Percutaneous carotid artery stenting

INTRODUCTION — For patients with indications for carotid revascularization, treatment options include carotid endarterectomy or carotid artery stenting (CAS), which is most commonly accomplished with stent delivery using a transfemoral (ie, TF-CAS) approach, but other percutaneous approaches (transaxillary, transcervical, transradial) have also been described.

Percutaneous CAS, and more specifically TF-CAS, has advantages and disadvantages and, as with other approaches to carotid artery revascularization, the patient's anatomy must meet specific anatomic requirements to undergo the procedure safely.

The technical aspects and outcomes of primarily TF-CAS are reviewed, with aspects of other percutaneous approaches provided where relevant.

Transcarotid artery revascularization (TCAR) requires a surgical cutdown to expose the common carotid artery for device placement and uses cerebral protection with flow reversal during introduction of a carotid stent. Because TCAR eliminates the risks associated with traversing the aortic arch, TCAR is gaining enthusiasm as an alternative approach to CAS among vascular clinicians and is reviewed separately. (See "Transcarotid artery revascularization".).

A comparison of CAS techniques is also provided separately. (See "Overview of carotid artery stenting", section on 'Approach to carotid artery stenting'.)

DEVICES USED FOR CAROTID REVASCULARIZATION — CAS systems were developed in the 1990s as a less invasive alternative to carotid endarterectomy (CEA) for carotid artery stenosis [1]. An endovascular approach is associated with fewer perioperative complications compared with open surgery for other vascular diseases, and it was felt that the same would be the case for CEA. A reduced rate of complications would be especially pertinent for patients deemed to be at "high risk" for CEA related to specific anatomic or physiologic risk factors [2]. While the risk of some perioperative complications was reduced with CAS, the risk for stroke was increased for CAS in trials comparing CEA with predominantly transfemoral CAS (TF-CAS). Over time, stroke rates associated with TF-CAS have decreased but remain concerning for certain subsets of patients. In an effort to reduce the potential for embolization and the risk of periprocedural stroke, refinement in carotid stents, embolic protection devices, and techniques are ongoing.

Carotid stent devices — Carotid stents can be grossly divided into two groups: open-cell architecture and closed-cell architecture [3,4]. With closed-cell stents, the stent struts are all interconnected, which is not the case for open-cell stents. As such, this architectural difference makes open-cell stents more flexible, and they may be more often chosen for more complex, angulated lesions or tortuous anatomy that may make delivery of the stent challenging. While closed-cell stents may be less flexible, they do have smaller free cell area between the stent struts, leaving smaller gaps uncovered, and may be more resistant to particle penetration that can lead to embolization [5]. A novel dual layer stent, which is available for use outside of the United States, has reported good early results [6,7]. This "covered" stent is designed to minimize and control plaque prolapse, thereby preventing plaque-related embolism after stent placement. In one trial, this mesh stent appeared to reduce the number and volume of new lesions identified on diffusion-weighted magnetic resonance imaging (DW-MRI) performed 2 days and 30 days after the procedure [8]. However, longer follow-up is needed to determine whether there is any sustained benefit.

Data from one trial, various retrospective studies, and registry reviews have failed to demonstrate any clinically important advantages for one stent type over another [9-12]. A systematic review that included nine predominantly retrospective studies did not find any significant differences in periprocedural (30-day) cerebrovascular complications comparing open- with closed-cell stent designs [9]. In a review of 740 patients who received carotid stents from the International Carotid Stenting Study (ICSS), the rate of ipsilateral stroke beyond 30 days was similar for each group [10]. However, the rate of restenosis ≥50 percent occurred in significantly fewer patients who received open- compared with closed-stent designs (36 versus 46 percent; hazard ratio [HR] 0.68, 95% CI 0.53-0.88), and there was a trend toward a reduced rate of severe stenosis (≥70 percent) or occlusion for the open-stent design (8.6 versus 12.7 percent; HR 0.63, 95% CI 0.37-1.05).

The dual-layered stent combines a stent frame with a micromesh lattice to provide better coverage of the carotid plaque compared with conventional stent designs. In the SCAFFOLD trial, 265 patients were treated with a 30-day stroke rate of 1.1 percent [13]. In a meta-analysis looking at four single-arm prospective studies evaluating two different dual-layered stents, the 30-day stroke rate was 1.25 percent [14]. While the early results are promising, longer follow-up in these patients is needed to ensure that subsequent rates of stroke, stent thrombosis, or restenosis are not higher compared with other stents.

There are no data supporting the use of drug-eluting stents or drug-coated balloons in treating carotid stenosis. The rate of restenosis following TF-CAS with bare metal stents is generally low.

Embolic protection devices — There are two basic types of embolic protection devices (EPDs): distal filters and proximal occlusion (flow arrest, flow reversal) [15-23]. Filter devices are used in the majority of percutaneous CAS procedures.

In a review of over 24,000 patients undergoing CAS, 74 percent were performed using TF-CAS with distal embolic protection, 2.3 percent using TF-CAS with proximal balloon occlusion, and 22.9 percent using transcarotid artery revascularization (TCAR) with flow reversal [24].

Distal filters — Distal filter designs allow continuous antegrade flow through the internal carotid artery during stent placement and are designed to catch debris dislodged during stent placement. Although filter devices are the most commonly used type of EPD for percutaneous CAS, they have several disadvantages [3,25-27]:

●They must pass unprotected across the stenosis, and tight lesions may require additional unprotected predilatation before the filter can be placed, a process that may dislodge emboli.

●There may be incomplete apposition of the filter device against the arterial wall, which may lead to incomplete capture of embolizing particles.

●The presence of the filter in the distal internal carotid artery may induce vasospasm that can severely compromise outflow and cause stroke if prolonged. Spasm can be treated with an intra-arterial vasodilator such as nitroglycerin or papaverine, but such treatment can lead to systemic hypotension.

●Filters can cause complications related to vessel wall injury or to difficulty in removal of the device once the carotid stent has been placed.

●By their inherent design that allows for flow through the filter, all filters allow some particles to pass into the internal carotid artery and cerebral circulation. In some instances, particles as large as 200 to 250 microns can pass, potentially resulting in small or minor stroke.

Proximal occlusion — Proximal occlusion devices redirect the flow of blood, including particulate matter, away from the internal carotid artery. Proximal occlusion is used in <5 percent of TF-CAS procedures [24]. Proponents of proximal devices emphasize that the embolic protection system is set up proximal to the lesion before intervention, which avoids unprotected engagement of the lesion as is necessary with distal filters. In a systematic review of proximal devices, the pooled rate of periprocedural adverse events was low at 1.7 percent [28].

There are two general categories of proximal occlusion.

●Flow arrest designs deploy occlusion balloons in the external carotid artery and common carotid artery, which results in cessation of flow in the internal carotid artery [29-31]. The proximal internal carotid artery is suctioned to remove debris prior to deflating the occlusion balloons. A single flow arrest system is commercially available (ie, MoMA).

●Flow reversal designs promote retrograde flow, with blood directed from the internal carotid artery through the device into the venous circulation. The flow reversal device originally used for TF-CAS has not been commercially available for several years.

Of note, the flow reversal systems require traversing the aortic arch to access the carotid artery. One flow arrest or occlusion system (eg, MoMa) that has been used with TF-CAS requires traversing the aortic arch to access the common carotid artery, but the internal carotid lesion is not traversed with the wire platform until flow occlusion is established. Another flow reversal system (Gore) was withdrawn from the market and is no longer commercially available. The flow reversal system designed for use with TCAR provides flow reversal before the lesion is crossed and with delivery of the flow reversal system and carotid stent directly through a common carotid artery cutdown, embolization from an aortic arch source is eliminated. (See "Transcarotid artery revascularization", section on 'Transcarotid stenting system'.)

Disadvantages associated with proximal embolic protection devices include [26]:

●They are larger than filter-type devices (6 French), requiring larger sheaths (9 French) to be placed into the femoral artery with potential higher risk of access-related complications.

●Cerebral ischemia can occur with proximal occlusion. Regardless of the design, some patients will be intolerant to the transient loss of flow up the internal carotid artery [32]. Using a flow arrest system, the rate of intolerance was as high as 30 percent in one study [32]. The rates of intolerance are much lower for flow reversal devices, ranging from <1 to 2.4 percent [31,33].

●Injury to the common and external carotid arteries can occur with balloon inflation.

Effectiveness of embolic protection — A benefit for the use of EPDs during TF-CAS in preventing periprocedural stroke and death has not definitively been established, and the available evidence consisting of randomized trials, retrospective reviews, and registry studies has been conflicting. In addition, the clinical significance of any new microvascular lesions, which is often used to compare devices, has yet to be determined [25]. Nevertheless, many consider the use of an EPD to be standard of care. In the United States, the use of an EPD is mandatory for reimbursement for CAS.

Stroke rates with versus without — Data from some [34,35], but not all [36], carotid stent trials (predominantly TF-CAS) suggest that EPDs are not effective for preventing symptomatic stroke or new ischemic brain lesions. In a meta-analysis that included two trials (Stent-Protected Angioplasty versus Carotid Endarterectomy [SPACE], Endarterectomy versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis [EVA-3S]), the combined endpoint of death or any stroke was similar for CAS with compared to without cerebral protection (odds ratio 0.77, 95% CI 0.41-1.46) [37].

●In the SPACE trial, the decision to use an EPD was left to the discretion of the enrolling center; only 27 percent of patients undergoing stenting received embolic protection. Four different EPDs were used. In a prespecified subgroup analysis, there was no significant difference in the 30-day outcome of ipsilateral stroke or death for those who underwent CAS with (n = 151) compared to without (n = 416) embolic protection (7.3 and 6.7 percent, respectively) [34].

●In the EVA-3S trial, which began enrollment in 2000, embolic protection was initiated in 2003, but the study was stopped in 2005. The 30-day risk of stroke and death was lower for those undergoing CAS with protection compared with those undergoing CAS without protection (8 versus 25 percent) [38].

One explanation for the inability of EPDs to prevent all perioperative strokes is that they do not prevent all emboli from reaching the distal cerebral vessels.

●The risk of stroke may be related to embolic load. This was suggested in a study that analyzed aspirated debris from 54 patients who had CAS with proximal balloon occlusion [39]. The risk of a neurologic event was associated with higher numbers of relevant particles, larger maximum particle diameters, and larger maximum particle areas.

●Filter type EPDs may paradoxically increase the microembolic load by leading to disintegration of macroemboli into smaller microemboli that can pass through the micropores of the EPD or through gaps that exist between the EPD and the arterial wall [40]. In addition, thrombus may form on the distal filter surface or on the tip of the EPD wire or result from EPD-related microtrauma to the vascular wall.

It is possible that some or all of the reduction in complication rates attributed to EPDs in observational studies is related to improvements in stent technology and the increasing experience of operators over time rather than the use of the EPDs [41,42]. In support of this hypothesis, a single-center case series of 528 patients who had CAS without protection over a five-year study period noted a significant reduction in the 30-day minor stroke rate in the fifth year compared with the first year (3.1 versus 7.1 percent, respectively) [41].

In a 2020 review of over 24,000 patients undergoing CAS, among 464 matched pairs undergoing TF-CAS with distal embolic protection or TF-CAS with proximal balloon occlusion, adverse event rates were low and outcomes were similar between the groups [24]. For distal embolic protection and proximal balloon occlusion these were, respectively:

●Stroke or death: 3.7 and 3.2 percent

●Stroke: 2.5 and 2.4 percent

●Death: 1.5 and 1.1 percent

●Transient ischemic attack: 1.5 and 1.7 percent

●Myocardial infarction (MI): 0.6 and 0.4 percent

Microembolization — There is increasing interest in quantifying microembolization events during and following CAS, but their clinical significance has yet to be established. Ischemic brain lesions discovered on DW-MRI after CAS may be associated with an increased risk for recurrent cerebrovascular events [43]. The number of events detected ranges widely between 33 and 72 percent and may be lower with use of EPDs [44]. Some have suggested that proximal flow reversal devices may cause less stent-related microembolization, but this is debated [45].

●In a systematic review of observational studies that included nearly 700 patients, the rate of new ipsilateral lesions on DW-MRI was lower for CAS procedures using an EPD compared with those without an EPD (33 versus 45 percent) [46].

●However, in a sub-study of the ICSS trial, more patients assigned to CAS at centers using EPDs had at least one new lesion on DW-MRI (largely asymptomatic) compared with those assigned to CAS at centers where EPDs were not used (37 of 51 [73 percent] versus 25 of 73 [34 percent]) [36,47,48].

●A small review evaluated the number of microembolic signals detected by transcranial Doppler or the number of new lesions identified on DW-MRI in patients undergoing flow reversal compared with filter-type EPDs, or no filter [49]. Flow reversal was associated with fewer microembolic signals during the procedure relative to historic controls with filter protection.

CAROTID REVASCULARIZATION — Carotid artery stenosis most commonly results from atherosclerotic degeneration. Disease in the carotid arteries can lead to embolization or thrombosis, resulting in neurologic events (eg, transient ischemia attack, stroke). The treatment of carotid stenosis includes maximal medical therapy and carotid revascularization for patients with appropriate indications. (See "Management of symptomatic carotid atherosclerotic disease", section on 'Intensive medical management' and "Management of asymptomatic extracranial carotid atherosclerotic disease", section on 'Intensive medical therapy and follow-up'.)

The general indications for carotid revascularization for stenotic atherosclerotic lesions are the same, regardless of revascularization approach (carotid endarterectomy [CEA], transfemoral CAS [TF-CAS], transcarotid artery revascularization [TCAR]). Indications in patients with asymptomatic or symptomatic carotid artery stenosis, whether to proceed with CEA or CAS, and whether one approach to CAS is preferable over another are discussed elsewhere. (See "Management of asymptomatic extracranial carotid atherosclerotic disease" and "Management of symptomatic carotid atherosclerotic disease" and "Overview of carotid artery stenting", section on 'Approach to carotid artery stenting'.)

Contraindications for transfemoral approach — Contraindications to CAS can be grouped into those that contraindicate the procedure, in general, and those that contraindicate a specific approach [50]:

Absolute contraindications to CAS (regardless of approach) include the following (see "Overview of carotid artery stenting", section on 'Contraindications'):

●Visible thrombus within the lesion detected on preoperative or intraoperative imaging (eg, ultrasound, angiography)

●Inability to gain vascular access

●Active infection

Relative complications to CAS include the following:

●Severe carotid plaque calcification, circumferential carotid plaque

●Severe carotid tortuosity

●Near occlusion of the carotid artery (figure 1) [51,52]

●Small internal carotid artery (unable to accommodate available commercial carotid stents)

For patients undergoing TF-CAS, the following may also preclude the ability to safely deliver the devices necessary to perform the procedure:

●Age >80 years (possibly a surrogate for a more heavily diseased aortic arch)

●Heavily calcified, severely ulcerated or thrombus-lined aortic arch

●Inability to track and deploy a cerebral protection device because of marked tortuosity of the proximal internal carotid artery

●Patients with marked truncal obesity; colonization of groins with bacteria or yeast

●Tortuous aortic arch (eg, type III arch) or aberrant arch anatomy (eg, bovine arch)

PATIENT PREPARATION — The preparatory management for CAS is similar regardless of technique. Preoperative imaging, considerations for anesthesia, and prophylactic measures (eg, antibiotics) are reviewed separately. Medication management specific to transfemoral CAS (TF-CAS) is reviewed below. (See "Overview of carotid artery stenting", section on 'Medication management'.)

Antiplatelet/statin therapy — Dual antiplatelet (DAPT) using aspirin and clopidogrel and statin therapy are recommended for all patients prior to undergoing TF-CAS. The efficacy of DAPT and statin therapy are reviewed separately. (See "Overview of carotid artery stenting", section on 'Dual antiplatelet therapy' and "Overview of carotid artery stenting", section on 'Statin therapy'.)

We use the regimen from the Carotid Revascularization Endarterectomy versus Stent Trial (CREST) [53]:

●For those patients not on chronic aspirin therapy, we start aspirin (325 mg twice daily) at least 48 hours before the procedure, or, if within 48 hours of the procedure, we give a loading dose of aspirin 650 mg four or more hours before the procedure.

●For those patients not on chronic clopidogrel therapy, we start clopidogrel 75 mg twice daily at least 48 hours before the procedure, or if within 48 hours of the procedure, we give a loading dose of clopidogrel 450 mg four or more hours before the procedure.

●For those patients not on chronic statin therapy, we start atorvastatin 40 mg daily for seven days before the procedure or we give a loading dose of 80 mg 12 hours before the procedure.

For TF-CAS, guidelines have supported a range of periprocedural aspirin therapy from 75 mg to 325 mg daily [54,55].

Following the CAS procedure, DAPT is continued for at least four weeks. We provide aspirin 325 mg daily plus clopidogrel 75 mg once daily. For patients with a history of neck irradiation, we continue DAPT indefinitely. For all other patients after CAS, we continue aspirin 325 mg daily (range 75 to 325 mg) indefinitely.

TECHNIQUES — Transfemoral CAS (TF-CAS) can be performed in an angiography suite or appropriately equipped operating room with a mobile fluoroscopy unit.

Complications of CAS may be directly related to the length of the CAS procedure. CAS should be performed expeditiously; if technical roadblocks are encountered (such as challenging aortic arch anatomy or extreme tortuosity that makes it difficult to insert the platform), it is very appropriate to abort the procedure. (See 'Complications' below.)

Percutaneous vascular access — Percutaneous access is most commonly obtained via the right (or left) common femoral artery, but transaxillary, transbrachial, transradial, and transcervical percutaneous access have all been described [56-78]. Percutaneous access is obtained in the standard fashion using ultrasound guidance. (See "Percutaneous arterial access techniques for diagnostic or interventional procedures".)

After obtaining access, an arch aortogram should be performed unless the arch anatomy is already known from preoperative imaging, such as computed tomographic (CT) angiography or magnetic resonance (MR) angiography. Older patients may have significant atherosclerotic disease of the aortic arch and origin vessels increasing their risk for atheroembolism.

Selective cerebral arteriography is also performed. Cerebral arteriography following CAS is compared with that obtained before the stent is placed to evaluate for any distal embolic debris.

Anticoagulation — Before manipulation of the guidewires and catheters within the aortic arch and carotid artery, the patient should be anticoagulated (heparin or an alternative agent) to maintain the activated whole blood clotting time at 250 to 300 seconds. For patients who cannot receive heparin (eg, heparin-induced thrombocytopenia), bivalirudin is an alternative and may be associated with a lower incidence of bleeding compared with heparin [79-82]. (See "Heparin and LMW heparin: Dosing and adverse effects" and "Direct oral anticoagulants (DOACs) and parenteral direct-acting anticoagulants: Dosing and adverse effects", section on 'Bivalirudin'.)

Whether to reverse heparin with protamine at the end of the procedure is generally driven by issues pertaining to the percutaneous access site. The increased use of closure devices reduces the need for reversal; however, for patients in whom a closure device is not used at a femoral access site, reversal of anticoagulation reduces sheath dwell time and duration of bedrest. In a review from the Vascular Quality Initiative, among over 17,000 patients who underwent transfemoral carotid artery stenting, 15 percent received protamine [83]. The use of protamine was not associated with significant differences in perioperative complications (eg, bleeding requiring reintervention, blood transfusion, transient ischemic attack, stroke, myocardial infarction, death, others) compared with no protamine. For patients treated for symptomatic carotid disease, protamine was associated with lower risk of stroke or death (3 versus 4.3 percent; relative risk 0.69, 95% CI 0.47-0.99), a difference that was not seen for asymptomatic patients.

Embolic protection device placement — Following placement of a sheath into the common carotid artery, embolic protection devices (EPDs) are deployed and then removed once the carotid artery stent has been positioned, deployed, and expanded [84]. Two general types of EPDs (distal filter or proximal occlusion) are discussed above. (See 'Embolic protection devices' above.)

●For protection using a distal filter, the filter is either deployed over a wire that is placed across the lesion or the filter is built into the wire and deployed after it crosses the lesion.

●For protection using proximal occlusion and flow occlusion designs, the occlusion balloons are placed prior to crossing the lesion.

Distal filter devices require "unprotected" tracking over a wire, through the stenotic lesion to be treated, and are deployed in the distal internal carotid artery. The most common technical problem associated with filter devices is maneuvering them up into a tortuous distal internal carotid artery. Various techniques can be used to assist in straightening the internal carotid artery (eg, use of a "buddy" wire). Another difficulty that may be encountered is passing a filter-type EPD through a severely stenotic internal carotid artery. Predilation of the lesion can be performed; however, without a filter in place, unprotected predilation is a recognized risk factor for periprocedural stroke. Vasospasm associated with the device can also be problematic.

Stent positioning and dilation — With the EPD in position, the carotid artery stenosis is predilated (if needed) and the carotid stent positioned and then deployed [85]. A post-stenting angioplasty is performed within the stent to ensure its full deployment and apposition against the arterial wall, though the need to do so routinely has been questioned [86-88]. Bradycardia due to baroreceptor activation can occur and lead to hypotension. The reaction is usually transient but may require the administration of atropine. Prophylactic administration of glycopyrrolate, an antimuscarinic anticholinergic agent, may prevent the hemodynamic response seen during carotid bulb manipulation. We give 0.2 mg glycopyrrolate intravenously prior to balloon dilation and provide a repeat dose of 0.2 mg, if necessary. (See "Anesthesia for carotid endarterectomy and carotid stenting", section on 'Hemodynamic monitoring'.)

Completion arteriography — Repeat carotid arteriography is performed before and after removal of the EPD, with attention not only to the carotid lesion but also the intracranial internal carotid vessels. Carotid arteriography should demonstrate brisk flow through the previously stenotic carotid artery.

POSTPROCEDURE CARE AND FOLLOW-UP — Many vascular surgeons will reverse heparin at the completion of a carotid endarterectomy (CEA); this can also be done at the completion of CAS. This allows normalization of activated whole blood clotting time to facilitate removing the access sheath(s). Alternatively, arterial closure devices can be used to reduce sheath dwell times and without the need for heparin reversal. (See 'Anticoagulation' above and "Percutaneous arterial access techniques for diagnostic or interventional procedures", section on 'Hemostasis at the access site'.)

Postprocedure monitoring following CAS is similar to CEA. Following CAS, the patient is transferred to a monitored setting for frequent blood pressure and neurologic assessment. The importance of tight blood pressure control cannot be overemphasized. Dual antiplatelet and statin therapy should be continued postprocedure. (See 'Antiplatelet/statin therapy' above.)

Routine duplex imaging is performed to identify restenosis. (See "Overview of carotid artery stenting", section on 'Postprocedure care and duplex surveillance'.)

COMPLICATIONS — The most serious acute complication associated with CAS is stroke. For transfemoral CAS (TF-CAS), the stroke rate is 3 to 4 percent and has steadily decreased with improvements in device technology and operator experience [89]. Stroke and other complications that are not specific to the approach to stenting, such as myocardial infarction, renal failure related to intravenous contrast, carotid thrombosis and restenosis, and stent fracture are reviewed separately. (See "Overview of carotid artery stenting", section on 'Complications'.)

Access-related issues are the most common complications following TF-CAS and include hematoma, bleeding, pseudoaneurysm formation, and atheroembolization to the lower extremities. Following percutaneous access procedures, inadequate closure of the femoral artery puncture site may lead to bleeding, hematoma, or the formation of a pseudoaneurysm. In a review of the Vascular Quality Initiative, bleeding complications occurred in 3.8 percent; however, only 0.8 percent required intervention [89].

The incidence of femoral pseudoaneurysm is approximately 3 percent [90-92]. While the narrow profile of most carotid stenting devices requires a smaller sheath size compared with some vascular interventions (eg, iliac artery stenting), it might be expected that the incidence of pseudoaneurysm might lower; however, the concomitant administration of antiplatelet therapy and anticoagulation contributes to pseudoaneurysm formation. Risk factors associated with pseudoaneurysm include inadequate postprocedure compression of the puncture site, postprocedural anticoagulation, antiplatelet therapy during the intervention, age >65 years, obesity, hypertension, peripheral artery disease, and hemodialysis. The diagnosis and treatment of access site pseudoaneurysm are discussed elsewhere. (See "Femoral artery pseudoaneurysm following percutaneous intervention".)

During any aortic catheterization procedure, atheromatous debris can become dislodged from the aortic wall. Clinical symptoms and signs are dependent upon the size of the debris and are reviewed in detail separately.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Occlusive carotid, aortic, renal, mesenteric, and peripheral atherosclerotic disease".)

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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Carotid artery disease (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Carotid revascularization to treat carotid atherosclerotic disease can be accomplished using open surgery (carotid endarterectomy) or using a carotid artery stent (CAS), with the most common CAS approach using a percutaneous approach. Transfemoral carotid artery stenting (TF-CAS) involves accessing the femoral artery percutaneously to place the necessary guidewires and sheaths, traversing the aortic arch to gain access to the carotid artery, deployment of an embolic protection device, and subsequently dilation of the artery and placement of the stent. (See 'Introduction' above and 'Carotid revascularization' above.)

●For patients in whom CAS is scheduled or anticipated, dual antiplatelet therapy (DAPT) using aspirin and clopidogrel is recommended. Furthermore, periprocedural statin therapy is also recommended. (See 'Patient preparation' above and "Overview of carotid artery stenting", section on 'Summary and recommendations'.)

For percutaneous CAS (transfemoral or other percutaneous approach), we use the following regimen, which is generally consistent with multidisciplinary guidelines:

•For those patients not on chronic aspirin therapy, we start aspirin (325 mg twice daily) at least 48 hours before the procedure, or, if within 48 hours of the procedure, we give a loading dose of aspirin 650 mg four or more hours before the procedure.

•For those patients not on chronic clopidogrel therapy, we start clopidogrel 75 mg twice daily at least 48 hours before the procedure, or if within 48 hours of the procedure, we give a loading dose of clopidogrel 450 mg four or more hours before the procedure.

•For those patients not on chronic statin therapy, we start atorvastatin 40 mg daily for seven days before the procedure or we give a loading dose of 80 mg 12 hours before the procedure.

●Following percutaneous access and sheath placement, the patient is systemically anticoagulated, typically using heparin. Whether to reverse heparin with protamine is left to the discretion of the operator and generally based on issues pertaining to the percutaneous access site. For those in whom a vascular closure device will not be used at a femoral access site, we suggest reversal of anticoagulation (Grade 2C). Reversal of anticoagulation reduces sheath dwell time and duration of bedrest. (See 'Anticoagulation' above.)

●Following the CAS procedure, DAPT with aspirin (325 mg once daily) plus clopidogrel (75 mg once daily) is continued for at least four weeks. For patients with a history of neck irradiation, we continue DAPT indefinitely. For all other patients, after clopidogrel is discontinued, we continue aspirin 325 mg daily indefinitely. (See "Overview of carotid artery stenting", section on 'Dual antiplatelet therapy'.)

●Several types of embolic protection devices (EPDs) are available and are intended to prevent embolic complications of angioplasty and stenting. Filter devices are used in most percutaneous CAS procedures. Although a benefit for EPDs has not been definitively established, many consider the use of an EPD to be standard of care. In the United States, the use of an EPD is mandatory for reimbursement for CAS. (See 'Embolic protection devices' above.)

●The most serious acute complication associated with CAS is stroke, which can occur due to thromboembolism, hypoperfusion, hyperperfusion syndrome, or hemorrhage. The overall stroke rate for TF-CAS is 3 to 4 percent and has steadily decreased with improvements in device technology and operator experience. Other complications associated with CAS include access-related issues (eg, hematoma, bleeding, pseudoaneurysm formation, and distal atheroembolization), myocardial infarction, contrast-related renal failure, restenosis of the target lesion, and carotid stent fracture. (See 'Complications' above and "Overview of carotid artery stenting", section on 'Complications'.)

ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledges Ronald M Fairman, MD, who contributed to an earlier version of this topic review.