Atherosclerotic Disease of the Carotid Artery

Atherosclerosis is a degenerative disease of the arteries that results in the formation of plaques composed of necrotic cells, lipids, and cholesterol crystals (see the images below). These plaques can result in symptoms by causing stenosis, by embolizing, or by thrombosing. Atherosclerosis is a diffuse process with a predilection for certain arteries. This article describes the history and impact of this process as it occurs in the extracranial carotid artery.

Carotid plaque.

Atherosclerotic plaque removed at time of carotid endarterectomy (areas of ulceration with thrombus and intraplaque hemorrhage are present).

For patient education resources, see the Brain and Nervous System Center and the Cholesterol Center, as well as Stroke, High Cholesterol, Understanding Your Cholesterol level, and Lifestyle Cholesterol Management.

The carotid artery originates from the innominate artery on the right and directly from the aortic arch on the left. The carotid artery enlarges in the midneck, forming the carotid bulb, before bifurcating into the external and internal carotid arteries. The carotid sinus and carotid body are located at the bifurcation (see the image below).

Arteriogram of aortic arch and its branches.

Currently, embolization is considered the most common mechanism causing ischemic strokes from atherosclerotic lesions in the carotid bulb. Thrombosis and low flow are other possible mechanisms.

Stroke is one of the most devastating complications of carotid stenosis. However, carotid stenosis is not the only cause of stroke. In fact, among patients with asymptomatic stenosis of 60-99%, as many as 45% of strokes may be caused by lacunar infarcts or cardiac emboli.

Stroke from any cause represents the third leading cause of death in the United States. About 610,000 new strokes occur each year in the United States, and about 185,000 occur in people who have previously had a stroke.[2] Stroke is the leading cause of serious long-term disability in the United States. Between 2014 and 2015, the direct and indirect cost of stroke in the United States was estimated at nearly $46 billion.[2]

Cranial nerve injuries occur in 2-7% of patients. Recurrent laryngeal and hypoglossal nerve dysfunctions are the most common. Postoperative stroke occurs in 1-5% of patients.[1] The perioperative mortality is 0.5-1.8%. Recurrent stenosis develops in 1-20% of cases, and reoperation is necessary in 1-3% of cases.

Pharmacotherapy vs intervention

In the North American Symptomatic Carotid Endarterectomy Trial (NASCET), the 2-year stroke risk after a successful carotid endarterectomy (CEA) was 1.6%, compared with 12.2% for the medically managed patients.[1] The cumulative risk of an ipsilateral stroke was 9% for the surgical patients and 26% for the medically managed patients.

In the Asymptomatic Carotid Atherosclerosis Study (ACAS), the 5-year risk for ipsilateral stroke was 5.1% for the surgical group and 11% for the medical group.[3] The stroke risk of arteriography was attributed to the surgical group and was 1.2%.

Endarterectomy vs stenting

The Endarterectomy Versus Stenting in Patients With Symptomatic Severe Carotid Stenosis (EVA-3S) trial revealed a higher stroke and death rate with carotid artery stenting (CAS); however, cerebral protection was not uniformly used, and dual antiplatelet therapy was not initiated on all patients.[4]

A meta-analysis revealed that protected CAS (with the use of an embolic protection wire) was associated with an 8.2% rate of stroke or death at 30 days, compared with 6.2% for surgery[5] ; however, the rates of disabling stroke or death within this period were not significantly different between the two groups.

Meier et al conducted a systematic review and meta-analysis of 11 randomized controlled clinical trials to evaluate the relative short-term safety and intermediate-term efficacy of CEA versus CAS.[6] CEA carried a lower risk of periprocedural mortality or stroke than CAS did, mainly because of a decreased risk of stroke. However, the risk of death and the composite endpoint of mortality or disabling stroke did not differ significantly between the two procedures. In addition, the odds of periprocedural myocardial infarction (MI) or cranial nerve injury (CNI) were higher among the CEA group as compared with the CAS group. In the intermediate term, the risk of stroke or death did not differ significantly between the two.

Numerous studies, including the Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial, have found that CAS is not inferior to CEA at 1 year. Published long-term results show no significant difference between groups in the prespecified secondary endpoint trial, a composite at 3 years of death, stroke, or MI within 30 days of the procedure (or death or ipsilateral stroke between 31 and 1080 days).[7]

A study by Illuminati et al suggested that with regard to the timing of CEA, previous or simultaneous CEA in patients with unilateral severe asymptomatic carotid stenosis (>70%) undergoing coronary artery bypass grafting (CABG) was better able to prevent stroke than delayed CEA was.[8] The overall surgical risk was not increased.

A study by Brown et al suggested that the risk of external carotid artery occlusion may be lower with CEA than it would be with CAS, though such occlusion after CAS was still uncommon overall (~4%) and was not associated with in-stent restenosis.[9]

The Carotid Revascularization Endarterectomy vs Stenting Trial (CREST) evaluated the outcomes of 2502 patients with symptomatic or asymptomatic carotid stenosis after undergoing CAS or CEA, and found that the risk of stroke, MI, or death was similar between the two procedures.[10]

Although there was no difference in the primary outcome of CREST, there was a higher risk of periprocedural stroke in the group who underwent CAS, whereas there was a higher risk of MI in the group undergoing CEA.[10]  Additional analysis, however, indicated that stroke had an adverse long-term effect on quality-of-life measures, whereas MI did not. Further study of the CREST data showed that 4-year mortality was significantly higher in patients who had a stroke after intervention (21.1% vs 11.6%).[11]

Whereas CNI occurred in 4.6% of the CREST patients who underwent CEA, there was a 80% rate of resolution at 1 year, and there was no statistical difference in health-related quality-of-life outcomes between patients who had CNI and those who did not.[12]

Brott et al carried out a pooled analysis of individual patient data (N = 4754) from the EVA-3S, SPACE (Stent-Protected Percutaneous Angioplasty of the Carotid Artery versus Endarterectomy), ICSS (International Carotid Stenting Study), and CREST trials to compare long-term outcomes of CEA and CAS for treatment of symptomatic carotid stenosis.[13]  Patients were followed for a maximum of 12.4 years (median follow-up, 2.0-6.9 years). The primary outcome was the composite risk of stroke or death within 120 days after randomization (periprocedural risk) or subsequent ipsilateral stroke up to 10 years after randomization (postprocedural risk). 

In patients who underwent CEA, 129 periprocedural and 55 postprocedural outcome events occurred, compared with 206 periprocedural and 57 postprocedural outcome events in those who underwent CAS.[13] After the periprocedural period, annual rates of ipsilateral stroke per person-year were 0.60% for CEA and 0.64% for CAS. Overall, the combined periprocedural and postprocedural risks favored CEA; treatment differences at 1, 3, 5, 7, and 9 years ranged from 2.8% to 4.1%. However, the similarity in postprocedural rates suggested that improvements in the periprocedural safety of CAS could yield outcomes similar to those of CEA in the future.

Transcarotid artery revascularization

Transcarotid artery revascularization (TCAR) represents an alternative to CAS in which the risk of navigating the often diseased atherosclerotic arch is eliminated through the use of direct, open surgical access to the proximal common carotid artery. Additionally, the use of flow reversal as embolic protection allows the institution of cerebral protection before the lesion is engaged, which has been shown to be the primary mechanism of stroke reduction in TCAR.[14]

The initial ROADSTER 1 and 2 trials evaluating the 30-day and 1-year safety of TCAR demonstrated high technical success rates (96.5%) and favorable safety outcomes, with a 30-day ipsilateral stroke rate of 1.4%, a 1-year ipsilateral stroke rate of 0.4%, respectively, a composite 30-day stroke/death rates of 2.3%, and a stroke/MI/death rates of 3.2%.[15, 16]  

Multiple studies have demonstrated the safety of TCAR in comparison with both CEA and transfemoral CAS. Observational comparative registry studies evaluating TCAR and CEA among patients entered into the Society for Vascular Surgery (SVS) Vascular Quality Initiative (VQI) TCAR Surveillance Project (TSP) registry and the CEA database, respectively, demonstrated comparable stroke/death rates among patients undergoing TCAR as compared with CEA, despite higher rates of medical comorbid conditions.[17]

Other comparative studies evaluating in-hospital outcomes of TCAR and transfemoral CAS demonstrated that patients undergoing TCAR, despite having higher rates of comorbid conditions, had a significantly lower risk of stroke or death.[18, 19]

Atherosclerotic disease of the carotid artery may be associated with the following:

• Amaurosis fugax (transient ipsilateral visual loss)
• Transient ischemic attacks (TIAs)
• Crescendo TIAs
• Stroke-in-evolution
• Cerebral infarction

Atherosclerosis of the carotid artery can be associated with a carotid bruit heard on auscultation.

Complications of carotid endarterectomy (CEA) and carotid artery stenting (CAS) include the following:

• Cardiac ischemia
• Cranial nerve injury (CNI)
• Hematoma with or without airway compromise
• Hypertension and hypotension
• Perioperative stroke
• Recurrent stenosis

In the absence of symptoms, screening is warranted for patients aged 65 years or older who have one or more of the following:

• Coronary artery disease (CAD)
• History of smoking
• Hypercholesterolemia 

Screening is warranted for all patients with carotid-territory ischemic symptoms.

Laboratory studies to be considered in the workup of carotid atherosclerosis include the following:

• Complete blood count (CBC)
• Electrolytes, blood urea nitrogen (BUN), and creatinine
• Lipid profile
• Prothrombin time (PT) and activated partial thromboplastin time (aPTT) - Heparin is administered during carotid endarterectomy (CEA), and knowing the PT or aPTT preoperatively is important

Computed tomography (CT) angiography (CTA) of the neck can provide important anatomic details useful for preoperative planning of CEA and transfemoral carotid stenting, including arch type, atherosclerotic burden, location of carotid bifurcation, and degree of stenosis. Additionally, it can be useful for determining anatomic suitability for transcarotid artery revascularization (TCAR).

Carotid duplex ultrasonography (US), with or without color, is the screening test of choice to evaluate for carotid stenosis. Many surgeons operate after seeing the results of a carotid duplex study alone if the laboratory has credentials and is validated. (See the images below.)

Normal carotid arteries on color flow duplex ultrasonography.

Color flow duplex ultrasonogram reveals 80-99% left carotid stenosis and normal right carotid.

In a study by van Engelen et al that used three-dimensional US  to evaluate 298 patients with carotid atherosclerosis, changes in carotid plaque texture and volume were found to be strong predictors of vascular events (eg, myocardial infarction [MI], transient ischemic attack [TIA], and stroke).[20]

Aortic arch and carotid arteriography was used in the North American Symptomatic Carotid Endarterectomy Trial (NASCET) to evaluate the percentage of stenosis. The diameter of the narrowest portion of the lesion is divided by the normal internal carotid artery diameter distal to the lesion. This procedure may be associated with a 1-2% risk of stroke.

Arteriogram of carotid stenosis.

All symptomatic patients should undergo a head scan with CT or magnetic resonance imaging (MRI) to rule out other intracranial lesions and identify the presence of new and old cerebral infarcts.

Evidence of prior MI and ischemic changes on electrocardiography (ECG) are important to identify. The most common cause of mortality after CEA is MI.

Carotid magnetic resonance angiography (MRA) has a tendency to overstate the significance of the stenosis. Its exact role is not well defined; it may be useful in collaborating the finding of an occluded carotid with duplex.

Lifestyle or medical interventions are implemented in order to address the following risk factors:

• Hypertension
• Hypercholesterolemia
• Smoking 

Aspirin (30-1350 mg/day) irreversibly acetylates the cyclooxygenase of platelets, thus inhibiting platelet synthesis of thromboxane A2. Prostacyclin production in the endothelium is reduced, but this effect is reversible and short-lived. A reduction in transient ischemic attacks (TIAs), stroke, and death in men was shown in the Canadian Cooperative Study Group.[21]

Statins, which include atorvastatin, rosuvastatin, simvastatin, pravastatin, and lovastatin, are 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors that lower LDL cholesterol levels. Statin therapy, with a target low-density lipoprotein (LDL) level below 100 mg/dL, is recommended for all patients with extracranial carotid atherosclerotic disease. A lower target LDL level, 70mg/dL, has been recommended in high-risk patients.[22]

Ticlopidine (250 mg q12hr) is a thienopyridine that irreversibly alters the platelet membrane and inhibits platelet aggregation. It is approximately 10% more effective than aspirin. Toxicity includes neutropenia and diarrhea. Clopidogrel (75 mg/day) is similar to ticlopidine; the risk of neutropenia is low.

Warfarin (titrated international normalized ratio [INR] 2-3) use in patients with noncardiac emboli is controversial.

Antiplatelet therapy (cilostazol) may reduce the progression of carotid artery stenosis after stent implantation.[23]

The following are indications for carotid endarterectomy (CEA), based on prospective randomized trials:

• Symptomatic patients with 70-99% stenosis ^[24] - Clear benefit was found in the North American Symptomatic Carotid Endarterectomy Trial (NASCET); the incidence of ipsilateral stroke in 2 years was 9% with surgery and 26% with medical management ^[1]
• Symptomatic patients with 50-69% stenosis ^[24] - Benefit is modest and appears to be greater for male patients
• Asymptomatic patients with greater than 60% stenosis - Benefit is significantly less than for symptomatic patients with 70-99% stenosis ^[25]
• Available literature includes considerable overlap in the percent of stenosis used as the threshold for CEA; in general, symptomatic patients with 50-99% stenosis and healthy, asymptomatic patients with greater than 60% stenosis warrant consideration for CEA
• Symptomatic trials include patients with transient ischemic attacks (TIAs) or minor strokes within 3 months of entry

Contraindications for CEA include the following:

• Patients with a severe neurologic deficit after a cerebral infarction
• Patients with an occluded carotid artery
• Concurrent medical illness that would significantly limit the patient’s life expectancy

For the indications listed above, medical management was found to be inferior to CEA.

The Society for Vascular Surgery (SVS) has published clinical practice guidelines for management of extracranial cerebrovascular disease.[26]

Cardiac evaluation

Patients with carotid artery stenosis have a high incidence of concomitant coronary artery disease (CAD). American Heart Association (AHA) recommendations regarding cardiac evaluation for noncardiac surgery should therefore be adhered to. In brief, the AHA recommends a functional assessment be performed on all patients with a history of new-onset angina and new symptoms following coronary angioplasty or bypass.

Nondiabetic patients younger than 70 years with no cardiac symptoms and normal findings on electrocardiography (ECG) may undergo CEA without further cardiac workup.

Preoperative imaging studies

Imaging studies should be performed preoperatively to determine the extent of stenosis, as well as to evaluate for kinks and coils that may affect the conduct of the operation (see Workup). Many surgeons who work with certified laboratories proceed with surgery on the basis of carotid duplex ultrasonography (US) alone. If any doubt exists regarding the degree of stenosis or the distal extent of the disease, arteriography of the arch and the carotid is indicated.

The extent of the disease should also be noted, with particular attention to the superior extent of the stenosis. The superior disease extent may influence the type of anesthesia chosen, and additional measures may prove necessary to expose an unusually high lesion.

Anatomic considerations

Anatomic issues that would be unfavorable for CEA include the following:

• Lesions that extend above C2
• Prior irradiation of the neck
• Prior neck operation

Anesthesia

Local anesthesia has the advantage of allowing direct evaluation of the patient’s neurologic status without sophisticated monitoring. This enables the surgeon to operate on most patients without the need for a shunt, which is a technical nuisance and may pose an increased risk of stroke to the patient.

General anesthesia has the advantage of improved airway control and patient comfort during prolonged operations. However, it does require the use of routine or selected shunting, and selective shunting requires the use of electroencephalography (EEG), stump pressures, transcranial Doppler, or some other form of cerebral monitoring to assess the need for a shunt.

Procedure

A vertical skin incision is made along the anterior border of the sternocleidomastoid. The dissection is carried down to the carotid sheath, which is opened longitudinally to expose the carotid arteries. (See the image below.)

Carotid artery exposed prior to carotid endarterectomy (coil present in internal carotid artery).

The endarterectomy is carried out in a smooth plane in the media of the artery. The most important aspect of this portion of the procedure is to obtain a smooth, tapering endpoint on the internal carotid (see the image below). Occasionally, tacking sutures are required to accomplish this.

Carotid artery following endarterectomy and prior to closure (tapered endpoint and smooth appearance of lumen).

The endarterectomy is closed either primarily or with a patch (see the image below). The technical result should be verified by means of completion angiography or duplex US.

Carotid artery following Dacron patch angioplasty.

Postoperative care

Postoperatively, a complete blood count (CBC) is obtained, electrolyte concentrations assessed, and ECG performed. Hemodynamic monitoring is instituted, with a focus on maintaining the patient’s blood pressure at its preoperative range. The patient is observed for the formation of a hematoma that may compromise the airway. Antiplatelet therapy is necessary.

Patients are evaluated 2 weeks postoperatively for wound or neurologic complications. Carotid duplex US is performed after 6 months and annually thereafter.

Carotid angioplasty and stenting (CAS) has emerged as a viable option in the treatment of carotid artery stenosis. Rapid growth and technologic advances have allowed this procedure to become a treatment strategy, particularly in high-risk patients. Most of the trials published to date have shown varying results with CAS.[27] Many are industry-sponsored, and some have different patient populations (eg, symptomatic and asymptomatic patients). Further randomized prospective studies are needed before any conclusion can be made.

Advances in CAS notwithstanding, CEA has remained the standard of care. Currently, the Centers for Medicare and Medicaid Services (CMS) has approved reimbursement for CAS only in the following patients[28] :

• Symptomatic patients with high-grade stenosis (≥70%) who are considered to be at high risk for CEA, provided that FDA-approved CAS systems and FDA-approved or -cleared embolic protection devices are used
• Symptomatic patients with 50-70% stenosis who are considered to be at high risk for CEA, in accordance with category B IDE clinical trials regulation, as a routine cost under the clinical trials policy, or in accordance with the National Coverage Determination on postapproval studies
• Patients who are at high risk for CEA and have asymptomatic carotid stenosis of 80% or higher, in accordance with category B IDE clinical trials regulation, as a routine cost under the clinical trials policy, or in accordance with the National Coverage Determination on postapproval studies

Anatomic considerations

The following factors are considered to increase the risk of CAS and should be taken into account in procedural planning[22] :

• "Soft" lipid-rich plaque identified on noninvasive imaging
• Extensive (≥15 mm) disease
• Preocclusive lesion
• Circumferential heavy calcification 
• Aortoiliac tortuosity
• Type III aortic arch
• Carotid lesion with more than two 90º bends within a short distance of the target lesion
• Significant tortuosity of the distal internal carotid artery
• Severe aortic arch atherosclerosis

In a study aimed at identifying angiographic features that would account for the difference in periprocedural stroke and death rates between CAS and CEA, the higher stroke and death rate in patients who underwent CAS was found to be associated with a longer lesion length (≥12.85 mm),  sequential lesions, or remote lesions extending beyond the bulb.[29]

Procedure

The procedure is performed either in an operating room with C-arm capabilities or in an angiographic suite. Local anesthesia with limited sedation is used so that the patient’s neurologic status can be constantly monitored.

Femoral artery access is achieved and arch arteriography performed. The affected side is cannulated, and selective carotid arteriograms are then obtained (see the images below).

Selective left carotid angiogram.

Oblique view of left carotid artery demonstrating lesion within internal carotid artery.

Next, a long sheath is placed over a wire into the common carotid artery, and a 0.014-in. filter wire is placed into the internal carotid distal to the lesion to provide embolic protection. After appropriate sizing, the lesion is quickly predilated with a small balloon. The stent is then placed and postdilated with a larger balloon. (See the images below.)

Placement of stent into internal carotid artery. Note filter wire in upper photos (dots at top of internal carotid artery).

Angioplasty after stent placement; again, note filter wire protecting distal carotid artery.

Next, a completion arteriogram is obtained to confirm that the lesion has been treated and that no other abnormalities exist within the internal carotid or cerebral views (see the image below). The procedure is completed, and the access site in the femoral artery is typically closed with a closure device. The patient is usually monitored overnight and discharged the next day.

Completion arteriogram displaying improvement in diameter of internal carotid artery.

Transcarotid artery revascularization (TCAR) represents an alternative to transfemoral CAS in patients deemed to be at high risk for CEA because of the presence of medical comorbidities or certain high-risk anatomic factors (eg, high carotid bifurcation, previous neck surgery, or previous irradiation).

Multiple studies have compared safety outcomes between TCAR and CEA,[17]  with TCAR having lower rates of stroke in comparison with transfemoral CAS.[18, 19]  The primary benefit of TCAR over transfemoral CAS is the ability to avoid navigating an often diseased aortic arch, by virtue of the direct common carotid access that is obtained surgically in TCAR. Additionally, the use of dynamic flow reversal allows the institution of embolic protection before crossing of the carotid lesion is attempted.

Much as with CAS, CMS has approved reimbursement for TCAR in the following patients[28] :

• Symptomatic patients with high-grade stenosis (≥70%) who are considered to be at high risk for CEA

However, the creation of the Society for Vascular Surgery (SVS) TCAR Surveillance Project extended coverage to the following patients:

• Asymptomatic high-risk patients with ≥80% stenosis
• Symptomatic high-risk patients with ≥50% stenosis

Anatomic considerations

In addition to the above, to be eligible for TCAR, the following anatomic requirements must be met:

• Distance greater than 5 cm exists between the access site and the carotid lesion
• Common carotid artery diameter  exceeds 6 mm
• Common carotid artery access site and the site of proximal clamp placement on the common carotid artery are free of disease.

The following anatomic features and lesion characteristics are not favorable for carotid stenting and thus represent contraindications for TCAR:

• Severe, circumfirentially calcified lesion
• Severe carotid tortuosity

Preparation for procedure

Dual antiplatelet therapy (DAT) with aspirin (75-325 mg/day) and clopidogrel (75 mg/day), initiated prior to the proedure, is strongly recommended. Statin therapy should also be initiated at the initial preoperative appointment, if it has not already been started.

Procedure

The procedure is performed either in an operating room with C-arm capabilities or in an angiographic suite. With the patient under either local or general anesthesia, the proximal ipsilateral common carotid artery is exposed through a short (3-cm) incision at the base of the neck, with dissection carried down between the two heads of the sternocleidomastoid.

After proximal circumferential control of the common carotid artery is gained, the patient is anticoagulated with heparin to achieve an activated clotting time (ACT) greater than 250 s. A 5-0 polypropylene "U" stitch is placed at the planned puncture site to aid in later closure. The common carotid artery is directly punctured with the use of a micropuncture access kit, and initial angiography is performed to confirm the carotid anatomy.

The carotid artery sheath is carefully advanced over a stiff, floppy-tipped wire, with care taken to ensure that the lesion is not engaged in the process; after successful placement, this sheath is flushed. A femoral venous sheath is then placed in the right or left common femoral vein percutaneously under US guidance, and the dynamic flow reversal system is connected. The patient is pretreated with glycopyrrolate (0.2 mg) prior to common carotid clamp placement to prevent hypotension and bradycardia during carotid bulb angioplasty and stenting.

The common carotid artery proximal to the arterial sheath is clamped, and flow reversal is started. The internal carotid artery stenosis can then be crossed with a 0.014-in. wire, and the lesion is predilated before stent placement. Postdilation of the stent is optional and depends on the amount of residual stenosis present.

Completion angiography is performed in two views to confirm adequate stent expansion. The wire is then removed, the proximal common carotid artery clamp is removed, and antegrade perfusion to the carotid artery is restored. The flow reversal system is disconnected, allowing the return of all blood to the patient, and the arterial sheath is removed. The already placed polypropylene suture is used to close the carotid artery access site, and protamine is given to reverse anticoagulation. The femoral venous sheath can be removed, with hemostasis obtained by means of direct manual pressure.

After the procedure, the patient is usually monitored within an intensive care unit (ICU) and discharged the next day.

Cranial nerve injuries occur in 2-7% of patients. Recurrent laryngeal and hypoglossal nerve dysfunctions are the most common. Postoperative stroke occurs in 1-5% of patients.[1] The perioperative mortality is 0.5-1.8%. Recurrent stenosis occurs in 1-20% of cases, and reoperation is necessary in 1-3% of cases.

In the CREST data, the rate of restenosis or occlusion at 2 years was approximately 6%, and there was no difference between CAS and CEA.[30] Secondary analysis of the CREST data sought to identify predictors of restenosis or occlusion. Female sex, diabetes and dyslipidemia were independent predictors of restenosis or occlusion at 2 years after either CEA or CAS. Smoking was also found to be an independent predictor; however, this was only noted in patients who had undergone CEA.

In June 2021, the Society for Vascular Surgery (SVS) published clinical practice guidelines for management of extracranial cerebrovascular disease.[26] Recommendations included the following:

• Carotid endarterectomy (CEA) is recommended as first-line treatment for symptomatic low-risk surgical patients with stenosis of 50-99% and asymptomatic patients with stenosis of 70-99%.
• Carotid revascularization is appropriate for symptomatic patients with recent stable stroke and >50% stenosis. It should be performed as soon as the patient is neurologically stable (after 48 hr but before 14 d from symptom onset).
• Screening for clinically asymptomatic carotid artery stenosis in patients without symptoms or risk factors for carotid artery disease is not recommended.
• In selected asymptomatic patients at increased risk for carotid stenosis, screening for clinically asymptomatic carotid artery stenosis is suggested, as long as the patients are potentially fit for and willing to consider carotid intervention upon discovery of significant stenosis.
• In patients with symptomatic carotid stenosis of 50-99% who require both CEA and coronary artery bypass grafting (CABG), CEA before or concomitant with CABG is suggested.

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Class Summary

Antiplatelet agents inhibit platelet aggregation and reduce ischemic events.

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

Aspirin inhibits prostaglandin synthesis, which prevents the formation of platelet-aggregating thromboxane A2.

Clopidogrel (Plavix)

Clopidogrel selectively inhibits adenosine diphosphate (ADP) binding to platelet receptors and subsequent ADP-mediated activation of the glycoprotein (GP) IIb/IIIa complex, thereby inhibiting platelet aggregation.

Ticlopidine

Ticlopidine hydrochloride interferes with platelet membrane function by inhibiting ADP-induced platelet-fibrinogen binding and subsequent platelet-platelet interaction. It is used as a second-line antiplatelet therapy for patients who are intolerant to aspirin therapy or in whom such therapy fails.

Class Summary

Anticoagulants are given to prevent an acute thrombotic or embolic event.

Warfarin (Coumadin, Jantoven)

Warfarin interferes with hepatic synthesis of vitamin K–dependent coagulation factors. It is used for the prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. Tailor the dose to maintain an international normalized ratio (INR) in the range of 2-3.

Class Summary

Statins are 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors that lower LDL cholesterol levels

Atorvastatin (Lipitor)

Simvastatin (Zocor)

Rosuvastatin (Crestor)

Pravastatin (Pravachol)

Lovastatin (Altoprev, Mevacor)