CAROTID STENOSIS

Naureen Rafiq, MD • Theophile Lyotard, MD

BASICS
Carotid stenosis may be caused by atherosclerosis, intimal
fibroplasia, vasculitis,
adventitial cysts, or vascular tumors; atherosclerosis is the
most common
etiology.
DESCRIPTION
• 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% diameterreducing 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
EPIDEMIOLOGY
More common in men and with increasing age (see
“Risk Factors”)
Incidence
Unclear (asymptomatic patients often go undiagnosed)
Prevalence
• Moderate stenosis
– Age <50 years: men 0.2%, women 0%

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– 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.
Genetics
• 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.
RISK FACTORS
• Nonmodifiable factors: advanced age, male sex,
family history, cardiac
disease, congenital arteriopathies
• Modifiable factors: smoking, diet, dyslipidemia, physical
inactivity, obesity,
HTN, DM
GENERAL PREVENTION
• Antihypertensive treatment to maintain 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

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• Transient ischemic attack (TIA)/stroke
• Coronary artery disease (CAD)/myocardial infarction (MI)
• Peripheral vascular disease (PVD)
• HTN
• DM
• Hyperlipidemia

DIAGNOSIS
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.
HISTORY
• Identification of modifiable and nonmodifiable
comorbidities (see “Risk
Factors”)
• History of cerebral ischemic event
• Stroke, TIA, amaurosis fugax (monocular blindness),
aphasia
• Coronary artery disease/MI
• Peripheral arterial disease
• Review of systems, with focus on risk factors for
– Cardiovascular disease
– Stroke (HTN and arrhythmias)
PHYSICAL EXAM
• 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)
DIFFERENTIAL DIAGNOSIS
• Aortic valve stenosis
• Aortic arch atherosclerosis

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• Arrhythmia with cardiogenic embolization
• Migraine
• Brain tumor
• Metabolic disturbances
• Functional/psychological deficit
• Seizure
DIAGNOSTIC TESTS & INTERPRETATION
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/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

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Tends to overestimate degree of stenosis
Diagnostic Procedures/Other
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
Test Interpretation
• 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

TREATMENT
Smoking cessation, BP control, antiplatelet medication, and
statin medication are
the primary treatments for both asymptomatic and
symptomatic carotid stenosis.
GENERAL MEASURES
• 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

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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.
MEDICATION
• 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.
• 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.
SURGERY/OTHER PROCEDURES
• 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 (1)[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%.
– 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 (2)[B].

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– Carotid artery stenting (CAS) provides similar long-term
outcomes as CEA
(3)[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 (4)[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.
Dual antiplatelet therapy with aspirin (81 to 325
mg/day) plus clopidogrel
(75 mg/day) is recommended for 30 days post-CAS.
• 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% (3),(5)[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 (6)[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

ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Patient Monitoring
• Duplex at 2 to 6 weeks postoperatively

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• 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.
DIET
Low-fat, low-cholesterol, low-salt diet at discharge
PATIENT EDUCATION
For patient education materials on this topic, consult the
following:
• American Heart Association: http://www.heart.org
• Mayo Clinic Information:
http://www.mayoclinic.org/diseasesconditions/carotid-artery-disea
se/basics/definition/con-20030206
COMPLICATIONS
• Untreated: TIA/stroke (risk of ipsilateral stroke
approximately 1.68% per year
• Postoperative (s/p 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

REFERENCES
1. Rerkasem K, Rothwell PM. Carotid endarterectomy
for symptomatic carotid
stenosis. Cochrane Database Syst Rev. 2011;(4):CD001081.
2. 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.
3. 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