Atherosclerotic Disease of the Carotid Artery Treatment & Management

Updated: Mar 22, 2023
  • Author: Jake F Hemingway, MD; Chief Editor: Vincent Lopez Rowe, MD, FACS  more...
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Risk Factor Modification

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

  • Hypertension
  • Hypercholesterolemia
  • Smoking 

Pharmacologic Therapy

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]


Carotid Endarterectomy

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


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.


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 endarterec 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 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. 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

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]


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. Selective left carotid angiogram.
Oblique view of left carotid artery demonstrating 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. N 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 fil 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 d Completion arteriogram displaying improvement in diameter of internal carotid artery.

Transcarotid Artery Revascularization

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.


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.