Carotid artery stenosis is a narrowing of the common and internal carotid arteries secondary to atherosclerosis.
- Affects more men than women until the age of 75
- Risk increases with age:
- 0.5% prevalence in the 6th decade
- 10% prevalence in patients > 80 years of age
- Major cause of disability and fatal stroke
- Modifiable risk factors:
- Alcohol use
- Sedentary lifestyle
- Diabetes mellitus
- Non-modifiable risk factors:
- Increasing age
- Family history
Carotid stenosis can cause symptoms from a state of low flow or embolization.
Low flow results from progressive narrowing of the carotid artery:
- Development of atherosclerosis (local thickening of the arterial wall due to plaque deposition)
- Atherosclerotic plaques consist of a lipid core covered with a fibrous cap.
- Atherosclerosis commonly develops at the site of endothelial injury secondary to increased blood turbulence.
- Plaques, therefore, typically develop at the bifurcation of the common carotid artery.
- Narrowing of the lumen can produce symptoms, especially if there is inadequate collateral circulation to the brain.
- Calcified plaques are less likely to be inflamed and are less prone to rupture.
- Plaques are more susceptible to rupture when the fibrous cap becomes thin with the remodeling of the extracellular matrix by matrix metalloproteinases.
- Rupture of the plaque can lead to thrombosis and embolization, resulting in a stroke.
- Important features of rupture-prone carotid plaques:
- Increased numbers of inflammatory cells (e.g., macrophages)
- Large lipid core
- Thin fibrous cap
- Endothelial denudation
- Platelet aggregation
- Transient ischemic attack (TIA):
- Results from transient cerebral ischemia without acute infarction
- Produces transient neurological symptoms:
- Embolic: usually lasts a few hours
- Low flow: usually lasts a few minutes
- Ischemic stroke:
- Brain ischemia to thrombosis, embolism, or hypoperfusion
- Can result in acute brain-tissue infarction
- Persistent neurological symptoms may result in permanent damage
- Symptoms include:
- Amaurosis fugax (painless monocular vision loss)
- Hand/arm weakness, numbness, or heaviness
- Contralateral hemiplegia
- Ipsilateral facial weakness
- Aphasia (dominant hemisphere)
- Anosognosia (neglect; non-dominant hemisphere)
- Previous documented strokes or TIAs
- Transient weakness, numbness, speech impairment, or vision loss
- History of atherosclerosis, hypercholesterolemia/hypertension
- Focal neurological deficits (would indicate a stroke)
- Carotid bruit: heard with a stethoscope over the bifurcation/proximal internal carotid artery
- Diminished carotid pulse (severe stenosis/occlusion)
- Carotid duplex ultrasound:
- Detects focal increase in blood-flow velocity, which is indicative of stenosis
- Accurate in determining the degree of stenosis
- Does not provide information on plaque morphology
- CT angiogram (CTA):
- Provides anatomical image of vessels and surrounding structures
- Useful in detecting high-grade stenosis and occlusion
- Accurately detects the degree of stenosis
- Provides an image of anatomy and plaque morphology
- Cerebral angiography:
- Considered the gold standard
- Provides information on the entire carotid artery system, including contralateral side and collateral circulation
- Invasive, expensive, and carries the risk of complications
- Stop smoking.
- Weight loss
- Limit alcohol intake.
- Regular exercise
- DASH diet (a diet rich in fruits and vegetables, and low in fats, dairy, and saturated/total fats)
- Antiplatelet therapy (e.g., aspirin, clopidogrel)
- High-intensity statin treatment (promotes plaque stability)
Carotid endarterectomy (CEA):
- Involves surgical removal of the atherosclerotic plaque from the carotid artery
- Indications are based on risk-benefit analysis:
- Stenosis 80%–99% in asymptomatic patients
- Stenosis > 50% in symptomatic patients (men) or > 70% (women)
- Annual or biannual surveillance for patients not undergoing surgery (usually with duplex)
- Patients can become candidates for surgery over time with disease progression.
- Contraindications to CEA:
- Symptomatic carotid artery stenosis < 50%
- Ipsilateral carotid occlusion (100% stenosis)
- Prior ipsilateral endarterectomy
- History of neck surgery or irradiation
- Life expectancy < 5 years
Carotid angioplasty and stenting:
- Less invasive alternative to CEA
- Greater risk of periprocedural stroke than CEA
- Recommended for patients with:
- A carotid lesion that is not accessible with surgery
- Radiation-induced stenosis
- Restenosis after endarterectomy
- Cardiac, pulmonary, or other diseases, which greatly increase the risk of anesthesia and surgery
- Unfavorable neck anatomy including contralateral vocal-cord paralysis, open tracheostomy, or prior radical surgery
- Vertebrobasilar insufficiency: stenosis of vertebral and basilar arteries secondary to atherosclerosis, which results in compromised circulation to the posterior brain. Symptoms include dizziness/vertigo, numbness, slurred speech, weakness, confusion, and loss of coordination. Diagnosis is based on MRA or CTA, and treatment is focused on the control of hypertension and cholesterol, and lifestyle modifications.
- Embolic strokes from other sources: Carotid atherosclerotic plaques are a very common source of emboli to cerebral vessels, but other sources include the heart and aortic arch. Presenting symptoms are very similar to TIA and strokes originating from the carotids. Diagnosis is established based on imaging studies, and treatment includes management of acute stroke and the underlying disease.
- Carotid artery dissection: a tear in the intimal layer of the carotid wall that results in separation of the wall layers with blood getting in between the layers, resulting in occlusion of the vessel lumen. Carotid artery dissection is the most common cause of stroke in young adults and may occur spontaneously or secondary to neck trauma. Diagnosis is established with imaging. Treatment is with anticoagulants and surgical interventions in some cases.
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