A 72-year-old Caucasian man presented 1 week after an episode where he spontaneously dropped a cigarette he was holding in his right hand. He had immediately noted an inability to grasp objects and numbness in his right hand. These symptoms lasted for 2 minutes and then spontaneously resolved. After this episode his right hand felt completely normal. He denied other symptoms such as amaurosis, paralysis, paresthesias, speech disturbance, or gait disturbance. His past medical history was significant for hypertension, hypercholesterolemia, and cramping in his calves when he walked long distances. He had a 40 pack-year history of smoking and denied use of alcohol. A carotid duplex ultrasound examination showed a left 70% to 99% internal carotid artery (ICA) stenosis.

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  Stroke ranks third among all causes of death in the United States behind heart disease and cancer, with 795,000 strokes occurring per year.¹

  
  
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  Annually, 55,000 more women than men are affected, and over 60% of all stroke deaths occur in women. African Americans have twice the stroke risk of Caucasians. Mexican Americans also have an increased incidence of stroke compared to Caucasians.²

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  One-third of all strokes are related to cervical carotid disease.

  
  
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  Standard risk factors for coronary and systemic atherosclerosis apply to carotid disease such as age, male sex, family history, smoking, hypertension, hyperlipidemia, sedentary lifestyle, and high dietary saturated fatty acids and cholesterol.

  
  
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  The mechanism of cervical carotid stroke is usually embolization from a carotid bifurcation plaque, but hemodynamic compromise from stenosis may also play a role. The risks of embolization and hemodynamic compromise increase with increasing ICA stenosis.³

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  When carotid territory stroke or transient ischemic attack (TIA) is suspected, carotid duplex in an accredited vascular laboratory to define degree of stenosis is mandatory.

  
  
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  When carotid duplex is nondiagnostic, computed tomography (CT) or magnetic resonance angiography (MRA) may be used.

  
  
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  Catheter angiography is indicated in the setting of conflicting noninvasive studies and when carotid artery stenting (CAS) is planned.⁴

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  Neurologic examination may reveal motor or sensory deficits contralateral to the affected carotid artery. Aphasia, dysphasia, or apraxia may also be reported.

  
  
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  Amaurosis fugax, or sudden complete or partial loss of vision in one eye, is a result of embolization from the cervical carotid artery to the ipsilateral central retinal artery.

  
  
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  Up to 70% of stroke survivors can regain functional independence; however, 15% to 30% become permanently disabled and 20% will require long-term care.⁵ In patients over 65 years old, 6 months after stroke 50% have some residual hemiparesis, 30% require some assistance with walking, 26% cannot perform activities of daily living independently, 19% have aphasia, and 26% are institutionalized.⁶

  
  
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  Mean lifetime cost of an ischemic stroke in the United States is $140,048. In 2007, the total cost of stroke exceeded $40 billion.¹

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  Carotid endarterectomy (CEA) has been well established as a treatment for cervical carotid disease. Recently, debate has centered on CEA versus CAS in the management of carotid disease. The decision to revascularize should be relatively independent of the method of revascularization, with case-specific nuances contributing more to the decision of CAS versus CEA.

  
  
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  All patients should receive optimal medical therapy. Aspirin is indicated for all patients with atherosclerotic carotid disease.

  
  
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  Warfarin may be indicated to treat patients who have had stroke from cardiac embolization, but there is no evidence supporting the use of heparin and warfarin or clopidogrel to prevent or treat stroke related to cervical carotid disease.

  
  
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  Management of hypertension and hypercholesterolemia, smoking cessation, and dietary and activity modification are all mainstays of treatment.

  
  
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  Patients with asymptomatic carotid stenosis greater than and equal to 60% gain stroke risk reduction with carotid revascularization. However, that risk reduction must be considered in light of the patient’s life expectancy, with intervention reserved for patients with at least a 5-year life expectancy.^7,8

  
  
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  Current medical therapy may outperform intervention in certain low-risk asymptomatic patients, and there is low absolute risk reduction with intervention for asymptomatic patients. Overall stroke risk in medically managed asymptomatic patients is only 2% per year, thus careful patient selection in asymptomatic carotid disease is paramount.

  
  
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  Carotid intervention is indicated in patients with symptomatic carotid stenosis if greater than 50% diameter reduction is demonstrated.^9,10

  
  
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  Patients considered high risk for CEA include those with anatomically inaccessible lesions, cervical immobility, prior neck dissection, tracheostomy, contralateral cranial nerve injury, prior radiation therapy, contralateral occlusion, and recurrent stenosis after CEA. Medical comorbidities considered high risk for CEA include presence of chronic obstructive pulmonary disease, New York Heart Association (NYHA) class III or IV heart failure, ejection fraction less than 30%, recent myocardial infarction (MI), and unstable angina.

  
  
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  Short-term risks in centers of excellence for both CEA and CAS may be equivalent for the composite endpoint of any stroke, death, or MI.

  
  
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  Center for Medicare and Medicaid Services (CMS) approval for CAS continues to undergo scrutiny, but currently CAS is reimbursed only for high-risk patients with symptomatic high-grade stenosis. Patients who are at high risk and symptomatic with 50% to 79% stenosis and high-risk asymptomatic patients with over 80% stenosis can be covered in the context of a trial. These criteria were put forth in the formative years of CAS when it was considered more reasonable to attempt CAS in patients with some contraindication to CEA. Evidence that these indications will evolve come in the form of recent FDA approval of several devices for use in nonhigh-risk patients.

  
  
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  Age alone increases risk with CAS, and this is thought to be related to increased arch calcification and changing arch morphology that can make access difficult (Figure 22-1). Carotid tortuosity (Figure 22-2) is also associated with age and may present problems with stent or embolic protection device deployment. Symptomatic patients may be better treated by CEA, especially when older than 70 years or if male.

  
  
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  Patients meeting high risk for CEA criteria with symptomatic high-grade stenosis may be offered CAS as primary treatment (Figures 22-3 and 22-4).

  
  
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  In the absence of being considered high risk for CEA, patients aged less than 70 years may be offered CAS or CEA with equivalent composite stroke or MI or death rates. In this group, CAS incurs higher stroke risk in exchange for lower MI risk, and CEA incurs higher MI risk in exchange for lower stroke risk.^{11,12,13,14,15, and 16}