eMedicine Specialties > Radiology > Vascular/Interventional

Carotid Artery, Stenosis

Author: Lennard A Nadalo, MD, Clinical Professor, Department of Radiology, University of Texas Southwestern Medical School; Consulting Staff, Envision Imaging of Allen and Radiological Consultants Association
Coauthor(s): Michelle C Walters, DO, Consulting Staff, Radiological Consultants Association
Contributor Information and Disclosures

Updated: Jul 23, 2009

Introduction

Background

Stroke (brain attack) represents one of the most serious causes of mortality and morbidity in the United States and throughout the world. Each year, 150,000 patients die as a direct result of a cerebrovascular accident (CVA), while 600,000 patients experience the morbidity of aphasia, blindness, or paralysis. Among patients with stroke, extracranial carotid disease represents the cause of approximately one half of cases. The goals of carotid imaging can be described as early detection, clinical staging, surgical road mapping, and postoperative therapeutic surveillance (see Image 1).

Imaging helps in detecting associated conditions early. Coronary artery disease, peripheral arterial stenosis, and hypertension are associated with an increased incidence of carotid arterial stenosis. Carotid arterial screening remains controversial. Good evidence supports evaluation for carotid stenosis prior to coronary arterial bypass surgery.^1,2,3

Detection of a carotid bruit is a common physical examination finding that may lead to a referral for carotid duplex sonography. The correlation between a carotid bruit and a hemodynamically important carotid stenosis is reported to be between 10-20%. A cardiac murmur may be transmitted to the neck. Stiff, calcified, or torturous vessels may generate a bruit in the absence of stenosis.

Recent study

The use of intravenous tissue plasminogen activator (t-PA) for stroke 3-4.5 hours after symptom onset has been endorsed by the American Heart Association, although time to treatment remains of extreme importance and should not be delayed. The European Cooperative Acute Stroke Study 3 (ECASS 3) showed benefit from t-PA in patients treated 3-4.5 hours after onset of symptoms of stroke.^4,5,6,7  

For excellent patient education resources, visit eMedicine's Stroke Center and Dementia Center. Also, see eMedicine's patient education articles Stroke, Transient Ischemic Attack (Mini-stroke), and Stroke-Related Dementia.

Pathophysiology

Transient ischemic attack (TIA) is the result of a brief interruption of blood flow to the brain. In 80% of cases, the interruption occurs as a result of blockage in the arterial circulation to the brain due to an embolus, an obstructing arterial thrombus, or the stenotic effects of atherosclerosis. In the other 20%, the interruption is caused by minor hemorrhage in the brain.

In both types of TIA, the lack of oxygen to the brain produces symptoms similar to those produced during a full stroke. Symptoms can affect vision, behavior, movement, speech, and thought processes. However, the symptoms of a TIA are temporary, generally lasting only 8-14 minutes with most clearing within an hour, although they can continue for as long as 24 hours. Permanent damage is unlikely because the oxygen supply to the brain is restored fairly quickly.

Thrombus causes 25-50% of all TIAs, and embolism causes 11-30%. A lacunar infarction occurs in 11-14% of patients with TIA. Less common causes of a TIA involve minor bleeding or sentinel leaks from a cerebral blood vessel (approximately 10% of cases). Mini strokes caused by bleeding are usually due to high blood pressure (hypertension). Since the underlying cause of this type of TIA is bleeding rather than blockage, the patient must receive an immediate and accurate medical evaluation. Treatment should not include thrombolytic drugs or aspirin because these agents increase bleeding.

Once blockage or bleeding occurs, whether the person is about to have a TIA or a full stroke depends greatly on host factors, eg, the person's age and general health status and the location and size of the blockage or bleed. Other blood vessels in the area may enlarge to improve blood flow to the affected area, thus ending the TIA. Although a TIA is characterized by a brief interruption of blood flow, symptoms of a TIA (eg, weakness on 1 side of the body) may last much longer than the time needed to dissolve the blockage completely or to absorb the bleed. For most people, symptoms last approximately 8-14 minutes and usually clear within an hour, but they can last as long as 24 hours.

Patients with symptoms of a TIA that persist for more than 24 hours usually are treated as though they have had a full stroke. More than 50,000 Americans have TIAs every year. In persons older than 65 years, 8.5% have been diagnosed with at least 1 mini stroke. The risk of stroke is highest soon after a TIA, and the risk continues to be approximately 5% during the first month following the TIA. Of patients with TIAs, 20-25% are estimated to develop a stroke within 2 years.

If the degree of carotid stenosis is severe, in the absence of adequate collateral circulation the ipsilateral cerebral hemisphere may become underperfused. When the arterial circulation falls, there is an increased risk of thrombosis within the middle cerebral artery (MCA), the anterior cerebral artery, and the more peripheral branches of the intracranial arterial circulation. Focal thrombosis may occur in areas of pre-existing atherosclerotic disease.

Other general medical issues which may exacerbate symptoms related to carotid stenosis include chronic lung disease, cardiac disease with restricted cardiac function, and attempts to low systemic hypertension. Any adverse physiological change which further limits oxygenation to the brain may result in cerebral ischemia in patients who otherwise tolerated even high-grade carotid stenosis.

The presence of 2 or more tandem arterial stenoses may result in symptomatic cerebral ischemia, even if any one of the narrowed arterial inflow circulation pathways was not critically narrowed.

Frequency

United States

The prevalence of hemodynamically significant carotid stenosis varies with age and other risk factors. Estimates indicate that 5 per 1000 persons aged 50-60 years and approximately 10% of persons older than 80 years have carotid stenosis greater than 50%.

Strokes were responsible for more than 150,000 deaths in 1998. Stroke is the third leading cause of death in the United States after heart disease and cancer. Each year, approximately 600,000 people have a stroke, and in 100,000 people, strokes recur annually. Approximately one half of all strokes result from significant extracranial arterial disease.

International

Carotid stenosis and CVA follow a similar pattern of occurrence within the developed world. A direct relationship exists between cigarette smoking and a diet rich in fat. The occurrence of carotid vascular disease probably is lower in underdeveloped countries; however, absolute incidence is difficult to measure.

Mortality/Morbidity

Patients with carotid artery stenosis are at increased risk for subsequent stroke, myocardial infarction (MI), and death. The risk of stroke is greatest for persons with neurologic symptoms such as TIAs, but it also is increased in patients with asymptomatic lesions. The proportion of all strokes attributable to previously asymptomatic carotid stenosis is small; however in patients older than 60 years who have cerebral infarction, approximately 15% have ipsilateral carotid stenosis of 70% or greater. The frequency of hemodynamically significant carotid artery stenosis is higher in symptomatic patients than in asymptomatic patients. In 40-50% of those with a complete stroke, the primary etiology of the stroke is related to extracranial carotid disease (stenosis).

Morbidity of a true transient CVA is nil. Without a completed infarction, the ischemic brain should return to a normal functional state. However, if the period of cerebral ischemia persists beyond 12-24 hours, even a seemingly full neurologic recovery is commonly associated with imaging findings of focal cerebral infarction. Beyond 24 hours and up to 48 hours following the initial CVA, neurologic recovery may be nearly complete, with small areas of infarction best demonstrated on T1-weighted diffusion cerebral MRIs.

The completed infarct syndromes involve neurologic defects that persist beyond the period of active medical treatment in patients with acute stroke. The specific morbidity related to a stroke is a reflection of the portions of the brain that have become ischemic and is related closely to the cerebral vessels that are stenotic or thrombosed.

Common stroke syndromes that may result from carotid stenosis, ulceration, or occlusion include the following:

• Regarding common and internal carotid artery (ICA) occlusion syndromes, young people with occlusion of the main trunk may be asymptomatic. Other manifestations of ICA occlusion include transient hemiplegia, persistent hemiparesis, unilateral loss of vision if the ophthalmic artery is involved, and aphasia when the dominant side is thrombosed.
• Embolization to the anterior cerebral artery or critical stenosis of carotid artery may affect the major branches of the anterior cerebral artery (medial striate artery, recurrent artery of Heubner, orbitofrontal artery, frontopolar artery, anterior internal frontal artery, middle internal frontal artery, posterior internal frontal artery, callosomarginal artery, pericallosal artery, and parieto-occipital artery).
• Anterior cerebral occlusion syndrome involving the main trunk results in contralateral hemiplegia (lower extremity), mild sensory deficits of the contralateral lower limb, and mental confusion or clouding of consciousness.
• The middle cerebral artery, including the major branches (striate arteries, anterior cerebral head of caudate septum pellucidum, middle cerebral globus pallidus, anterior temporal branch, and orbitofrontal, operculofrontal, central sulcus, posterior parietal, angular, and posterior temporal branches) may be directly affected by embolization, or a thrombosis may result due to proximal stenosis of the ipsilateral ICA.
• Middle cerebral occlusion syndrome of the main trunk results in coma, contralateral flaccid hemiplegia, hemianesthesia hemianopia, and motor and sensory aphasia (dominant hemisphere).
• Middle cerebral occlusion syndromes of the posterior parietal, angular, or posterior temporal branches result in contralateral hemiparesis, contralateral astereognosis, contralateral homonymous hemianopia, sensory aphasia, agnosia, apraxia, and alexia if on dominant side.
• Embolization to perforation branches results in contralateral hemiplegia, contralateral rigidity, and tremor.
• Posterior cerebral branches, including major branches (anterior temporal artery, posterior temporal artery, posterior occipital artery, calcarine artery, and collateral arteries), may be involved. The primary blood flow pattern to the posterior cerebral artery may arise from the ICA. The stroke pattern resulting from embolization or stenosis affects the related cerebral structures, ie, the anterior temporal artery (inferior temporal lobe), posterior temporal artery (inferior temporal lobe), posterior occipital artery (inferior and medial occipital lobe, posterior corpus callosum), calcarine artery (calcarine cortex occipital lobe), and collateral arteries (thalamogeniculate thalamoperforating branches).
• Posterior cerebral occlusion syndrome of the main trunk includes contralateral hemianesthesia, contralateral homonymous hemianopia, sensory aphasia if on the dominant side, ipsilateral cerebellar signs, contralateral rigidity, tremors, and choreiform movements.
• Retrolenticular capsule includes hemiplegia hemihypalgesia, hemianesthesia, and contralateral homonymous hemianopia.
• Involvement of the calcarine artery includes contralateral homonymous hemianopia, loss of half of the person's macular vision, visual agnosia if on the dominant side, thalamic syndrome, contralateral hemianalgesia, contralateral dysesthesia, and pain.

Race

Strokes are more common among blacks and Hispanics than others. The incidence of CVA tends mirror the incidence of hypertension and diabetes. The rate of diabetes among Hispanics is greater than in the population as a whole. Hypertension is both more severe and more common among blacks than among others. The factors of diet, obesity and family history interact to result in a greater risk of carotid stenosis in both blacks and Hispanics.

Treatment of patients who are asymptomatic for carotid stenosis and the overall management of hypertension tend to be less successful among patients of lower socioeconomic status, resulting in more frequent and more severe strokes. To the extent that blacks and Hispanics represent a greater percentage of the population in poverty, the medical treatment of strokes in minority patients has a worse outcome.

The complex interassociation of genetics, diet, and lifestyle is reflected by the relatively low rates of vascular disease reported among elderly persons living in remote areas of Italy and China.

Sex

Carotid stenosis requiring surgical treatment tends to occur in almost equal frequency in men and women. In general, women are more likely to seek and receive treatment for both benign and symptomatic carotid stenosis.

Age

Extracranial carotid disease tends to occur more frequently in elderly persons. In patients with increased risk factors, the age at first presentation tends to be younger.

Anatomy

Anatomy and variants

The aortic arch presents many anatomic variations that may affect the treatment of patients with carotid stenosis. The most common aortic arch variant has 3 primary branches, ie, the innominate artery, the left common carotid artery (CCA), and the left subclavian artery. The right CCA arises from the innominate artery. The most common variant has a single (bovine) origin of the innominate artery and the left CCA (see Image 2).

The right subclavian artery may take its origin from the aortic arch distal to the left subclavian artery, in which case, the first aortic arch branch usually is the right CCA. Stenosis of the proximal origin of the CCA or the innominate artery may result in clinical cerebral ischemia and must be differentiated from carotid stenosis because the surgical approach is entirely different. The CCA bifurcates in the cervical region to form the external carotid artery (ECA) and the ICA. The level in the cervical region at which the bifurcation occurs is highly variable.

Occasionally, the origin of the ICA occurs at or above the angle of the mandible. Four primitive connections that normally regress occur between the anterior and the posterior circulations. The persistent trigeminal artery is the most common anomaly. The persistent hypoglossal artery occurs at a rate of approximately 0.2%. Clinically, significant stenosis may occur at the origins of both normal and anomalous vessels. The normal internal diameter of the ICA is highly variable. Within the same normal vessel, the diameter of the ICA varies and is larger in the proximal carotid bulb. As a result of normal variations, the absolute internal diameter is less significant than the ratio of the diameter of a stenotic vessel to the normal diameter of the distal ICA.

Vascular causes of stroke

The cervical portion of the CCAs and ICAs form the primary basis for diagnosis and treatment of carotid stenosis (see Image 5). Surgical treatment and prevention of stroke is directed toward the detection of extracranial carotid vascular disease because effective surgical treatment is limited to the cervical carotid artery and the brachiocephalic branches of the aorta. Extracranial carotid occlusive disease accounts for more than one half of strokes. While stenosis, thrombosis, and anomalies of the aortic arch may contribute to unusual collateral blood flow, stenosis and plaque ulceration within the common carotid bulb and proximal ICA indicate the primary anatomic structures found in the surgical treatment of stroke.

The ECA and its branches provide important collateral pathways, which may reduce the ischemic effects of an ICA stenosis (see Image 19). The primary external carotid arterial pathways involve branches of the ophthalmic artery, the internal maxillary artery, and the occipital artery. Plaque in the proximal ECA may result in a bruit, which can result in diagnostic confusion. Rarely, the ECA may become the source of distal embolization through enlarged collateral pathways. The ICA can be divided into a cervical portion, an intrapetrosal portion to the cavernous sinus, an intracavernous segment, and a supraclinoid segment with major distal branches including the anterior cerebral and MCAs. Major branches of the ICA include the ophthalmic, meningohypophyseal, posterior communicating, anterior choroidal, anterior cerebral, and MCAs.

Decreased cerebral arterial perfusion can result in symptomatic cerebral ischemia if a significant degree of stenosis occurs at most points along the blood pathway from the aortic arch to the end intracranial vessels. Atherosclerotic stenosis tends to occur near the origins of major branch arteries and within the area of vascular turbulence. This is most likely related to intimal trauma, which tends to occur near the origins of arterial branches.

Assessment of a patient who presents with cerebral vascular disease should include a search for an inflow stenosis near the origin of the right innominate artery or the proximal left CCA. In the most common anatomic presentation, the right CCA and the right subclavian artery arise from the innominate artery. Stenosis of the innominate artery may result in right-sided vertebral arterial steal as well as symptomatic reduction of right carotid arterial blood flow. Because of the larger diameter of the innominate artery, symptomatically significant stenosis of the innominate artery is less common than stenosis of the proximal left common artery.

Presentation

Risk factors for carotid artery disease are similar to those for coronary artery disease, ie, atherosclerosis of the main arteries that carry the oxygen-rich blood to the heart (coronary arteries). Therefore, people with one condition often also have the other. Risk factors for both (as shown by a coronary risk profile) that can be modified include smoking, lack of regular exercise, eating a high-fat high-cholesterol diet, obesity (>20% over an individual's ideal weight), uncontrolled diabetes, uncontrolled hypertension, uncontrolled stress and anger, high low-density lipoprotein (bad cholesterol) levels, and low high-density lipoprotein (good cholesterol) levels.

Risk factors that cannot be modified include (1) sex, ie, men are more likely to have a stroke and survive, women are more likely to die as a result of stroke; (2) advanced age, ie, cardiovascular diseases tend to affect older people more than younger people; and (3) ethnicity, ie, African Americans have a higher risk of high blood pressure than others.

TIA is a warning sign of a future stroke. An estimated 25% of patients with TIA develop a stroke within the next 2 years. Symptoms of a TIA include weakness, numbness or tingling on one side of the body, confusion, trouble with speaking, difficulty understanding speech, vertigo, and severe headache. TIAs also may cause a variety of visual symptoms that include partial loss of vision or complete blindness, double vision, abnormal eye movements, blurred vision, and a gray shading or fogging within the field of vision.

Medical treatment for mild to moderate carotid stenosis is most appropriate. Treatment is directed toward reducing the progression of the atherosclerotic disease process by lowering serum cholesterol levels, controlling hypertension, and by the administration of a medication such as aspirin, which decreases the likelihood of platelet or small clot embolization.

Carotid endarterectomy of asymptomatic carotid stenosis is most commonly limited to lesions with a 70% or greater degree of stenosis.⁸ Asymptomatic carotid stenosis may be detected by the auscultation of a cervical (neck) bruit or other screening method. Symptomatic carotid stenosis (SCS) is characterized by an associated stroke, TIA, transient monocular (1 eye) blindness, or other objective symptom or sign of an ipsilateral cerebral vascular event. Treatment for most SCS is surgical.

More recently, carotid stenosis has been successfully managed by means of endovascular carotid stent placement. The selection of a specific clinical treatment is based upon the degree of stenosis, the condition of the arterial vessels proximal to the carotid stenosis, and the availability of specific treatment options.

Preferred Examination

A complete medical history should be taken first. On the basis of risk factors and the family history and current symptoms, selecting a screening examination such as duplex carotid sonography, CT angiography (CTA), or magnetic resonance angiography (MRA) of the carotid artery may be appropriate (see Image 1, Images 13-15).⁹

After obtaining the medical history, carotid duplex imaging is performed most commonly in patients with moderate risk factors. In the author's practice, duplex sonography is the initial triage examination for patients with an asymptomatic bruit, known asymptomatic carotid vascular disease, and in patients with a complete stroke without prior history of carotid stenosis.

In symptomatic patients and in most who present with abnormal carotid sonographic findings, another imaging test is performed. MRA or CTA offer full depiction of the cervical and cerebral portions of the CCA and ICA. In most cases, a diagnostic evaluation for cerebral vascular disease can be performed by using either MRA or CTA. The immediate availability of CTA in many critical hospitals on a 24-hour basis makes CTA attractive in the care of patients who present after hours in the emergency department.

In the selection of patients for acute treatment for cerebral ischemia, axial CT images should be reviewed by using the criteria of less than one-third involvement of the middle cerebral distribution or by using the Alberta Stroke Program Early CT Score (ASPECTS). The role of cervical-cerebral angiography is evolving as less invasive alternative tests have become available. Many experienced vascular surgeons are more comfortable with cervical-cerebral catheter angiography than with other studies. In the author's practice, clinicians perform carotid angiography routinely, and cerebral angiography or digital subtraction angiography (DSA) is reserved for patients who are likely candidates for surgery or for patients who may benefit from angiographically based carotid intervention.

Limitations of Techniques

Although carotid duplex imaging offers an excellent means of initial evaluation of the extracranial cerebral vessels, the presence of dense calcifications in the carotid plaque tends to make the study less accurate (see Image 20). Because carotid duplex imaging does not help in assessing the intracranial portion of the carotid artery, tandem lesions of the ICA may be missed. In a similar manner, proximal stenosis of the innominate artery and the left carotid artery cannot be evaluated near the origins from the aortic arch.

MRA is contraindicated in patients who have cardiac pacemakers or cerebral aneurysm clips or in those who have undergone certain other medical procedures. In addition, MRA is highly motion sensitive. Many patients require sedation. Because of artifacts related to the MRA image, the degree of stenosis may be overestimated.

CTA requires iodinated contrast agents to be injected at a relatively high flow rate. Patients with renal disease may not tolerate intravenous contrast agents. Motion artifacts remain a problem if the examination is performed by using older CT equipment (see Images 20-21).

Cerebral angiography also involves the injection of iodinated contrast agents. The overall contrast dose is similar to that required for CTA. The performance of catheter-based cervical-cerebral angiography depends on the skill and experience of the angiographer. Overall major morbidity rates are 0.1-1%. Injury may occur in the form of iatrogenic stroke or bleeding around the catheter introduction site. Angiograms do not provide much information concerning the nature of the plaque lesion. Cerebral angiography is the most costly means of carotid stenosis evaluation. If cases are selected carefully, the overall risk of diagnostic angiography together with the morbidity related to carotid surgery is less than the risk of stroke for the untreated patient (see Images 6-9, Image 11, Image 17).

Differential Diagnoses

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• Stroke Treatment
• Stroke-Related Dementia Overview

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