis and platelet aggregation than other salicylic acid derivatives. Acetyl group is responsible for inactivation of cyclooxygenase via acetylation. Aspirin is hydrolyzed rapidly in plasma, and elimination follows zero order pharmacokinetics.

Irreversibly inhibits platelet aggregation by inhibiting platelet cyclooxygenase. This, in turn, inhibits conversion of arachidonic acid to PGI2 (potent vasodilator and inhibitor of platelet activation) and thromboxane A2 (potent vasoconstrictor and platelet aggregate). Platelet-inhibition lasts for life of cell (approximately 10 d). May be used in low dose to inhibit platelet aggregation and improve complications of venous stases and thrombosis. Reduces likelihood of myocardial infarction. Also very effective in reducing risk of stroke. Early administration of aspirin in patients with AMI may reduce cardiac mortality in first mo.

Clopidogrel (Plavix)

Thienopyridine antiplatelet agent. Used off-label to maintain carotid artery stent patency. Selectively inhibits adenosine diphosphate (ADP) binding to platelet receptor and subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.