General description of procedure, equipment, technique

Carotid stenting is an effective therapy for patients with symptomatic and asymptomatic carotid atherosclerotic disease. Early results of endovascular treatment of carotid disease were limited by high risk of embolic stroke but ongoing improvement in technology (emboli protection devices and self-expanding stents), use of dual antiplatelet therapy, and improved operator experience, have made it a safe and effective procedure in carefully selected patients (Figure 1).

Figure 1.
A 65-year- old patient presented with transient left arm paresis. A carotid Doppler revealed severe stenosis of his right internal carotid artery (RICA) and total occlusion of the left carotid system. He was successfully treated with a carotid stent and the poststent cerebral angiogram demonstrated filling of the entire anterior circulation from the RICA.

The procedure is however currently performed in a small minority of patients undergoing carotid revascularization in the United States, although the safety and efficacy of this procedure have been established in well-designed, randomized controlled trials. This is mainly related in the U.S. to the decision by the Center for Medicare Services (CMS) to limit reimbursement for the procedure to a small subgroup of patients.

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Indications and patient selection

Carotid stenting should be considered as an alternative to carotid endarterectomy (CEA) in patients with symptomatic or asymptomatic carotid artery disease based on patient risk with either treatment. In general, randomized data have demonstrated a higher risk of periprocedural stroke with carotid artery stenting, while the risk of periprocedural myocardial infarction is higher in patients undergoing carotid endarterectomy.

The increased risk of periprocedural stroke with carotid artery stenting appears to be particularly relevant in older patents and those undergoing treatment for symptomatic disease, although this has not been a consistent finding in most of the recent studies.

Current guidelines support the use of carotid revascularization in patients with symptomatic carotid artery disease (defined as nondisabling hemispheric stroke or transient ischemic attack in the prior 6 months), a greater than 50% stenosis, and an anticipated procedural stroke or mortality risk of <6%. In asymptomatic patients, carotid revascularization is advised for patients with a stenosis >70%, a procedural risk of stroke or death of <3%, and a life expectancy of at least 5 years.

Carotid artery stenting (CAS) is favored in patients whose anatomy or comorbidities increase the risk of CEA. Anatomic features that make CEA higher risk are stenosis that is located higher than the second vertebral body, intrathoracic stenosis, prior CEA, contralateral vocal cord paralysis, open tracheostomy, prior radical neck surgery, or prior neck radiation.

CAS may be safer than CEA in patients with severe cardiac disease (class III-IV congestive heart failure or angina, need for cardiac surgery within 30 days, left ventricular ejection fraction <30%, class III-IV angina pectoris, left main or severe three-vessel coronary artery disease, myocardial infarction within 30 days) or pulmonary disease. These patients often have a poor life expectancy and the need for any revascularization should be carefully balanced against the risk of stroke on best medical therapy.


Contraindications to carotid artery stenting can be broadly divided into conditions that negate any procedural benefit or those with increased procedural risk.

1.    CAS should not be performed in patients where the procedural risk of stroke or mortality exceeds the risk associated with ongoing medical therapy. Thus, CAS should not be performed if the anticipated procedural risk of death or stroke for a symptomatic patient exceeds 6% or exceeds 3% for an asymptomatic patient. CAS should generally be avoided in asymptomatic patients if the life expectancy is <5 years.

2.    Inability of the patient to take dual antiplatelet therapy due to allergy, compliance, hematologic disorders such as thrombocytopenia, or active bleeding problems

3.    Relative contraindications:

  • Anatomic features that increase procedural risk.
  • Heavy calcification of the lesion (especially concentric), severe angulation of the carotid artery, excessive proximal or distal tortuosity that limits use of emboli protection devices, unfavorable arch anatomy (Type III arch), presence of heavy thrombus burden

4.    Recent hemispheric stroke – the optimal timing of CAS in these patients remains debatable. Early CAS has been associated with a high risk of hemorrhagic conversion and some observational studies suggest delaying the procedure for 2 weeks after the stroke.

5.    Prior multiinfarct dementia or cerebral microangiopathy with diminished vascular reserve

6.    Severe uncontrolled hypertension

Details of how the procedure is performed

Most patients who undergo CAS have known carotid artery stenosis that has been diagnosed with a noninvasive modality, such as duplex ultrasonography, magnetic resonance angiography, or computed (CT) angiography. It is our preference to perform CT angiography, if feasible, prior to CAS in most patients since it helps provide an accurate assessment of anatomic features that might increase procedural risk or might help guide choice of equipment.

The patient should be started on dual antiplatelet therapy (aspirin + a thienopyridine) prior to the procedure and blood pressure should be adequately controlled. We also routinely start high-dose statin therapy prior to the procedure based on better outcomes associated with statins in patients undergoing coronary stenting and the proven benefit of statin therapy in patients with advanced atherosclerosis.

There are no data, however, that demonstrate improved clinical outcomes with statin therapy in patients undergoing CAS.

The procedure is usually performed via femoral arterial access, although it can be performed using brachial or radial access.

Heparin or bivalirudin are used for procedural anticoagulation. Carotid angiography is performed followed by delivery of a guiding catheter or sheath to the common carotid artery. An emboli protection device is then deployed distal or proximal to the stenosis and the lesion is dilated with a small balloon to facilitate delivery of a stent.

Some operators prefer direct stenting when feasible. Most of the stents that are used clinically for carotid stenting are made of nitinol and are self-expanding in nature. The deployment of the stent is often followed by postdilation of the stent with a high pressure balloon, following which the emboli protection device is removed.

The pressure from the angioplasty balloons, as well as from the self-expanding stent, stimulates the carotid baroreceptors and patients can develop bradycardia and hypotension from diminished sympathetic outflow and increased vagal tone. This usually responds to atropine and low dose sympathomimetic drugs. Pacing is rarely required but should be considered in patients in whom such hemodynamic changes may not be well tolerated (such as patients with critical aortic stenosis or severe pulmonary hypertension).

Outcomes (applies only to therapeutic procedures)

Carotid stenting has favorable outcomes in the hands of experienced operators. In most recent large registries, the procedural risk of stroke and mortality has been less than 6% in symptomatic patients and less than 3% in asymptomatic patients.

The best data on the comparative outcome of contemporary CEA and CAS can be derived from the CREST trial. In this trial, a total of 2,502 average surgical-risk, symptomatic (53%), and asymptomatic (47%) patients were randomized to CAS or CEA by experienced operators.

There was no difference between CAS and CEA for the primary end point (any stroke, myocardial infarction [MI], or death within the periprocedural period, plus any ipsilateral stroke thereafter) at 4 years (CAS, 7.2% vs CEA, 6.8%, HR = 1.11, 95% CI: 0.81 to 1.51; P = .51). There was an excess of strokes with CAS (4.1% vs 2.3%) that was driven mainly by an excess of minor strokes with no difference in major strokes (CAS 0.9% vs CEA 0.7%).

An excess of myocardial infarction was seen with CEA (2.3% vs 1.1%). A significant interaction was seen with age, and younger patients (<69 years old) did better with CAS, and older patients did better with CEA. Long term, there was no difference in risk of stroke with either CEA or CAS, suggesting similar efficacy of the procedure.

Alternative and/or additional procedures to consider

CAS should be performed only after consideration of the alternative revascularization strategy (CEA) and carefully weighing the risk benefit ratio with respect to the best medical therapy. There is an increasing belief that aggressive contemporary medical therapy may suffice in many patients with severe carotid stenosis, although the randomized data to support this argument are still awaited.

A few centers have adopted a multidisciplinary approach to the care of patients with severe carotid stenosis and the decision to proceed with CAS or CEA or continued observation on optimal medical therapy is based on consensus of specialists with different skill sets. It is not clear if this approach is preferable to, or more cost-effective than current practice.

Our approach is to assess the patient risk with either CEA or CAS based on patient age, anatomic features, and comorbidities, and weigh it against the expected survival time (based on age and comorbidities). In symptomatic patients, unless the expected survival is dismal (<6 months), we generally recommend CEA or CAS based on anatomy and lesion characteristics, as well as patient comorbidities.

In asymptomatic patients, if the expected survival is >5 years, we recommend CEA for most patients and reserve CAS for patients with anatomic features that make them a high risk for CEA. In asymptomatic patients with severe comorbid medical illness, we base our assessment on the expected survival time and generally pursue optimal risk reduction and careful monitoring for development of symptoms.

Complications and their management

Complications after carotid stenting are uncommon but can be devastating. The major complications and possible strategies to prevent these are listed below.

1.    Death – The 30-day mortality associated with carotid stenting is less than 1%. Most of these deaths are related to major strokes, although patients have rarely died from other problems such as retroperitoneal bleeding, contrast-induced nephropathy, and airway obstruction from unrecognized perforation of external carotid artery branches. Careful attention to technique can reduce these complications but cannot totally negate the risk.

2.    Stroke – Stroke is the most feared complication of carotid stenting and the procedure should not be performed if the stroke rate is expected to be >3% for asymptomatic and >6% for the symptomatic patients. Most experienced operators and centers have demonstrated rates consistently lower than these benchmarks although this is not true for all institutions or operators, especially those with limited experience.

Stroke may develop due to thromboembolism of plaque debris, or from thrombosis that develops on the equipment that is used, or may be related to cerebral hemorrhage. Risk of embolic events can be reduced by meticulous attention to procedural detail, use of dual antiplatelet therapy, and by ensuring appropriate procedural anticoagulation for the entire duration of the procedure.

The EPD dwell time should be minimized since longer dwell times have been associated with an increased risk of stroke. In patients with symptomatic disease, or in those with large ulcerated plaques, the occurrence of slow flow phenomenon should be anticipated (discussed below) and appropriate equipment to treat it should be at hand.

A small but significant proportion of strokes following carotid stenting occur following successful completion of the procedure but prior to hospital discharge. These likely arise from either secondary thromboemboli that form on the stent or from areas of endothelial injury arising from the use of the embolic protection device (EPD) or guiding catheters.

Hemorrhagic stroke is much rarer but is usually more devastating. The commonest cause is usually hemorrhagic conversion of a recent stroke, or it may develop following the onset of hyperperfusion syndrome. It is our practice to avoid CAS for 2 weeks following a stroke to minimize the risk of hemorrhagic conversion although there are no randomized data to support this approach.

3.    Hyperperfusion syndrome – The sudden increase in perfusion pressure associated with CAS (and CEA) can dramatically increase cerebral blood flow and this can manifest clinically as hyperperfusion syndrome. Patients often complain of severe retro-orbital headache ipsilateral to the treated site, and if not treated, it can progress to seizures and intracerebral bleeding.

The predisposing factors for hyperperfusion syndrome are severe hypertension, severe ipsilateral stenosis, contralateral occlusion, or severe contralateral stenosis. Once hyperperfusion develops, it is important to maintain strict blood pressure control and hold anticoagulation or antiplatelet therapy.

Meticulous attention to blood pressure control can prevent hyperperfusion syndrome. It is our practice to ensure that blood pressure is normal before the patient leaves the catheterization suite.

We commonly use labetalol as the drug of choice for periprocedural blood pressure control and wean it off as patients start their routine antihypertensive therapy. Hyperperfusion can develop up to 2 weeks after carotid stenting, and it is our practice to have patients check their blood pressure twice a day and adjust their antihypertensive therapy for the first month following the procedure.

4.    Bradycardia and hypotension – Patients who have lesions involving the carotid bulb will often develop hypotension and bradycardia following carotid stenting. This is secondary to the stimulation of the carotid baroreceptors and is usually self-limited.

We will withhold beta-blockers and other medications with negative chronotropic effect prior to the procedure and slowly reintroduce these once the patient’s heart rate and blood pressure return to baseline. Very rarely, hypotension after CAS can persist for a few days and can be treated with pseudoephedrine or midodrine in the outpatient setting. Prolonged hypotension is especially common in patients with heavily calcific carotid stenosis.

5.    EPD-related complications – EPDs are routinely used for prevention of embolic stroke but are occasionally associated with complications.

  • Vasospasm – The commonest complication in our experience is spasm that occurs with use of filter type of devices. This is commonly seen in active smokers and can be reduced by ensuring that patients are tobacco free for at least a week before the procedure. Appropriate sizing of the device is important and spasm usually responds to local vasodilators.
  • Slow flow – This angiographic phenomenon manifests as stasis or markedly reduced flow due to plugging of the filter pores by plaque microemboli and detritus. This is usually associated with symptomatic, bulky ulcerated lesions and is treated with aspiration of the static column of blood with the suspended particulates before collapsing the filter. Patients who have slow flow have a 30-day stroke rate of close to 10%.
  • Inability to remove EPD – This is a rare complication that is usually associated with marked distal tortuosity of the carotid artery. Usually, this can be overcome by straightening the artery by having the patient turn his or her head to the contralateral side but occasionally surgical removal has been necessary.

6.    Vascular complications – Approximately 3% to 5% of patients will develop vascular complications after CAS in the form of hematomas, pseudoaneurysms, AV fistulas, and arterial thrombosis. Retroperitoneal bleeding and infections are rarely seen. Meticulous attention to vascular access and closure is necessary to minimize the occurrence of these complications.

7.    Contrast-induced problems – Contrast-induced nephropathy (CIN) can develop in patients with preexisting renal dysfunction. Adequate hydration and minimization of contrast volume are two proven strategies that are effective at reducing the likelihood of CIN.

8.    Stent thrombosis – Stent thrombosis is a rare complication and occurs in <1% of patients. It has been usually associated with premature cessation of dual antiplatelet therapy.

What’s the evidence?

Meier, P, Knapp, G, Tamhane, U, Chaturvedi, S, Gurm, HS. “Short term and intermediate term comparison of endarterectomy versus stenting for carotid artery stenosis: Systematic review and meta-analysis of randomised controlled clinical trials”. BMJ. vol. 340. 2010. pp. c1798A comprehensive meta-analysis of all trials that preceded CREST and provides a nice overview of changing outcomes with CAS relative to CEA with evolution of technology and improving experience.

Brott, TG, Hobson, RW, Howard, G. “Stenting versus endarterectomy for treatment of carotid-artery stenosis”. N Engl J Med. vol. 363. 2010. pp. 11-23. The best randomized trial of CEA and CAS that provides a contemporary comparison of experienced operators using state of the art devices and technique.

Bates, ER, Babb, JD, Casey, DE. “Accf/scai/svmb/sir/asitn 2007 clinical expert consensus document on carotid stenting: A report of the American College of Cardiology foundation task force on clinical expert consensus documents (accf/scai/svmb/sir/asitn clinical expert consensus document committee on carotid stenting)”. J Am Coll Cardiol. vol. 49. 2007. pp. 126-170. This consensus document, although dated and in need of an update in view of the CREST trial, provides a thorough overview of the literature surrounding CAS.

Gray, WA, Chaturvedi, S, Verta, P. “Thirty-day outcomes for carotid artery stenting in 6320 patients from 2 prospective, multicenter, high-surgical-risk registries”. Circ Cardiovasc Interv. vol. 2. 2009. pp. 159-166. One of the recent registries demonstrating outcomes of CAS in a nontrial, unselected population. The results demonstrated an acceptable rate of complications with CAS for both symptomatic and asymptomatic patients .