> Table of Contents > Carotid Stenosis
Carotid Stenosis
Edlira Yzeiraj, DO, MS
Maria M. Plummer, MD
image BASICS
Carotid stenosis may be caused by atherosclerosis, intimal fibroplasia, vasculitis, adventitial cysts, or vascular tumors; atherosclerosis is the most common etiology.
  • Narrowing of carotid artery lumen is typically due to atherosclerotic changes in the vessel wall. Atherosclerotic plaques are responsible for 90% of extracranial carotid lesions and up to 30% of all ischemic strokes.
  • A “hemodynamically significant” carotid stenosis produces a drop in pressure, reduction in flow, or both and corresponds approximately to a 60% diameter-reducing stenosis (1).
  • Carotid lesions are classified by the following:
    • Symptom status
      • Asymptomatic: tend to be homogenous and stable
      • Symptomatic (stroke, transient cerebral ischemic event): tend to be heterogeneous and unstable
    • Degree of stenosis
      • High grade: 80-99% stenosis
      • Moderate grade: 50-79% stenosis
      • Low grade: <50% stenosis
More common in men and with increasing age (see “Risk Factors”)
Unclear (asymptomatic patients often go undiagnosed)
  • Moderate stenosis (2)
    • Age <50 years: men 0.2%, women 0%
    • Age >80 years: men 7.5%, women 5%
  • Severe stenosis (2)
    • Age <50 years: men 0.1%, women 0%
    • Age >80 years: men 3.1%, women 0.9%
  • Atherosclerosis begins during adolescence, consistently at carotid bifurcation. The carotid bulb has unique blood flow dynamics. Hemodynamic disturbances cause endothelial injury and dysfunction. Plaque formation in vessel wall results and stenosis then ensues.
  • Initial cause not well understood, but certain risk factors are frequently present (see “Risk Factors”). Tensile stress on the vessel wall, turbulence, and arterial wall shear stress seem to be involved.
  • Increased incidence among family members
  • Genetically linked factors
    • Diabetes mellitus (DM), race, hypertension (HTN), family history, obesity
    • In a recent single nucleotide polymorphism study, the following genes were strongly associated with worse carotid plaque: TNFSF4, PPARA, TLR4, ITGA2, and HABP2.
  • Nonmodifiable factors: advanced age, male sex, family history, cardiac disease, congenital arteriopathies (1)
  • Modifiable factors: smoking, diet, dyslipidemia, physical inactivity, obesity, HTN, DM
  • Antihypertensive treatment to maintain BP <140/90 mm Hg (systolic BP of 150 mm Hg is target in elderly) (3)[A]
  • Smoking cessation to reduce the risk of atherosclerosis progression and stroke (3)
  • Lipid control: regression of carotid atherosclerotic lesions seen with statin therapy (3)
  • Transient ischemic attack (TIA)/stroke
  • Coronary artery disease (CAD)/myocardial infarction (MI)
  • Peripheral vascular disease (PVD)
  • HTN
  • DM
  • Hyperlipidemia
Screening for carotid stenosis is not recommended. However, in the setting of symptoms suggestive of stroke or TIA, workup for this condition may be indicated.
  • Lateralizing neurologic deficits: contralateral motor and/or sensory deficit
  • Amaurosis fugax: ipsilateral transient visual obscuration from retinal ischemia
  • Visual field defect
  • Dysarthria and in the case of dominant (usually left) hemisphere involvement, aphasia
  • Carotid bruit (low sensitivity and specificity)
  • Aortic valve stenosis
  • Aortic arch atherosclerosis
  • Arrhythmia with cardiogenic embolization
  • Migraine
  • Brain tumor
  • Metabolic disturbances
  • Functional/psychological deficit
  • Seizure
Initial Tests (lab, imaging)
Workup for suspected TIA/stroke may include the following:
  • CBC with differential
  • Basic metabolic panel
  • ESR (if temporal arteritis a consideration)
  • Glucose/glycated hemoglobin (HbA1c)
  • Fasting lipid profile
  • Duplex ultrasonography is the recommended initial diagnostic test in asymptomatic patients with known or suspected carotid stenosis (3)[C].
  • Duplex ultrasound (US) identifies >50% stenosis, with 98% sensitivity and 88% specificity.
Follow-Up Tests & Special Consideration
  • Proceed to imaging if there is suggestion of stenosis from history or physical exam.
  • Other noninvasive imaging techniques can add detail to duplex results:
    • CT angiography
      • 88% sensitivity and 100% specificity
      • Requires contrast load with risk for subsequent renal morbidity
    • MR angiography
      • 95% sensitivity and 90% specificity
      • Evaluates cerebral circulation (extracranial and intracranial) as well as aortic arch and common carotid artery
      • The presence of unstable plaque can be determined if the following characteristics are seen:
        • Presence of thin/ruptured fibrous cap
        • Presence of lipid-rich necrotic core
      • Tends to overestimate degree of stenosis
Diagnostic Procedures/Other
Cerebral (catheter) angiography is the traditional gold standard for diagnosis:
  • Delineates anatomy pertaining to aortic arch and proximal vessels
  • However, procedure is invasive and has multiple risks:
    • Contrast-induced renal dysfunction (1-5% complication rate)
    • Thromboembolic-related complications (1-2.6% complication rate) and neurologic complications
    • Should be used only when other tests are not conclusive
Test Interpretation
  • Stenosis consistently occurs at carotid bifurcation, with plaque formation most often at proximal internal carotid artery:
    • Plaque is thickest at the carotid bifurcation.
    • Plaque occupies the intima and inner media and avoids outer media and adventitia.
  • Plaque histology
    • Homogenous (stable) plaques seldom hemorrhage or ulcerate:
      • Fatty streak and fibrous tissue deposition
      • Diffuse intimal thickening
    • Heterogenous (unstable) plaques may hemorrhage or ulcerate:
      • Presence of lipid-laden macrophages, necrotic debris, cholesterol crystals
      • Ulcerated plaques
    • Soft and gelatinous clots with platelets, fibrin, and red and white blood cells
Smoking cessation, BP control, use of antiplatelet medication, and statin medication are the primary treatments for both asymptomatic and symptomatic carotid stenosis.
  • Lifestyle modifications: dietary control and weight loss, exercise of 30 min/day at least 5 days/week.
  • Patients should be advised to quit smoking and offered smoking cessation intervention to reduce the risk of atherosclerotic progression and stroke.
  • Control of HTN with antihypertensive agents to maintain BP <140/90 mm Hg (3)[A]; <150/90 mm Hg in the elderly

  • Antihypertensive treatment (<140/90 mm Hg) (3)[A], <150/90 mm Hg in the elderly
  • Diet, smoking cessation, and exercise are useful adjuncts to therapy.
  • Statin initiation is recommended to reduce LDL cholesterol <100 mg/dL (3)[B]; choose moderate- to high-intensity statin therapy for anti-inflammatory benefit.
  • In statin intolerance, LDL-lowering therapy with bile acid sequestrants and/or niacin is reasonable (3)[B].
  • Aspirin: 75 to 325 mg/day (3)[A]
  • If patient has sustained ischemic stroke or TIA, antiplatelet therapy with
    • Aspirin alone (75 to 325 mg/day) (3)[B] or
    • Clopidogrel alone (75 mg/day) (3)[B], or
    • Aspirin plus extended-release dipyridamole (25 and 200 mg BID, respectively) (3)[B]
    • A combination of clopidogrel plus aspirin is NOT recommended within 3 months post TIA or CVA (3)[B].
  • For acute symptomatic stroke, order imaging and contact neurology.
  • For known carotid stenosis, some suggest duplex imaging every 6 months if stenosis is >50% and patient is a surgical candidate.
  • Symptomatic carotid stenosis
    • Carotid endarterectomy (CEA) is recommended in symptomatic patients with a carotid stenosis of 70-99% without near-occlusion. Benefit in patients with carotid near-occlusion is uncertain in the long term (4)[A].
    • CEA is recommended for patients with a life expectancy of at least 5 years. The anticipated rate of perioperative stroke or mortality must be <6% (3)[A].
    • Treatment with aspirin (81 to 325 mg/day) is recommended for all patients who are having CEA. Aspirin should be started prior to surgery and continued for at least 3 months postsurgery but may be continued indefinitely (5)[B].
    • Carotid artery stenting (CAS) provides similar long-term outcomes as CEA (6)[A]. Age should be considered when planning a carotid intervention.
      • CAS has an increased risk of adverse cerebrovascular events in the elderly compared to the young but similar mortality risk. CEA is associated with similar neurologic outcomes in the elderly and young, at the expense of increased mortality (7)[A].
      • CAS is suggested in select patients with neck anatomy unfavorable for arterial surgery and those with comorbid conditions that greatly increase the risk of anesthesia and surgery (3)[A].
      • Dual antiplatelet therapy with aspirin (81 to 325 mg/day) plus clopidogrel (75 mg/day) is recommended for 30 days post CAS (3)[C].
  • Asymptomatic patients
    • CEA is recommended by some for asymptomatic men who have 60-99% stenosis, have a life expectancy of at least 5 years, and the perioperative risk of stroke and death is <3% (6),(8)[B].
    • The advantage of surgical compared with medical therapy has decreased with contemporary medical management. It is not possible to make an evidence-based recommendation for or against surgical therapy with current literature (9)[A].
Admission Criteria/Initial Stabilization
Any patient with presentation of acute symptomatic carotid stenosis should be hospitalized for further diagnostic workup and appropriate therapy.
Rapid evaluation for symptoms compatible with TIA should be obtained in the emergency department (ED) or inpatient setting.
Discharge Criteria
24 to 48 hours post CEA, if ambulating, taking adequate PO intake, and neurologically intact
Patient Monitoring
  • Duplex at 2 to 6 weeks postop
  • Duplex every 6 to 12 months
  • Reoperative CEA or CAS is reasonable, if there is rapidly progressive restenosis (3)[A].
  • Patients with any of the following: renal failure, heart failure, diabetes, and age >80 years have a high-readmission rate following CEA; thus, intensive medical therapy and rigorous follow-up is recommended (10).
Low-fat, low-cholesterol, low-salt diet at discharge
For patient education materials on this topic, consult the following:
  • American Heart Association: http://www.heart.org
  • Mayo Clinic Information: http://www.mayoclinic.org/diseases-conditions/carotid-artery-disease/basics/definition/con-20030206
1. Goldstein LB, Bushnell CD, Adams RJ, et al. Guidelines for the primary prevention of stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011;42(2):517-584.
2. de Weerd M, Greving JP, Hedblad B, et al. Prevalence of asymptomatic carotid artery stenosis in the general population: an individual participant data meta-analysis. Stroke. 2010;41(6):1294-1297.
3. Brott TG, Halperin JL, Abbara S, et al. 2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease: executive summary. J Am Coll Cardiol. 2011;57(8):1002-1044.
4. Rerkasem K, Rothwell PM. Carotid endarterectomy for symptomatic carotid stenosis. Cochrane Database Syst Rev. 2011;(4):CD001081.
5. Chaturvedi S, Bruno A, Feasby T. Carotid endarterectomy—an evidenced-based review: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2005;65(6):794-801.
6. Bonati LH, Lyrer P, Ederle J, et al. Percutaneous transluminal balloon angioplasty and stenting for carotid artery stenosis. Cochrane Database Syst Rev. 2012;(9):CD000515.
7. Antoniou GA, Georgiadis GS, Georgakarakos EI, et al. Meta-analysis and meta-regression analysis of outcomes of carotid endarterectomy and stenting in the elderly. JAMA Surg. 2013; 148(12):1140-1152.
8. Raman G, Moorthy D, Hadar N, et al. Management strategies for asymptomatic carotid stenosis: a systematic review and meta-analysis. Ann Intern Med. 2013;158(9):676-685.
9. Meschia JF, Bushnell C, Boden-Albala B, et al. Guidelines for the primary prevention of stroke: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45(12):3754-3832.
10. Fokkema M, Bensley RP, Lo RC, et al. In-hospital versus postdischarge adverse events following carotid endarterectomy. J Vasc Surg. 2013;57(6):1568-1575.
Additional Reading
  • Go C, Avgerinos ED, Chaer RA, et al. Long-term clinical outcomes and cardiovascular events after carotid endarterectomy. Ann Vasc Surg. 2015;29(6):1265-1271.
  • Jonas DE, Feltner C, Amick HR, et al. Screening for asymptomatic carotid artery stenosis: a systematic review and meta-analysis for the U.S. Preventive Services Task Force. Ann Intern Med. 2014;161(5):336-346.
  • Paraskevas KI, Mikhailidis DP, Veith FJ. Comparison of the five 2011 guidelines treatment of carotid stenosis. J Vasc Surg. 2012;55(5):1504-1508.
See Also
Algorithms: Transient Ischemic Attack and Transient Neurologic Defects; Stroke
  • I65.29 Occlusion and stenosis of unspecified carotid artery
  • I65.21 Occlusion and stenosis of right carotid artery
  • I65.22 Occlusion and stenosis of left carotid artery
Clinical Pearls
  • Atherosclerosis is responsible for 90% of all cases of carotid artery stenosis.
  • Duplex US is the best initial imaging modality.
  • Antiplatelet therapy and aggressive treatment of vascular risk factors are the mainstays of medical therapy.
  • Compared with CEA, CAS increases the risk of any stroke and decreases the risk of MI. For every 1,000 patients opting for stenting rather than endarterectomy, 19 more patients would have strokes and 10 fewer would have MIs.