Overview of carotid artery stenting

INTRODUCTION — The proximal internal carotid artery and the carotid bifurcation are the locations most frequently affected by carotid atherosclerosis. Progression of atherosclerotic plaque at the carotid bifurcation results in luminal narrowing, often accompanied by ulceration. This process can lead to cerebral ischemia (eg, transient ischemic attack, stroke) from arterial embolization, thrombosis, or less commonly from hemodynamic compromise. For patients with appropriate indications, options for carotid revascularization include carotid endarterectomy (CEA) or carotid angioplasty and stenting, which can be approached using several approaches, each with advantages and disadvantages.

An overview of carotid artery stenting (CAS), including approaches to CAS and factors that may favor one approach over the other, and general issues surrounding periprocedural care are reviewed, including complications. CEA is reviewed elsewhere. (See "Carotid endarterectomy".)

CAROTID ATHEROSCLEROTIC DISEASE — The management of symptomatic or asymptomatic carotid atherosclerotic disease, including the indications for carotid revascularization and the choice between carotid endarterectomy [CEA] and CAS), is discussed in detail separately. (See "Management of symptomatic carotid atherosclerotic disease" and "Management of asymptomatic extracranial carotid atherosclerotic disease".)

Indications for stenting — CAS is an option for selected patients with contraindications to CEA due to high-risk anatomical or physiological factors for symptomatic (≥50 percent) or asymptomatic high-grade (≥80 percent) internal carotid artery stenosis. (See "Management of asymptomatic extracranial carotid atherosclerotic disease", section on 'Carotid stenting' and "Management of symptomatic carotid atherosclerotic disease", section on 'Patients appropriate for CAS'.)

Risk assessment — Many of the risk factors for a worse outcome identified for CAS, such as symptomatic carotid disease, increasing degrees of carotid stenosis, parallel those identified in major trials of CEA. (See "Carotid endarterectomy", section on 'Risk factors for poor outcome'.)

Other factors that may affect CAS outcomes in patients undergoing CAS include age, sex, composition and morphology of the stenotic lesion, and the presence of white matter lesions, among others.

●Age – Data from the Stent-Protected Angioplasty versus Carotid Endarterectomy (SPACE) trial [1], Carotid Revascularization Endarterectomy versus Stent trial (CREST) [2-4], prospective series [5-7], and retrospective reports [8-10] suggest that patients ≥80 years old have a significantly higher risk of stroke and death at 30 days compared with younger patients following transfemoral CAS (TF-CAS). In addition, a retrospective study suggested that patients older than 80 had a higher incidence of unfavorable arterial factors that increased the technical difficulty of TF-CAS, such as aortic arch elongation, arch calcification, common carotid and innominate artery origin stenosis, common and internal carotid artery tortuosity, and a higher risk of residual stenosis post-stenting due to underlying vessel calcification [11]. It is also postulated that older patients have a lower cerebral reserve that makes them more sensitive to minor cerebral emboli, which may be one factor explaining their higher risk of stroke during TF-CAS [12].

Age does not appear to have an appreciable effect on patient outcomes after transcarotid artery revascularization (TCAR), which combines the benefits of avoiding a potentially diseased aortic arch with a low rate of distal embolization. The higher complication rates associated with age seen in those undergoing TF-CAS have not manifested among those undergoing the TCAR procedure. In a study evaluating all patients undergoing carotid procedures in the Vascular Quality Initiative between 2015 and November 2018, 10,381 TF-CAS cases (from 269 centers) and 3152 TCAR cases (from 174 centers) were evaluated [13]. The patients were divided into three different age groups: <70 years, 71 to 79 years, and >80 years. In-hospital mortality, stroke, myocardial infarction, and transient ischemic attack (TIA) were similar between the three age groups. TF-CAS was associated with an increased risk for stroke among older patients (>77 years) but TCAR was not.

●Sex – Clinical studies indicate that the perioperative risk of CAS compared with CEA may be higher in females compared with males [14-18]. Studies are conflicting whether the perioperative risk associated with CAS is more prevalent in symptomatic or asymptomatic women, although data favor increased risk in symptomatic females. Sex as it may impact the choice of CAS or CEA in symptomatic and asymptomatic individuals is discussed in detail elsewhere. (See "Management of asymptomatic extracranial carotid atherosclerotic disease", section on 'Factors influencing outcome' and "Management of symptomatic carotid atherosclerotic disease", section on 'Factors influencing benefit and risk'.)

●Composition and morphology of the stenotic lesion – For patients with atherosclerotic disease, heavily calcified carotid plaque [19], ulcerated plaque [6], increasing degree of carotid stenosis [8], longer lesions, and presence of thrombus have been associated with an increased risk for stroke. Retrospective reviews also suggest that long carotid lesions (>10 mm) [8,20] or carotid segments with more than one lesion separated by normal vessel wall are associated with a higher stroke risk [8]. An analysis of plaque characteristics derived from the CREST trial reported that only plaque length was associated with age with respect to stroke risk; however, it was responsible for only 8 percent of the excess stroke risk [21].

Among patients with radiation-induced stenosis, a systematic review identified 27 studies including 533 patients who underwent CAS or CEA [22]. For patients who underwent TF-CAS, the pooled estimate for any cerebrovascular adverse event was 3.9 percent, which was similar to that identified for CEA. However, the rate of restenosis (long-term) >50 percent and/or occlusion was significantly higher in patients treated with CAS compared with CEA (22.5 versus 10.7 percent). An earlier meta-analysis that included 21 studies found similar results [23].

●White matter lesions – White matter lesions are likely a consequence of degenerative changes in the deep perforating arterioles. Risk factors for the development of white-matter lesions include age and hypertension. In the International Carotid Stenting Study (ICSS), the number of lesions identified on baseline brain imaging was correlated with stroke rates at 30 days [24]. Patients who underwent CAS with ≥7 age-related white matter changes had a higher risk of stroke relative to those with <7 lesions (hazard ratio [HR] 2.76, 95% CI 1.17-6.51) and relative to CEA (any stroke: HR 2.98, 95% CI 1.3-6.9; non-disabling stroke: HR 6.34, 95% CI 1.45-27.71). No differences in stroke rates were detected for those with <7 lesions.

●Other risk factors — Other medical risk factors associated with an increased risk for periprocedural complications (mainly stroke) and worse outcome after TF-CAS have been identified in uncontrolled prospective and retrospective studies. The assessment of medical risk prior to stenting and stroke risk associated with asymptomatic and symptomatic carotid stenosis are discussed in detail elsewhere. (See "Evaluation of cardiac risk prior to noncardiac surgery".)

Other medical risk factors include [6,20,25-30]:

•Presence of aortic stenosis (may be an overall surrogate for atherosclerotic disease)

•Aortic arch calcification or variant aortic arch anatomy (transfemoral approach)

•Diabetes mellitus with inadequate glycemic control (hemoglobin A1C >7 percent)

•Symptomatic compared with asymptomatic ipsilateral carotid stenosis

•Hemispheric TIA or minor stroke compared with retinal TIA or no symptoms

•Chronic kidney disease

•Oral anticoagulant therapy

•Emergency admission

Contraindications — Contraindications to CAS can be grouped into those that contraindicate the procedure, in general, and those that contraindicate a specific approach (TF-CAS, TCAR). General contraindications are listed below. These and other specific contraindications are discussed in topics that discuss a specific approach [31] (see 'Indications for stenting' above and "Percutaneous carotid artery stenting", section on 'Contraindications for transfemoral approach' and "Transcarotid artery revascularization", section on 'Anatomic requirements and eligibility'):

Absolute

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

●Inability to gain vascular access

●Active infection

Relative — In general, relative contraindications to CAS include the following. Additional considerations depend upon the approach to carotid stenting.

●Severe plaque calcification, circumferential carotid plaque

●Severe carotid tortuosity

●Near occlusion of the carotid artery (figure 1) [32,33]

●Small internal carotid artery (may not accommodate available commercial artery stents)

Timing and other considerations — The timing of intervention in patients with symptomatic carotid disease depends on the nature and severity of symptoms (eg, TIA, stroke) and is discussed separately. Although the periprocedural risks associated with CAS are similar to CEA performed earlier (0 to 7 days), the stroke risk for CAS may be slightly higher [34,35]. (See "Management of symptomatic carotid atherosclerotic disease", section on 'Timing of revascularization'.)

Other considerations:

●Bilateral carotid stenosis – For patients with severe bilateral carotid stenosis, we suggest a staged approach rather than simultaneous CAS [8,36,37]. A staged approach limits the length of the procedure and intravenous contrast load, whereas simultaneous CAS theoretically increases the risk for cerebral hyperperfusion syndrome and the risk of severe bradycardia or hypotension related to bilateral baroreceptor irritation [38]. (See 'Hyperperfusion syndrome' below.)

●Prophylactic carotid stenting – Given that prophylactic CEA prior to another surgical procedure is generally not supported by available evidence, it may not be reasonable to offer CAS in this setting. A decision to proceed should be individualized based upon the risk of perioperative stroke weighed against the risk of bleeding associated with ongoing antiplatelet therapy (eg, clopidogrel, aspirin), which is recommended following CAS. (See "Coronary artery bypass grafting in patients with cerebrovascular disease", section on 'Method of carotid revascularization' and "Carotid endarterectomy", section on 'Carotid endarterectomy prior to other procedures' and 'Dual antiplatelet therapy' below.)

APPROACH TO CAROTID ARTERY STENTING — As experience using stents to treat atherosclerotic lesions at other peripheral sites increased, CAS was developed with the aim of reducing the systemic (eg, myocardial infarction [MI]) and local risks (eg, nerve injury) associated with carotid endarterectomy (CEA), which has been the established as the gold standard for carotid revascularization for atherosclerotic disease. To provide a durable benefit, the periprocedural risk of stroke and death for any carotid revascularization must be ≤3 percent for asymptomatic patients and ≤6 percent for symptomatic stenosis. (See "Management of asymptomatic extracranial carotid atherosclerotic disease" and "Management of symptomatic carotid atherosclerotic disease".)

With the introduction of CAS, some outcomes improved with CAS, but stroke rates were increased in early trials, likely related to certain aspects of the stent technology, the conduct, the procedure (eg, crossing a diseased aortic arch), and possibly the nature of cerebral protection. Improvements in stent devices, differing access approaches, and differing embolic protection methods (distal filter protection, proximal flow arrest, proximal flow reversal) have all been aimed at reducing the risk of stroke associated with CAS and stroke rates have improved for some, but not all patients. Alternative access approaches and technologic refinements continue.

CAS can be performed percutaneously or through a small incision in the neck.

●Percutaneous CAS obtains vascular access through the groin (transfemoral), axillary artery (transaxillary), brachial artery (transbrachial), radial artery (transradial) [39-42], or direct puncture of the carotid (transcervical). By far the most common approach is via the right (or left) common femoral artery (ie, transfemoral CAS [TF-CAS]). Percutaneous approaches for CAS are typically performed in conjunction with a distal filter-type embolic protection device; proximal occlusion has also been used [43-45]. (See 'Transfemoral carotid revascularization' below and "Percutaneous carotid artery stenting".)

●Transcarotid artery revascularization (TCAR) is a specific technique that accesses the carotid through a short incision at the base of the neck over the proximal ipsilateral common carotid artery [43-61]. The TCAR procedure is performed through a short carotid sheath in conjunction with flow reversal for embolic protection using a proprietary device. (See 'Transcarotid revascularization' below and "Transcarotid artery revascularization".)

Transfemoral carotid revascularization — Clinical trials have compared CEA with TF-CAS in patients with either symptomatic or asymptomatic carotid disease [1,2,4,62-69]. No trials have compared CAS with medical therapy alone. Compared with CEA, the periprocedural risk for stroke, and possibly longer-term risk, following TF-CAS is higher [70-72]. Combined 30-day stroke and death rates for TF-CAS in randomized trials range from 6 to 9 percent for symptomatic and from 2 to 4 percent for asymptomatic patients [73-76]. Stroke rates have improved since the introduction of CAS, achieving long-term benefit for symptomatic and asymptomatic patients [73-76].

Clinical trials — A meta-analysis of 16 trials (including CREST [2,4,68,69], ICSS [66,67], Endarterectomy versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis [EVA-3S] [63], Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy [SAPPHIRE] [64,65], and others) compared endovascular treatment (mainly TF-CAS) with CEA [74]. The risk of periprocedural stroke or death at 30 days was increased for CAS compared with CEA (8.2 versus 5.0 percent, odds ratio [OR] 1.72, 95% CI 1.29-2.31). In subgroup analysis, a higher risk of periprocedural stroke or death was seen for CAS patients ≥70 years of age compared with CEA (OR 2.20, 95% CI 1.47-3.29). By contrast, the risk of periprocedural stroke or death for patients <70 years of age was similar for CAS and CEA (OR 1.16, 95% CI 0.80-1.67). CAS had a higher rate of death or stroke during the periprocedural period or ipsilateral stroke during follow-up (10.4 versus 7.7 percent, OR 1.39, 95% CI 1.10-1.75), but a lower risk for MI (OR 0.44), cranial nerve palsy (OR 0.08), and access site hematoma (OR 0.37). The randomized trials of carotid stenting in symptomatic and asymptomatic patients are discussed in more detail elsewhere. (See "Management of asymptomatic extracranial carotid atherosclerotic disease", section on 'Carotid stenting' and "Management of symptomatic carotid atherosclerotic disease", section on 'Trials comparing CAS with CEA'.)

Registry data — The 30-day death and stroke rate was 3.6 percent in an analysis of two multicenter postmarket surveillance registries of CAS (EXACT, CAPTURE-2) that included 6320 high-risk patients [77]. In the SAPPHIRE worldwide registry, which included 2001 patients followed for 30 days, mortality was 1.1 percent and stroke rate was 3.2 percent [78]. A similar rate was found in later large reviews [10,79-81].

Transcarotid revascularization — The available clinical data on the TCAR procedure consist of safety and efficacy studies, institutional reports, and real-world outcomes reported in the TCAR Surveillance Project (TSP). The updated Society for Vascular Surgery guidelines on the management of extracranial cerebrovascular disease note that TCAR procedure is at least equivalent to CEA, with some potential improvements, and compared with TF-CAS, the overall data demonstrate better outcomes [82]. TCAR may be preferable to CEA and TF-CAS for high-risk patients (anatomic and physiologic) [83].

Safety and efficacy studies — The use of the TCAR procedure with internal carotid flow reversal was first described in 2004 [60,61]. However, the first report of TCAR performed with the neuroprotection system was published in 2011. The Silk Road Medical Embolic PROtectiOn System: First-In-Man (PROOF) study reported initial procedural success in 68 of 75 (91 percent) [43]. There were three device malfunctions and four artery dissections with device insertion. Of note, 9 percent had transient intolerance to flow reversal, which was managed successfully by minimizing the duration of flow reversal. At 30 days, there were no major strokes, MIs, or deaths [84]. In a subgroup of 31 patients who underwent a diffusion-weighted magnetic resonance imaging examination, 16 percent had evidence of new ischemic brain lesion without clinical sequelae.

The Safety and Efficacy Study for Reverse Flow Used During Carotid Artery Stenting Procedure (ROADSTER) study was a prospective, single-arm, multicenter clinical trial that enrolled 208 patients considered at high risk for complications from CEA who had either symptomatic ≥50 percent stenosis or asymptomatic ≥70 percent stenosis [85]. Between 2012 and 2014, 67 patients were enrolled as lead-in cases, and 141 were enrolled in the pivotal phase, and this latter group was evaluated for outcome analysis. The mean flow reversal time was 13 minutes, and there was one case (0.7 percent) of intolerance to high-flow reversal. The initial technical success rate was 99 percent and the all-stroke rate was 1.4 percent. The composite rate of stroke/death was 2.8 percent, and the composite rate of stroke/death/MI was 3.5 percent. One patient (0.7 percent) had postoperative hoarseness from potential 10th cranial nerve injury, which resolved at six months. In a follow-up study, 165 patients (112 of 141 pivotal ROADSTER patients as well as 53 of 78 extended-access patients) had outcomes analyzed at one year [86]. Patients aged 75 years and older comprised 43.3 percent of the cohort; 79.9 percent were asymptomatic. In this group, the ipsilateral incidence of stroke incidence was 0.6 percent; seven patients (4.2 percent) died during follow-up, but none of the deaths were neurologic in origin.

The ROADSTER 2 study was a prospective, single-arm, multicenter post-approval registry that enrolled 692 patients between 2015 and 2019. Patients were considered at high risk for complications from CEA with either symptomatic ≥50 percent stenosis or asymptomatic ≥80 percent stenosis. In the "per protocol" study population, which included 632 patients (ie, 60 protocol violations excluded), the primary endpoint of procedural success (ie, technical success plus absence of stroke/death/MI) was 97.9 percent [87,88]. In the per protocol group, the perioperative (30-day) stroke rate was 0.6 percent, the composite rate of stroke/death was 0.8 percent, and composite rate of stroke/death/MI was 1.7 percent.

Observational studies — Outcomes for the TCAR procedure appear to be at least equivalent to CEA in database reviews [89-93], and other observational studies [94]. A multi-institutional analysis reviewed 663 patients undergoing TCAR or CEA [94]. TCAR patients had higher prevalence of several comorbidities (diabetes, hyperlipidemia, coronary disease, and renal insufficiency). Overall stroke rates were similar at 30 days (1.0 percent TCAR versus 1.1 percent CEA) and one year (2.8 percent TCAR and 3.0 percent CEA) in the unmatched groups. After propensity matching based on preoperative comorbidities, 292 TCAR patients were compared with 292 CEA patients. Stroke (1.0 percent TCAR versus 0.3 percent CEA) and death (0.3 percent TCAR versus 0.7 percent CEA) were similar at 30 days and comparable at one year (stroke 2.8 percent TCAR versus 2.2 percent CEA; death 1.8 percent TCAR versus 4.5 percent CEA). The two groups had a similar composite endpoint of stroke/death/MI (2.1 percent TCAR versus 1.7 percent CEA), but TCAR was associated with a decreased rate of cranial nerve injury (0.3 percent TCAR versus 3.8 percent CEA).

TCAR surveillance project — The TCAR surveillance project (TSP) remains the largest source of data on the clinical outcome of TCAR. Although not all CEA and TF-CAS procedures are captured within the Vascular Quality Initiative (VQI), over 95 percent of all TCAR procedures performed in the United States are recorded in this registry [95]. Collection of such data provides real world outcomes. In one review of 400 consecutive patients treated with carotid revascularization, clinical practice differed from those included in carotid revascularization randomized trials in terms of patient eligibility, age, comorbidities and medications [96].

Several studies have used data from the TSP to compare outcomes between the different methods of carotid revascularization.

TCAR versus CEA

●In a study comparing in-hospital outcomes for patients treated between January 2016 and March 2018, 1182 TCAR patients were compared with 10,797 CEA patients. TCAR patients were older, more likely symptomatic, and had more medical comorbidities (including coronary artery disease, heart failure, and lung and kidney disease). TCAR patients were more likely to undergo redo carotid intervention, given higher rates of prior ipsilateral CEA (16 versus 2 percent) [90]. TCAR patients were more often treated with local or regional anesthesia (20 versus 7 percent). On unadjusted analysis, TCAR had a similar rate of in-hospital stroke/death (1.6 versus 1.4 percent) and stroke/death/MI (2.5 versus 1.9 percent) compared with CEA. There was no difference in the rate of stroke (1.4 versus 1.2 percent), in-hospital death (0.3 versus 0.3 percent), 30-day death (0.9 versus 0.4 percent), or MI (1.1 versus 0.6 percent). TCAR on average was 33 minutes shorter than CEA, and the patients were less likely to incur a cranial nerve injury (0.6 versus 1.8 percent). On adjusted analysis, there was no difference in terms of stroke/death, stroke/death/MI, or the individual outcomes [91].

●A retrospective propensity-matched cohort study compared TCAR (2692 patients) with carotid endarterectomy (8886 patients) in patients with standard surgical risk [89]. The primary composite outcome (30-day stroke, death or myocardial infarction, or stroke at one year) was similar between the groups at 3.0 and 2.6 percent, respectively. All-cause mortality was also similar (2.6 and 2.5 percent). There was a trend toward a slight increased risk of ipsilateral stroke at one year for TCAR (1.6 versus 1.1 percent; relative risk [RR] 1.49, 95% CI 1.05-2.11).

TCAR versus TF-CAS

●In a study that compared in-hospital outcomes for 638 patients undergoing TCAR from 2016 to 2017 with 10,136 patients who underwent TF-CAS between 2005 and 2017 [93], TCAR patients were found to be significantly older, had more cardiac comorbidities, were more likely to be symptomatic, and were less likely to have recurrent stenosis. TCAR procedures were more likely to be performed under general anesthesia (79 versus 12 percent) compared with TF-CAS. TCAR was associated with overall lower rates of in-hospital transient ischemia attacks (TIA)/stroke (1.9 versus 3.3 percent) and in-hospital TIA/stroke/death (2.2 versus 3.8 percent) compared with TF-CAS. On multivariate analysis, there was a trend but no statistically significant difference in stroke or death rates.

●In a later study using data between September 2016 and April 2019, there were 5251 TCAR procedures performed by 1035 surgeons from 319 centers [95]. Most procedures were performed by vascular surgeons (85 percent), followed by general surgeons (9 percent), neurosurgeons (2 percent), and cardiologists (1 percent). TCAR accounted for 46 percent of all carotid stenting procedures performed in 2018. There were 6640 TF-CAS patients included in the study. After propensity score matching, 3286 pairs of patients were identified. TCAR was associated with a lower risk of in-hospital stroke or death (1.6 versus 3.1 percent), stroke (1.3 versus 2.4 percent), and death (0.4 versus 1 percent). There was no statistically significant difference in the risk of perioperative MI (0.2 versus 0.3 percent). The TCAR procedure was also associated with less radiation exposure for the patient and less contrast utilized. At one year, TCAR also had a lower risk of ipsilateral stroke or death (5.1 versus 9.6 percent).

Selecting an approach

Anatomic evaluation — The evaluation of patients who may be candidates for CAS includes preoperative vascular imaging to characterize the carotid lesion and assure its patency, evaluate surrounding anatomy, and identify anatomic features that may influence the approach to CAS. (See "Evaluation of carotid artery stenosis".)

The evaluation of the carotid lesion may include duplex ultrasonography, computed tomographic (CT) angiography, or magnetic resonance imaging or catheter angiography depending on the clinical presentation (symptomatic, asymptomatic). These are typically sufficient to characterize the carotid lesion and surrounding anatomy. For TCAR, ultrasound examination of the neck also confirms adequate anatomy for arterial sheath insertion.

●For TF-CAS, CT angiography identifies any significant aortoiliac occlusive disease. For patients with occlusive disease, a decision needs to be made whether transfemoral access is feasible, or whether adjunctive endovascular procedure (eg, iliac artery angioplasty/stenting) is needed to safely achieve access. For some patients, an alternative access route may need to be selected.

●For TCAR, CT angiography defines anatomic candidacy related to the length of common carotid artery, presence of aortic arch atheroma, vessel tortuosity, and calcium burden within the carotid lesion.

Cross-sectional contrast-enhanced imaging from the aortic arch through to the Circle of Willis should also be performed to identify the presence of intracranial arterial disease that may affect patient outcome.

Factors favoring TF-CAS — For patients in whom CAS has been selected, the following factors may favor the TF-CAS.

●Severe radiation injury in the neck

●Prior neck ablative surgery (laryngectomy with tracheostomy or radical neck dissection)

The degree of radiation damage to the soft tissue in a patient who has undergone prior neck irradiation should be considered when selecting an approach for CAS. The TCAR procedure may be avoided because it requires limited dissection through a neck incision. Patients with prior neck irradiation tolerate TF-CAS with relative safety [5,97-99]. However, in many [100-102], but not all, studies [103,104], the rate of late carotid restenosis and occlusion following CAS was higher in patients who had radiation-induced occlusive disease compared with those who had atherosclerotic carotid disease [101]. A systematic review identified 27 studies that included 533 patients with radiation-induced carotid stenosis who underwent CAS or CEA [22]. Among patients who underwent TF-CAS, the pooled estimate for any cerebrovascular adverse event was 3.9 percent, which was similar to that identified for CEA. However, the rate of restenosis >50 percent and/or occlusion was significantly higher in patients treated with CAS compared with CEA (22.5 versus 10.7 percent). An earlier meta-analysis that included 21 studies found similar results [23]. However, carotid restenosis and occlusion in these reports was largely asymptomatic.

Factors favoring TCAR — For patients in whom CAS has been selected, the following factors may favor the TCAR procedure.

●Peripheral arterial disease with unfavorable peripheral artery (eg iliac, femoral) access

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

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

●Variations in aortic arch anatomy, such as a type III arch or bovine anatomy

●Patients with marked truncal obesity with groin colonization with bacteria and yeast

●Age >80

PERIOPERATIVE CARE — Transfemoral CAS (TF-CAS) is most commonly performed using local anesthesia with sedation and close cardiopulmonary monitoring by the anesthesia provider. It is important for the patient to be able to communicate freely during the procedure with the anesthesia provider. The patient needs to be comfortable, but not so heavily sedated that they are disinhibited or unable to follow commands. Transcarotid artery revascularization (TCAR) may be more commonly performed using general anesthesia. In a study looking at 2609 patients undergoing TCAR, 82.3 percent were performed with general anesthesia and 17.7 percent under local anesthesia with no differences in clinical outcomes (eg, mortality, myocardial infarction [MI], neurologic events) [105]. General anesthesia is generally recommended for TCAR proceduralists early during their experience; however, when procedural familiarity is obtained, TCAR is well suited for use of local anesthesia as with TF-CAS. (See "Anesthesia for carotid endarterectomy and carotid stenting".)

Some degree of periprocedural bradycardia or hypotension occurs in up to 68 percent of patients who undergo CAS [106-113]. Given that bradycardia or even cardiac arrest can develop during ballooning of the stent, both atropine and glycopyrrolate should be available for immediate infusion. Bradycardia is due to carotid baroreceptor stimulation during inflation of the post-stent angioplasty balloon.

Following CAS, patients are typically discharged in one to two days. Outpatient CAS may become feasible, but the safety of this practice needs to be established. Reimbursement in the United States for CAS mandates an overnight hospitalization of at least one day.

Medication management

Preoperative control of blood pressure — Poorly controlled hypertension preoperatively is predictive of prolonged length of stay due to postoperative hypertension. Thus, we make an effort to have hypertension under control before proceeding with CAS [114]. (See "Anesthesia for carotid endarterectomy and carotid stenting", section on 'Hemodynamic monitoring'.)

Prophylactic antibiotics — Although not routinely recommended for all percutaneous interventional procedures, antibiotic prophylaxis prior to CAS is standard practice, regardless of approach. Appropriate antibiotic choices are given in the table (table 1).

Dual antiplatelet therapy — Prior to CAS, we recommend pretreatment with dual antiplatelet therapy (DAPT) using aspirin and clopidogrel (algorithm 1); however, data are limited regarding the effectiveness of DAPT; the optimal timing, dose and duration of treatment for CAS is unknown [115]. Our specific pretreatment and post-treatment dosing regimens for percutaneous CAS and TCAR are provided separately. (See "Percutaneous carotid artery stenting", section on 'Antiplatelet/statin therapy' and "Transcarotid artery revascularization", section on 'Dual antiplatelet therapy and statins'.)

A systematic review identified only two small trials comparing single with dual antiplatelet therapy in patients undergoing CAS. In a meta-analysis of these two trials [116-118], the risk for transient ischemic attack (TIA) was reduced for dual compared with single antiplatelet therapy (1.3 versus 14.6 percent; risk difference -0.13; 95% CI -0.22 to -0.05). However, there were no differences in stroke, major bleeding, or hematoma formation, or incidence of MI or death. In a separate meta-analysis of these same trials, the risk for restenosis was similar [119]. In the absence of any other robust data, we initiate DAPT using aspirin and clopidogrel prior to the procedure (at least 48 hours for percutaneous CAS; the TCAR trial favored 72 hours pretreatment) and continue dual antiplatelet therapy post-procedure for at least four weeks. Thereafter, aspirin should be continued indefinitely to reduce the risk for future cardiovascular events. (See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk", section on 'Antiplatelet therapy'.)

In an observational study from the Vascular Quality Initiative looking at 31,036 total CAS procedures (approximately 50/50 TCAR and TF-CAS), perioperative P2Y12 inhibitors (clopidogrel, prasugrel, or ticagrelor taken within 36 hours of the procedure) markedly reduced the perioperative neurologic event rate [120]. Among patients on P2Y12 inhibitors, 92.7 percent were also taking aspirin. P2Y12 inhibitors were significantly more likely to be used in TCAR cases compared with TF-CAS cases (87.3 versus 76.8 percent). Of the patients on P2Y12 inhibitors, 77.3 percent were on clopidogrel. This study demonstrated there is considerable room for improving compliance with recommended perioperative DAPT.

For patients with a history of neck irradiation, we suggest long-term DAPT with aspirin and clopidogrel following CAS, provided the risk of bleeding remains low. While there are no studies available that have specifically evaluated such a protocol in this subset of patients, radiated patients are at high risk for recurrent carotid stenosis following CAS, as high as 30 percent in some series.

In CAS trials, the following protocols were used:

●In the CREST trial, patients were treated with aspirin (325 mg twice daily) and clopidogrel (75 mg twice daily) starting at least 48 hours before the CAS procedure [4]. Those scheduled for CAS within 48 hours received aspirin 650 mg and clopidogrel 450 mg at least four hours before the CAS procedure. Following CAS, treatment included aspirin 325 mg once or twice daily and clopidogrel 75 mg daily (or ticlopidine 250 mg twice daily) for at least 30 days, with a recommendation to continue aspirin indefinitely (at least one year).

●In a survey of participants of the Asymptomatic Carotid Surgery Trial 2 (ACST2 trial), 82 percent of sites used dual antiplatelet therapy (DAPT) preoperatively and 86 percent postoperatively with a mean postprocedural duration of three months (range 1 to 12), while 9 percent continued DAPT lifelong [121]. For those prescribing postprocedural mono antiplatelet therapy (76 percent), aspirin was more commonly prescribed than clopidogrel (59 versus 6 percent), and 11 percent did not show a preference for either aspirin or clopidogrel. Eleven centers (16 percent) tested for antiplatelet therapy resistance.

●In the ROADSTER 2 study, early postoperative outcomes in the intention-to-treat population (692 patients) included stroke in 13 patients (1.9 percent), death in 3 patients (0.4 percent), and MI in 6 patients (0.9 percent) [88]. Sixty patients had major protocol deviations, and among these, 48 patients were not on dual antiplatelet and statin therapy while undergoing carotid intervention or during the periprocedural follow-up period. Among the 60 patients with protocol violations, perioperative (30-day) stroke occurred in 9 (26 percent); death in 2 (3.3 percent); MI in none.

Guidelines have suggested a range of periprocedural aspirin therapy ranging from 75 mg to 325 mg daily [82,83,122,123]. Various loading doses of clopidogrel have also been used.

Other doses of clopidogrel have also been investigated. In the Clopidogrel and Atorvastatin Treatment During Carotid Artery Stenting (ARMYDA-9 CAROTID) trial, 156 patients were randomly assigned to receive a loading dose of clopidogrel (600 mg or 300 mg) before stenting with or without a statin reload (2 x 2 trial design) [124]. The perioperative (30-day) incidence of TIA/stroke or new ischemic lesions on magnetic resonance imaging was lowest in the 600 mg clopidogrel plus statin reload group. By contrast, in a smaller trial, no differences were seen between groups for asymptomatic patients (n = 35) undergoing CAS assigned to 300 mg or 600 mg of clopidogrel with respect to the sum of all microembolic signals on transcranial Doppler, or platelet aggregation measurements [125].

Cilostazol is a phosphodiesterase inhibitor that is commonly used in the treatment of claudication. A systematic literature review identified seven studies evaluating outcomes using cilostazol in association with CAS [126]. Major outcomes included in-stent restenosis within the observation period, revascularization rate, major/minor bleeding, and MI/stroke/death rate at 30 days and within the observation period. A significantly lower rate of in-stent stenosis was seen with cilostazol treatment after a mean follow-up of 20 months (odds ratio [OR] 0.158, 95% CI 0.072-0.349). No significant differences were found between the groups among five studies (649 patients) for periprocedural MI/stroke/death or in three studies (1076 patients) for MI/stroke/death for the entire follow-up period.

Statin therapy — Statin therapy is recommended for patients following TIA or ischemic stroke or in those with coronary artery disease risk equivalents. (See "Management of low density lipoprotein cholesterol (LDL-C) in the secondary prevention of cardiovascular disease" and "Overview of secondary prevention of ischemic stroke", section on 'LDL-C lowering therapy'.)

Whether statin therapy can reduce the risk of cerebral embolization during or after CAS is debated [124,127-132]. A small study compared debris collected from embolic protection devices in 62 patients who were or were not taking statins [132]. Statin use (HMG-CoA-reductase inhibitor) was associated with significantly fewer embolic particles (16.4 versus 42.4 particles). Coronary artery disease, prior coronary artery bypass grafting, and hyperlipidemia were more prevalent in those receiving statins. The authors speculated that statin use stabilizes atherosclerotic plaque, resulting in a more fibrous plaque that is less vulnerable.

Our specific pretreatment and post-treatment dosing regimens for percutaneous CAS and TCAR are provided separately. (See "Percutaneous carotid artery stenting", section on 'Antiplatelet/statin therapy' and "Transcarotid artery revascularization", section on 'Dual antiplatelet therapy and statins'.)

Patients requiring long-term anticoagulation — A decision to stop versus bridge long-term oral anticoagulation (OAC) prior to carotid stenting is individualized and made together with the patient's cardiologist or medical physician [133]. Regardless of whether OAC is continued or temporarily discontinued (with or without bridging anticoagulation), antiplatelet therapy (ie, aspirin and clopidogrel) is initiated prior to the carotid procedure in the manner discussed above. (See 'Dual antiplatelet therapy' above and "Perioperative management of patients receiving anticoagulants".)

Following carotid stenting, if OAC was temporarily discontinued, it is resumed and aspirin and clopidogrel initiated preoperatively are continued for at least four weeks, at which point aspirin is discontinued while clopidogrel is continued along with the anticoagulation. Any new ischemic or bleeding episodes (or change in bleeding risk) should lead to a re-evaluation of antithrombotic therapy. This approach is based on outcomes from coronary stenting. There are no data to suggest that a different approach is warranted when performing a carotid stent. (See "Coronary artery disease patients requiring combined anticoagulant and antiplatelet therapy", section on 'Our approach'.)

Outcomes from studies of percutaneous coronary procedures with or without stenting also do not demonstrate any increase in adverse outcomes for uninterrupted compared with interrupted OAC, suggesting that continuing OACs is safe [134,135]. In one retrospective review of patients undergoing CAS, among 502 patients, there were 20 patients who did not discontinue OACs. There were no complications in this group [136]. In another review that included 511 CAS procedures, among 30 patients taking OACs, outcomes were similar to those not taking OACs [30].

Postprocedure care and duplex surveillance — Postprocedure care following CAS is similar to that following carotid endarterectomy [114]. (See "Carotid endarterectomy", section on 'Postoperative care'.)

Patients are transferred to a monitored setting for frequent blood pressure and neurologic assessment. CAS is associated with a slightly higher rate of postprocedural hypotension compared with CEA, likely related to the continued outward force of the implanted stent on the carotid body [112,113]. As such, measures should be taken to closely monitor for this occurrence and aggressively treat postoperative hypotension.

Repeat duplex ultrasonography should be obtained within three months following CAS to establish a new baseline for future comparison. Duplex surveillance is performed every six months for two years and then annually thereafter until stable (ie, no restenosis observed in two consecutive annual scans) [137]. More frequent intervals may be warranted if a contralateral stenosis is being observed.

COMPLICATIONS — Complications associated with carotid revascularization can be grouped into systemic complications that, in general, are related to the revascularization (stroke), patient comorbidities (eg, myocardial infarction [MI], chronic kidney disease), related to the stent (in-stent restenosis, stent fracture), and related to the revascularization approach. Complications specific to the approach include complications related to arterial access or related to the embolic protection system. Approach-specific complications are reviewed separately. (See "Percutaneous carotid artery stenting", section on 'Complications' and "Transcarotid artery revascularization", section on 'Complications'.)

In a study that evaluated the timing of complications following CAS, 53 percent of postoperative events/complications occurred within 6 hours of CAS, 5.3 percent between 6 and 12 hours, 8 percent between 12 and 24 hours, and 34.2 percent >24 hours postprocedure [108]. Late events >24 hours were access site-related, and neurologic events included transient ischemia, minor stroke, and major stroke.

Stroke — The most serious acute complication associated with CAS is stroke. Periprocedural stroke related to CAS may be due to several mechanisms, alone or in combination, including the following [138]:

●Thromboembolism

●Hypoperfusion due to bradycardia and/or baroreceptor stimulation

●Cerebral hyperperfusion

●Intracerebral hemorrhage

●Stent thrombosis

●Noncompliance with antiplatelet therapy

Combined 30-day stroke and death rates for transfemoral CAS (TF-CAS) in randomized trials range from 6 to 9 percent for symptomatic patients and 2 to 4 percent for asymptomatic patients [1,66,139]. Stroke rates have improved since the first introduction of CAS. The 30-day death and stroke rate was 3.6 percent in an analysis of two multicenter postmarket surveillance registries of CAS (EXACT, CAPTURE-2) that included 6320 high-risk patients [77]. A similar rate was found in later large reviews [10,79-81]. (See 'Transfemoral carotid revascularization' above.)

Transcarotid artery revascularization (TCAR) appears to be associated with a lower risk for stroke compared with TF-CAS. In a study in which 3286 propensity matched pairs were studied, stroke rates were 1.3 and 2.4 percent in the TCAR and TF-CAS groups, respectively [95]. The theoretical explanation for these observations is that TCAR eliminates the need to traverse the aortic arch during the intervention where there is often considerable concomitant atherosclerotic thromboembolic debris. The effectiveness of flow reversal in preventing distal embolization may also play a role. (See 'Transcarotid revascularization' above.)

The main strategies used to reduce the risk of thromboembolic complications during and following CAS are appropriate patient selection, perioperative treatment with optimal medical therapy (including dual antiplatelet therapy [aspirin and clopidogrel] and statin), optimal intraoperative anticoagulation, strict postprocedural blood pressure control, and possibly choice of approach (TCAR versus TF-CAS) and choice of embolic protection. (See 'Dual antiplatelet therapy' above and 'Transcarotid revascularization' above and "Percutaneous carotid artery stenting", section on 'Embolic protection devices' and "Transcarotid artery revascularization", section on 'Establishing flow reversal and carotid stenting'.)

Hyperperfusion syndrome — Cerebral hyperperfusion syndrome is an uncommon sequela of CAS, and its occurrence after carotid stenting follows a similar path to that following carotid endarterectomy (CEA) [140]. The syndrome is often heralded by headache ipsilateral to the revascularized internal carotid artery. Focal motor seizures and intracerebral hemorrhage may follow. As with CEA, hypertension is a frequent predecessor of the syndrome, underscoring the importance of adequate control of perioperative blood pressure. (See 'Preoperative control of blood pressure' above and "Complications of carotid endarterectomy", section on 'Hyperperfusion syndrome'.)

Scant data exist concerning the incidence of the hyperperfusion syndrome after carotid stenting. In a retrospective review of 450 patients treated with CAS, the following observations were made [141]:

●Hyperperfusion developed in five patients (1.1 percent), all of whom had correction of a severe internal carotid stenosis (mean 96 percent).

●All five patients with hyperperfusion syndrome had contralateral carotid stenosis >80 percent or occlusion, and baseline hypertension.

●Intracerebral hemorrhage developed in three of the five patients, two of whom developed significant periprocedural hypertension preceding the intracerebral hemorrhage. Two of the patients with intracerebral hemorrhage died.

Myocardial infarction — In major randomized trials, the periprocedural incidence of MI with CAS has ranged from <1 to 4 percent [4,66]. In a study comparing 3286 propensity-matched pairs of patients undergoing TCAR and TF-CAS, there was no statistically significant difference in the risk of perioperative MI (0.2 versus 0.3 percent). In the author's experience, acute coronary syndromes can be precipitated by profound bradycardia and transient hypotension associated with ballooning the stent. Even with routine prophylactic strategies to avoid bradycardia, cardiac ischemia still sometimes occurs. Other risk factors for cardiac complications in noncardiac surgery and management of perioperative MI are discussed in detail elsewhere. (See "Evaluation of cardiac risk prior to noncardiac surgery" and "Perioperative myocardial infarction or injury after noncardiac surgery".)

Data from the National Inpatient Sample on 1,083,688 patients who underwent CEA or CAS found that 11,341 (approximately 1 percent) developed non-ST elevation MI (NSTEMI) during hospitalization. NSTEMI was associated with a significantly higher rate of in-hospital mortality (6.2 versus 0.4 percent), neurologic complications (6 versus 1.4 percent), and longer hospital stay (12.2 versus 2.8 days) [142]. (See "Acute coronary syndrome: Terminology and classification" and "Overview of the acute management of non-ST-elevation acute coronary syndromes".)

Renal dysfunction — Renal dysfunction following CAS can be related to contrast-induced nephropathy, renal atheroemboli (during TF-CAS), or renal hypoperfusion due to hemodynamic instability. The risk of contrast nephropathy following CAS is greatest in patients with moderate-to-severe renal insufficiency and diabetes. (See "Contrast-associated and contrast-induced acute kidney injury: Clinical features, diagnosis, and management" and "Prevention of contrast-associated acute kidney injury related to angiography".)

Instrumentation of the aorta during TF-CAS can lead to atheroembolic events, which in turn can result in renal dysfunction. (See "Clinical presentation, evaluation, and treatment of renal atheroemboli" and "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)".)

Carotid thrombosis and restenosis — Acute and subacute in-stent thrombosis has been reported in 0.5 to 5 percent of patients with CAS [143,144]. Some cases of carotid restenosis following CAS may be related to inadequate or discontinued antiplatelet therapy [145-147]. Beyond 30 days, early restenosis after CAS is mainly due to neointimal hyperplasia, which is related to vascular injury related to the stent regardless of the technique used to place the stent (ie, TF-CAS, TCAR) [148-150]. Neointimal hyperplasia related to CAS may be due to stent overdilation or imperfect positioning of the carotid stent in the vessel leading to ongoing vascular injury, and it may occur more often in women and in patients with poorly controlled diabetes or hyperlipidemia [151]. Prior radiation is also a risk factor. Data regarding restenosis come primarily from trials and observational studies evaluating TF-CAS.

Reported rates of early restenosis after CAS vary widely [64,151-157]. In a systematic review that analyzed 34 carotid stenting studies involving 3814 arteries, angiographic restenosis, defined as ≥50 to 70 percent stenosis (a lower threshold), occurred in approximately 6 percent of arteries after one year [152]. This compares favorably with reported rates of restenosis in the first 12 to 18 months after CEA, which range from 5.2 to 11.4 percent [153-155]. In a review of 1060 patients, independent risk factors for restenosis ≥70 percent identified on logistic regression included hypertension (hazard ratio [HR] 6.2, 95% CI 1.9-19.9), impaired vasoreactivity (HR 1.7, 95% CI 1.09-2.8), and angioplasty without stent (HR 2.9, 95% CI 1.2-6.8) [157].

In the SAPPHIRE trial, target vessel revascularization (TVR) was performed for a stenosis of ≥50 percent with ischemic neurologic symptoms or a stenosis of ≥80 percent without neurologic symptoms [64,158]. At one year after the procedure, the rate of TVR was significantly lower for the stenting group compared with the endarterectomy group (0.6 versus 4.3 percent) [64]. At three years postprocedure, the rate of TVR remained lower for TF-CAS compared with endarterectomy (2.4 versus 5.4 percent), but the difference was not significant [158]. In the Asymptomatic Carotid Trial I (ACT-1), the one-year rate of TVR was also lower for the stenting group (0.6 versus 2.6 percent) [62].

In a secondary analysis of the CREST trial, 2191 patients with appropriate postoperative ultrasonography were available for study (CAS 1086, CEA 1105) [151]. The rates for restenosis at two years were similar for CAS compared with CEA. Female sex, diabetes, and dyslipidemia were independent predictors of restenosis or occlusion after the two procedures. Smoking predicted an increased rate of restenosis after CEA but not after CAS. At 10-year follow-up, there was no statistically significant difference in the development of restenosis or need for revascularization between transfemoral CAS and CEA (12.2 versus 9.7 percent) [69].

A single-center case series with long-term follow-up of 221 carotid stenting procedures on 193 patients showed a restenosis rate (>50 percent on duplex scan) at 10 years was 6.8 percent [159]. [152]

Stent fracture — Stent fracture may be a common complication of CAS, but its clinical significance is unknown. Data regarding stent fracture come from studies evaluating TF-CAS. In a retrospective report of 48 carotid stents in 43 patients, stent fracture was detected at a mean radiologic follow-up of 18 months in 29 percent [160]. The risk of stent fracture was associated with the presence of arterial calcification in the region of the deployed stent (odds ratio 7.7, 95% CI 1.9-32.0). Restenosis >50 percent was present in 3 of the 14 fractured stents and 3 of 34 stents without fracture. In a review of the outcomes of the ACT-1 trial, in which CAS was used in 1021 standard surgical risk patients with asymptomatic carotid stenosis, stent fracture was detected in 5.4 percent of 939 patients who had at least one radiograph during follow-up [161]. There was no association between stent fracture and the occurrence of carotid restenosis or for a primary composite endpoint of stroke, death, or MI.

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".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

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 artery stenting – Carotid artery stenting (CAS) can be performed percutaneously (eg, transfemoral CAS [TF-CAS]) or through a small incision in the neck (ie, transcarotid artery revascularization [TCAR]). A technical comparison of these methods is provided above. During CAS, several methods of embolic protection are used and are intended to prevent stroke; however, the superiority of one method over another, and furthermore, an overall benefit has not been definitively established. (See 'Approach to carotid artery stenting' above.)

●Bilateral carotid stenosis – For patients with severe bilateral carotid stenosis, we prefer a staged approach rather than simultaneous CAS. Simultaneous CAS theoretically increases the risk for cerebral hyperperfusion syndrome, as well as severe bradycardia or hypotension related to bilateral baroreceptor irritation. (See 'Timing and other considerations' above.)

●Antiplatelet therapy – For patients in whom CAS is scheduled or anticipated, we recommend pretreatment with dual antiplatelet therapy (DAPT) using aspirin and clopidogrel, rather than monotherapy or no antiplatelet therapy (Grade 1B).

•Duration of therapy

-DAPT is continued for at least four weeks after the procedure. Aspirin alone is subsequently continued indefinitely to reduce the risk of future cardiovascular events. (See 'Dual antiplatelet therapy' above and "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk".)

-For patients with a history of neck irradiation, we suggested continuing DAPT using aspirin and clopidogrel indefinitely (Grade 2C). Radiated patients are at high risk for recurrent carotid stenosis following CAS (See 'Dual antiplatelet therapy' above.)

•Dosing regimens – Specific pre- and post-treatment DAPT dosing regimens for TF-CAS and TCAR are provided separately. Statin therapy is also recommended. (See "Percutaneous carotid artery stenting", section on 'Antiplatelet/statin therapy' and "Transcarotid artery revascularization", section on 'Dual antiplatelet therapy and statins'.)

●Stroke – The most serious acute complication associated with carotid artery stenting (CAS) is stroke, which can occur due to thromboembolism, hypoperfusion, hyperperfusion syndrome, or hemorrhage. Potential factors that have an impact on the risk of stroke with CAS include older age, carotid plaque morphology, prior neck irradiation, and contralateral carotid occlusive disease. The main strategies used to reduce the risk of thromboembolic complications during and following CAS are appropriate patient selection, perioperative treatment with aspirin and clopidogrel (dual antiplatelet therapy), and optimal intraoperative anticoagulation. (See 'Complications' above and 'Risk assessment' above.)

●Other complications – 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 "Percutaneous carotid artery stenting", section on 'Complications' and "Transcarotid artery revascularization", section on 'Complications'.)

ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges Emile R Mohler, III, MD (deceased), who contributed to an earlier version of this topic review.

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