Carotid stenosis may be caused by atherosclerosis, intimal fibroplasia, vasculitis, adventitial cysts, or vascular tumors; atherosclerosis is the most common etiology.
- Narrowing of the 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 or a reduction in flow. It corresponds approximately to a 60–99% diameter-reducing stenosis.
- Carotid lesions are classified by the following:
- Symptom status
- Asymptomatic: tend to be homogenous and stable
- Symptomatic: tend to be heterogeneous and unstable; present with stroke or transient cerebral ischemic attack
- Degree of stenosis
- High grade: 80–99% stenosis
- Moderate grade: 50–79% stenosis
- Low grade: <50% stenosis
- Symptom status
More common in men and with increasing age (see “Risk Factors”)
Unclear (Asymptomatic patients often go undiagnosed.)
- Moderate stenosis
- Age <50 years: men 0.2%, women 0%
- Age >80 years: men 7.5%, women 5%
- Severe stenosis
- Age <50 years: men 0.1%, women 0%
- Age >80 years: men 3.1%, women 0.9%
Etiology and Pathophysiology
- Atherosclerosis begins during adolescence, consistently at the 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 is 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 (>65 years old), male sex, family history, coronary artery disease (CAD), peripheral artery disease, aortic aneurysmal disease, congenital arteriopathies
- Modifiable factors: smoking, diet, dyslipidemia, physical inactivity, obesity, HTN, DM
- Possible factors: Chlamydia pneumoniae and Cytomegalovirus
- Antihypertensive treatment to maintain blood pressure (BP) <140/90 mm Hg (Systolic BP of 150 mm Hg is target in elderly.)
- Smoking cessation to reduce the risk of atherosclerosis progression and stroke
- Lipid control: regression of carotid atherosclerotic lesions seen with statin therapy
Commonly Associated Conditions
- Transient ischemic attack (TIA)/stroke
- CAD/myocardial infarction (MI)
- Peripheral vascular disease (PVD)
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.
- Identification of modifiable and nonmodifiable comorbidities (see “Risk Factors”)
- History of cerebral ischemic event
- Stroke, TIA, amaurosis fugax (monocular blindness), aphasia
- Peripheral arterial disease
- Review of systems, with focus on risk factors for
- Cardiovascular disease
- Stroke (HTN and arrhythmias)
- Lateralizing neurologic deficits: contralateral motor and/or sensory deficit
- Amaurosis fugax: ipsilateral transient visual obscuration from retinal ischemia
- Visual field defect
- Dysarthria, aphasia (in the case of dominant hemisphere involvement, usually left)
- Carotid bruit (low sensitivity and specificity)
- Aortic valve stenosis
- Aortic arch atherosclerosis
- Arrhythmia with cardiogenic embolization
- Brain tumor
- Metabolic disturbances
- Functional/psychological deficit
Diagnostic Tests & InterpretationInitial Tests (lab, imaging)
Workup for suspected TIA/stroke may include the following:
- Complete blood count with differential
- Basic metabolic panel
- Erythrocyte sedimentation rate (if temporal arteritis a consideration)
- Glucose/hemoglobin A1c
- Fasting lipid profile
- Duplex ultrasonography is the recommended initial diagnostic test in asymptomatic patients with known or suspected carotid stenosis.
- Duplex ultrasound (US) identifies ≥50% stenosis, with 98% sensitivity and 88% specificity.
Follow-Up Tests & Special Considerations
- 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 IV contrast 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
- CT angiography
Cerebral angiography is the traditional gold standard for diagnosis:
- Delineates the anatomy pertaining to aortic arch and proximal vessels
- The 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
- Stenosis consistently occurs at the carotid bifurcation, with plaque formation most often at the level of the 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
- Homogenous (stable) plaques seldom hemorrhage or ulcerate:
Smoking cessation, BP control, 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; <150/90 mm Hg in the elderly. In carefully selected individuals, tighter blood pressure control might reduce cerebrovascular events, but this remains uncertain.
- Antihypertensive treatment (<140/90 mm Hg), <150/90 mm Hg in the elderly
- Diet, smoking cessation, and exercise are useful adjuncts to therapy.
- Statin initiation is recommended; choose moderate- to high-intensity statin therapy for anti-inflammatory benefit.
- A comprehensive program that includes tight control of HTN with ACE inhibitor or angiotensin receptor blocker treatment reduces the risk in individuals with diabetes. Stroke prevention benefit of intensive glucose lowering therapy has not been established (1)[A].
- Aspirin: 75 to 325 mg/day
- If patient has sustained TIA or ischemic stroke, antiplatelet therapy with
- Aspirin alone (75 to 325 mg/day), or
- Clopidogrel alone (75 mg/day), or
- Aspirin plus extended-release dipyridamole (25 and 200 mg BID, respectively)
- A combination of clopidogrel plus aspirin is NOT recommended within 3 months post-TIA or CVA.
Issues For Referral
- 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 (history of ischemia ipsilateral to stenosis)
- Carotid endarterectomy (CEA) is of some benefit in 50–69% symptomatic stenosis, highly beneficial for those with 70–99% stenosis without near occlusion and has no benefit in people with carotid near-occlusion (2)[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)[B].
- 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 (3)[B].
- Carotid artery stenting (CAS) provides similar long-term outcomes as CEA (4)[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 (5)[A].
- CAS is suggested in selected patients with neck anatomy unfavorable for arterial surgery and those with comorbid conditions that greatly increase the risk of anesthesia and surgery.
- Dual antiplatelet therapy with aspirin (81 to 325 mg/day) plus clopidogrel (75 mg/day) is recommended for 30 days post-CAS.
- Asymptomatic patients
- As compared with CAS, CEA is the preferred option for the management of asymptomatic carotid stenosis if a surgical option is chosen. CAS has the potential for increased risks of periprocedural stroke and periprocedural death (6)[A].
- 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 (1)[A].
Admission, Inpatient, and Nursing Considerations
- 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
Follow-up RecommendationsPatient Monitoring
- Duplex at 2 to 6 weeks postoperatively
- Duplex every 6 to 12 months
- Reoperative CEA or CAS is reasonable, if there is rapidly progressive restenosis.
- 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.
Heart-healthy diet low in saturated fat, no trans fat
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/basic...
- Untreated: TIA/stroke (risk of ipsilateral stroke approximately 1.68% per year)
- Postoperative (status post CEA)
- Perioperative (within 30 days)
- Stroke/death, cranial nerve injury, hemorrhage, hemodynamic instability, MI
- Late (>30 days postop)
- Recurrent stenosis, false aneurysm at surgical site
- Perioperative (within 30 days)
- 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. [PMID:26004951]
- 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. [PMID:25004169]
- Paraskevas KI, Mikhailidis DP, Veith FJ. Comparison of the five 2011 guidelines for the treatment of carotid stenosis. J Vasc Surg. 2012;55(5):1504–1508. [PMID:22542347]
- Rundek T, Sacco R. Risk factor management to prevent first stroke. Neurol Clin. 2008;26(4):1007–1045. [PMID:19026901]
- I63.031 Cerebral infrc due to thrombosis of right carotid artery
- I63.032 Cerebral infarction due to thrombosis of left carotid artery
- I63.039 Cerebral infarction due to thrombosis of unsp carotid artery
- I63.131 Cerebral infarction due to embolism of right carotid artery
- I63.132 Cerebral infarction due to embolism of left carotid artery
- I63.139 Cerebral infarction due to embolism of unsp carotid artery
- I65.21 Occlusion and stenosis of right carotid artery
- I65.22 Occlusion and stenosis of left carotid artery
- I65.23 Occlusion and stenosis of bilateral carotid arteries
- I65.29 Occlusion and stenosis of unspecified carotid artery
- 433.10 Occlusion and stenosis of carotid artery without mention of cerebral infarction
- 433.11 Occlusion and stenosis of carotid artery with cerebral infarction
- 433.30 Occlusion and stenosis of multiple and bilateral precerebral arteries without mention of cerebral infarction
- 433.31 Occlusion and stenosis of multiple and bilateral precerebral arteries with cerebral infarction
- 195185009 cerebral infarct due to thrombosis of precerebral arteries (disorder)
- 195186005 Cerebral infarction due to embolism of precerebral arteries
- 266254007 carotid artery occlusion (disorder)
- 285191000119103 left carotid artery stenosis (disorder)
- 285201000119100 right carotid artery stenosis (disorder)
- 64586002 Carotid artery stenosis (disorder)
- 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.
Evangelos Giakoumatos, MD, MSc
Naureen Bashir Rafiq, MBBS
- Meschia JF, Bushnell C, Boden-Albala B, et al; and American Heart Association Stroke Council, Council on Cardiovascular and Stroke Nursing, Council on Clinical Cardiology, Council on Functional Genomics and Translational Biology, Council on Hypertension. 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. [PMID:25355838]
- Orrapin S, Rerkasem K. Carotid endarterectomy for symptomatic carotid stenosis. Cochrane Database Syst Rev. 2017;(6):CD001081. [PMID:16186516]
- Chaturvedi S, Bruno A, Feasby T, et al. Carotid endarterectomy—an evidence-based review: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2005;65(6):794–801. [PMID:16186516]
- 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. [PMID:24154858]
- 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. [PMID:28679848]
- Moresoli P, Habib B, Reynier P, et al. Carotid stenting versus endarterectomy for asymptomatic carotid artery stenosis: a systematic review and meta-analysis. Stroke. 2017;48(8):2150–2157. [PMID:25355838]
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