Atherosclerotic Disease of the Carotid Artery

Updated: May 15, 2017
  • Author: April L Rodriguez, MD, MS; Chief Editor: Vincent Lopez Rowe, MD  more...
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Overview

Practice Essentials

Atherosclerosis is a diffuse, degenerative disease of the arteries resulting in plaques that consist of necrotic cells, lipids, and cholesterol crystals. These plaques can cause stenosis (see the image below), embolization, and thrombosis. Atherosclerosis has a predilection for certain arteries, including the extracranial carotid artery.

Arteriogram of carotid stenosis. Arteriogram of carotid stenosis.

Signs and symptoms

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

See Overview for more detail.

Indications and contraindications for carotid endarterectomy

Indications

Indications for carotid endarterectomy (CEA) based on prospective randomized trials include the following:

  • Symptomatic patients with greater than 70% stenosis - Clear benefit was found in the North American Symptomatic Carotid Endarterectomy Trial (NASCET) [1]
  • Symptomatic patients with greater than 50-69% stenosis - Benefit is marginal; appears to be greater for male patients
  • Asymptomatic patients with greater than 60% stenosis - Benefit is significantly less than for symptomatic patients with greater than 70% stenosis

Note: Available literature includes considerable overlap in the percentage of stenosis used as the threshold for CEA. Generally, symptomatic patients with greater than 50% stenosis and healthy, asymptomatic patients with greater than 60% stenosis warrant consideration for CEA.

Contraindications

Contraindications for CEA include the following:

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

Laboratory and radiologic studies

Studies to be considered include the following:

  • Complete blood count
  • Levels of electrolytes, blood urea nitrogen, creatinine
  • Lipid profile
  • Coagulation studies - Prothrombin time/activated partial thromboplastin time
  • Electrocardiography - To identify evidence of prior MI as well as ischemic changes
  • Carotid duplex ultrasonography, with or without color - Screening test of choice to evaluate for carotid stenosis
  • Cranial computed tomography scanning or magnetic resonance imaging - To rule out other intracranial lesions and to identify the presence of new and old cerebral infarcts
  • Carotid magnetic resonance angiography - May be useful in collaborating the finding of an occluded carotid with duplex sonography; however, this modality tends to overstate the significance of the stenosis
  • Aortic arch and carotid arteriography - To evaluate the percentage of stenosis

See Workup for more detail.

Management

Treatment of atherosclerosis of the carotid artery is dependent on the severity and degree of the disease.

Pharmacotherapy

Medications used to manage atherosclerotic disease of the carotid artery include the following:

  • Antiplatelet agents (eg, aspirin, ticlopidine, clopidogrel)
  • Anticoagulants (eg, warfarin) - Note that use of warfarin in patients with noncardiac emboli is controversial

Surgery

Endovascular management of atherosclerotic disease of the carotid artery includes the following procedures:

  • CEA
  • Carotid angioplasty and stenting (CAS)

See Treatment for more detail.

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Background

Atherosclerosis is a degenerative disease of the arteries resulting in plaques consisting of necrotic cells, lipids, and cholesterol crystals (see the images below). These plaques can result in symptoms by causing stenosis, embolizing, and 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. Carotid plaque.
Atherosclerotic plaque removed at time of carotid 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.

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Anatomy

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

Arteriogram of aortic arch and its branches. Arteriogram of aortic arch and its branches.
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Pathophysiology

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, as many as 45% of strokes in patients with asymptomatic stenosis of 60-99% may be caused by lacunar infarcts or cardiac emboli.

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Epidemiology

Stroke from any cause represents the third leading cause of death in the United States. Half a million new strokes occur each year in the United States, resulting in approximately 150,000 deaths. Stroke is the leading cause of serious long-term disability in the United States. Direct and indirect cost of stroke in the United States in 1997 was estimated at $40 billion.

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Prognosis

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.

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. [2] 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. [3]

A meta-analysis revealed that protected (use of embolic protection wire) CAS was associated with an 8.2% rate of stroke or death rate at 30 days, compared with 6.2% for surgery [4] ; however, the rates of disabling stroke or death within this period were not significantly different in 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 against those of CAS. [5] 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 in the CEA group than in the CAS group. In the intermediate term, the risk of stroke or death did not differ significantly between the two treatments.

Numerous studies, including the Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial, have found that carotid artery stenting (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). [6]

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. [7] 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. [8]

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, finding that the risk of stroke, MI, or death was similar with the two procedures. [9]

Although there was no difference in the primary outcome, there was a higher risk of periprocedural stroke in the group who underwent CAS, as well as a higher risk of MI in the group undergoing CEA. [9]  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%). [10]

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. [11]

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