Carotid Artery Stenosis

Carotid artery stenosis is atherosclerotic narrowing of the extracranial internal carotid artery, usually at the bifurcation and proximal internal carotid artery. It accounts for 10 to 15% of ischaemic strokes. The dominant mechanism is artery-to-artery embolism from plaque rupture or surface thrombus. Haemodynamic failure is much less common and needs severe stenosis or occlusion with poor collateral supply.

Epidemiology and risk

• Stenosis of 50% or more is present in about 5 to 7% of men and 3 to 5% of women over 65 years.
• Risk factors are smoking, hypertension, diabetes, dyslipidaemia, older age, coronary and peripheral arterial disease, and prior neck radiotherapy.
• Non-atherosclerotic causes include fibromuscular dysplasia, dissection, radiation arteritis, Takayasu arteritis and giant cell arteritis.

Severity is graded by comparing the narrowest residual lumen with the diameter of the normal distal internal carotid artery beyond the bulb:

• Mild: under 50%.
• Moderate: 50 to 69%.
• Severe: 70 to 99%.
• Near-occlusion (string sign) and occlusion are categorised separately.

Stroke risk depends on symptom status

• Untreated symptomatic stenosis of 70 to 99% carries an ipsilateral stroke risk of about 26% over 2 years, falling to about 9% with timely endarterectomy.
• The risk is highest in the first 2 weeks after a TIA or minor stroke, and falls steeply after that.
• Asymptomatic stenosis of 60 to 99% carries an annual ipsilateral stroke risk of roughly 1 to 2% with modern medical therapy.

Features of a plaque at higher risk of embolism

• Ulceration, intraplaque haemorrhage, a lipid-rich necrotic core with a thin fibrous cap, and low echogenicity on ultrasound.
• Stenosis progression, silent ipsilateral infarcts on imaging, and microembolic signals on transcranial Doppler.

Most patients are asymptomatic and are found through a bruit or incidental imaging. A bruit is a poor predictor of stenosis severity, and its disappearance may signal either improvement or tight stenosis with minimal flow.

Symptomatic disease presents as

• Amaurosis fugax: painless monocular visual loss lasting seconds to minutes, often described as a curtain descending. It reflects retinal embolism, and Hollenhorst plaques may be seen on fundoscopy.
• TIA or stroke: contralateral weakness or sensory loss, aphasia in dominant hemisphere disease, neglect in non-dominant disease, and dysarthria.
• Crescendo TIAs: repeated stereotyped events in a short period, which is a medical emergency.
• Haemodynamic symptoms: limb-shaking TIAs, transient events on standing, and border-zone infarcts, typically with occlusion or tight bilateral disease.
• Ocular ischaemic syndrome: with severe stenosis or occlusion, producing eye pain, rubeosis and venous stasis retinopathy.

Symptoms must be attributed to the correct vascular territory. Symptoms in the posterior circulation, syncope and non-focal dizziness are not caused by unilateral carotid stenosis.

Differential diagnosis includes cardioembolic stroke from atrial fibrillation, small vessel disease, carotid dissection, migraine aura, retinal vein or artery occlusion, giant cell arteritis, hypoglycaemia and focal seizures.

Red flags needing emergency evaluation: new focal deficit, crescendo events, fluctuating deficit, and amaurosis fugax with headache or jaw claudication in patients over 50 years.

Carotid duplex ultrasound is the first-line test

• Peak systolic velocity above 125 cm/s suggests 50% or greater stenosis.
• Peak systolic velocity above 230 cm/s with an end-diastolic velocity above 100 cm/s suggests 70% or greater stenosis.
• An internal carotid to common carotid velocity ratio above 4 supports severe stenosis.
• Near-occlusion shows low or variable velocities and needs confirmation with angiography.

Confirmation and planning

• CT angiography from the aortic arch to the circle of Willis gives stenosis severity, plaque morphology, calcification and arch anatomy. It also shows intracranial disease and tandem lesions.
• MR angiography is an alternative, though it can overestimate severity.
• Catheter angiography is reserved for discordant results because it has a 1% risk of neurological complications.

Brain and cardiac assessment

• MRI with diffusion sequences or CT of the brain to identify the infarct and silent lesions.
• ECG, prolonged rhythm monitoring (14 to 30 days) and echocardiography to exclude atrial fibrillation and a cardiac source. Stenosis and atrial fibrillation often coexist.
• Fasting lipids, HbA1c, creatinine and eGFR, CBC, and ESR with CRP when giant cell arteritis is possible.
• Assessment for coronary artery disease before surgery, since it is the main cause of perioperative death.

Medical therapy (all patients)

• Antiplatelet: aspirin 75 to 100 mg daily, or clopidogrel 75 mg daily if intolerant. After minor stroke (NIHSS 3 or less) or high-risk TIA, give aspirin 75 to 100 mg with clopidogrel 75 mg (after a 300 mg clopidogrel load) for 21 days, started within 24 hours, then a single agent.
• Statin: atorvastatin 40 to 80 mg or rosuvastatin 20 to 40 mg daily, targeting LDL cholesterol below 55 mg/dL (1.4 mmol/L). Add ezetimibe 10 mg if needed, then a PCSK9 inhibitor.
• Blood pressure: below 130/80 mmHg for stable disease. In symptomatic severe stenosis, avoid abrupt lowering in the acute phase. Ramipril 5 to 10 mg with amlodipine 5 to 10 mg is a typical combination.
• Diabetes: HbA1c around 7%, with a GLP-1 receptor agonist or SGLT2 inhibitor when indicated.
• Lifestyle: smoking cessation (varenicline 1 mg twice daily after titration for 12 weeks), Mediterranean diet, exercise and weight loss.
• Anticoagulation is added only when atrial fibrillation is present, and aspirin is then usually stopped unless there is a recent stent.

Revascularisation for symptomatic stenosis

• Stenosis 70 to 99%: carotid endarterectomy is recommended, ideally between 48 hours and 14 days of the last event, since benefit falls with delay. Benefit is greatest in men, patients over 75 years, and those operated on within 2 weeks.
• Stenosis 50 to 69%: endarterectomy is considered for selected patients, especially men with recent hemispheric events and low surgical risk.
• Stenosis under 50%: medical therapy alone.
• Near-occlusion with full collapse and occlusion: medical therapy, and surgery is rarely beneficial.
• Carotid artery stenting is an alternative in patients under about 70 years, and in those with hostile necks (previous neck surgery or radiotherapy), restenosis after endarterectomy, a high bifurcation, contralateral laryngeal nerve palsy, or significant cardiac or respiratory comorbidity. Procedural stroke risk rises with age above 70, and with plaque ulceration and symptomatic status.

Asymptomatic stenosis

• Medical therapy is the foundation.
• Intervention can be considered for stenosis of 60 to 99% with a life expectancy over 5 years, a perioperative stroke and death risk below 3% at the treating centre, and high-risk features (progression, silent infarcts, microemboli, impaired cerebrovascular reserve, large ulcerated plaque).

Periprocedural care for stenting

• Dual antiplatelet therapy with aspirin 75 to 325 mg and clopidogrel 75 mg started at least 3 days before, or a loading dose (aspirin 300 mg and clopidogrel 300 to 600 mg) given before the procedure, and continued for at least 4 weeks.
• Unfractionated heparin during the procedure to an activated clotting time of 250 to 300 seconds. An embolic protection device is used.
• Atropine 0.5 to 1 mg IV for bradycardia and hypotension from baroreceptor stimulation, with vasopressors for persistent hypotension.

Complications and monitoring

• Hyperperfusion syndrome (headache, seizures, focal deficit, haemorrhage) after revascularisation of severe stenosis: control systolic pressure below 140 mmHg using labetalol 10 to 20 mg IV or a nicotinamide-free infusion of nicardipine 5 to 15 mg/h.
• Restenosis in 5 to 10% within 2 years. Duplex follow-up at 1 month, 6 months and annually.
• Acute stroke with tandem lesions is treated with thrombolysis and thrombectomy per stroke pathways.