Carotid artery stenosis

• Carotid artery stenosis is atherosclerotic narrowing at the carotid bifurcation or the first part of the internal carotid artery. It causes 10–15% of cerebrovascular events.^[1]
• Most plaques are silent. Symptoms come from emboli: transient loss of vision in one eye, a transient ischaemic attack (TIA), or a stroke in the territory of the middle cerebral artery.
• Duplex ultrasound is the first test; the degree of narrowing is reported by the NASCET method, and CT or MR angiography clarifies uncertain or discordant results.
• Everyone needs intensive medical treatment. A fit patient with a recent symptom and a 70–99% stenosis should be offered carotid endarterectomy, ideally within 14 days. Moderate (50–69%) stenosis is a shared decision; mild stenosis is treated medically.
• Asymptomatic stenosis is managed selectively. Modern medical therapy has lowered the annual stroke risk, and new trial data are changing the balance between treatment and intervention.

By the end of this page you should be able to:

1. Define carotid stenosis, distinguish symptomatic from asymptomatic disease, and grade its severity.
2. Explain how an atherosclerotic plaque ruptures, embolises, and produces amaurosis fugax, TIA, or stroke.
3. Recognise the symptoms and signs, including the carotid bruit, and separate carotid disease from other causes of focal neurological symptoms.
4. Choose and interpret duplex ultrasound, CT angiography (CTA), and MR angiography (MRA), and calculate a NASCET percentage.
5. Build a best-medical-therapy plan with the correct antiplatelet, statin, blood-pressure, and glucose targets.
6. Decide between carotid endarterectomy (CEA) and carotid artery stenting (CAS), and explain the importance of timing.
7. Manage asymptomatic stenosis and discuss the uncertainty created by recent trials.
8. Adapt follow-up and treatment to older patients, women, and low-resource settings.

The common carotid artery divides into the external and internal carotid arteries in the mid-neck. The internal carotid artery supplies the retina through the ophthalmic artery and the anterior and middle cerebral hemispheres. A plaque at the bifurcation can therefore cause symptoms in the eye, the cortex, or both.

Figure 1. Carotid artery stenosis: atherosclerotic narrowing at the bifurcation. Source: Wikimedia Commons (CC BY-SA).

Carotid stenosis matters for two reasons. First, it is a direct cause of disabling stroke, and it is treatable. Second, it is a marker of atherosclerosis elsewhere: people with carotid plaque have more coronary and peripheral arterial disease, and they die more often from vascular causes.^[1][3] The consultation is therefore never only about the neck artery.

This page covers atherosclerotic stenosis of the extracranial internal carotid artery. It does not cover intracranial atherosclerosis, vertebral artery stenosis, or carotid dissection in detail, although these appear in the differential diagnosis.

The definition has two parts: the degree of narrowing and the clinical status. Both are needed, because a 70% stenosis in a patient with a recent TIA carries a very different risk from the same stenosis found by chance.

By severity. Most guidelines report the NASCET percentage and divide disease into mild (less than 50%), moderate (50–69%), severe (70–99%), and occlusion.^[2] The cut-offs are not natural boundaries; they are the thresholds at which trials showed that the balance of benefit and harm changed.

By symptoms. Symptomatic means an ipsilateral retinal or cerebral event within six months. Most guidelines use this window, although a few use three months and others use one year.^[1][2] Asymptomatic means no such event, even if the plaque looks dangerous.

By plaque behaviour. A stenosis can be tight but stable, or moderate but ulcerated and inflamed. Plaque vulnerability is now part of the ESVS 2023 approach, especially for asymptomatic disease.^[1]

Carotid atherosclerosis is common, and its clinical consequences are concentrated in older people and in low- and middle-income countries.

• Stroke burden. Atherosclerotic carotid stenosis accounts for 10–15% of all cerebrovascular events.^[1] About 15–20% of patients presenting with acute ischaemic stroke or TIA are thought to have carotid stenosis.^[4]
• Global prevalence. About 816 million people aged 30–79 years have some carotid plaque, and about 58 million have significant stenosis, roughly 1.5% of the population.^[1]
• Age and sex. The prevalence of stenosis greater than 50% ranges from 0.2% to 3.1% in women and from 0.1% to 3.1% in men, depending on age. For stenosis greater than 70%, the range is 0.1% to 1.7% in women and 0.1% to 2.3% in men.^[1] A separate estimate for significant stenosis in people aged 30–79 years is 1.8% in men and 1.2% in women.^[4]
• Other vascular disease. Carotid stenosis is present in 5–9% of patients with coronary artery disease and 14–19% of those with peripheral arterial disease.^[1]
• Inequality. About 87% of stroke deaths and 89% of disability-adjusted life years are concentrated in low- and middle-income countries.^[1]

The incidence of stroke from carotid stenosis has fallen over recent decades as statins, antiplatelet drugs, and blood-pressure control have improved. Contemporary cohorts suggest an annual risk of about 0.49% in asymptomatic patients on best medical treatment,^[3] and about 1% per year in general populations.^[1] This fall is the reason old trial results cannot be applied without adjustment.

Most carotid stenosis is atherosclerotic. The familiar risk factors cluster together: older age, hypertension, diabetes mellitus, dyslipidaemia, and smoking.^[1] These are the same factors that produce coronary and peripheral plaque, which is why the presence of carotid disease should prompt a search for atherosclerosis elsewhere.

A minority of narrowing is non-atherosclerotic.^[4] Dissection, fibromuscular dysplasia, radiation-induced arteriopathy, vasculitis, and carotid webs can all narrow the artery or cause emboli. They matter because the treatment is different: an inflammatory or dissecting artery is not managed by simply removing a plaque.

Plaque vulnerability is not the same as plaque size. Features associated with a higher risk of events include a large lipid-rich necrotic core, a thin or ruptured fibrous cap, intraplaque haemorrhage, ulceration, neovascularisation, and active inflammation.^[1][4] These features explain why two stenoses of the same percentage can behave very differently.

Atherosclerosis begins with endothelial injury and the entry of low-density lipoprotein (LDL) cholesterol into the arterial wall. Monocytes become macrophages, take up lipid, and form foam cells. A fatty streak develops, then a fibroatheroma with a lipid core and a fibrous cap. The artery remodels outwards at first, so the lumen can stay open while the wall thickens. Once remodelling is exhausted, the plaque encroaches on the lumen and the stenosis becomes visible on imaging.

The carotid bulb and bifurcation are favoured sites because flow there is disturbed, with low and oscillating shear stress. This is a local mechanical explanation for a systemic disease.^[1]

The dominant mechanism is artery-to-artery embolism.^[1] A plaque ruptures or erodes, exposing the lipid core and tissue factor. Platelets adhere, thrombin is generated, and a thrombus forms on the surface. Fragments of thrombus or plaque break off and travel with the blood.

The destination determines the symptom:

• Ophthalmic artery: transient monocular visual loss (amaurosis fugax), retinal artery occlusion, or chronic ocular ischaemia.
• Middle cerebral artery: contralateral weakness or numbness, aphasia if the dominant hemisphere is affected, neglect if the non-dominant hemisphere is affected, and hemianopia.
• Border-zone territories: a pattern of watershed infarction, especially when perfusion is marginal.

A haemodynamic mechanism is less common. A very tight stenosis or occlusion can reduce pressure and flow distally, and the brain may not compensate through the circle of Willis. This mechanism is more likely with bilateral disease, poor collateral flow, or a sudden fall in blood pressure.^[1] It explains why some patients become symptomatic with hypotension or anaemia rather than with a new embolus.

A recently symptomatic plaque is unstable. Recurrent ischaemic events occur in up to 24% of patients with symptomatic carotid stenosis within the first two weeks after the index event.^[4] This early clustering is the rationale for operating quickly rather than waiting for the plaque to "settle".

An atherosclerotic plaque is an eccentric, yellowish-white thickening of the intima. It may be smooth and fibrous, or irregular, ulcerated, and calcified. Fresh or organised thrombus can sit on the surface. In a tight stenosis, the residual lumen is a narrow slit or a small circle, and the post-stenotic artery may be reduced in calibre.

The typical plaque has a necrotic core containing cholesterol clefts, lipid-laden foam cells, and debris, covered by a fibrous cap of smooth-muscle cells and collagen. Inflammatory cells, especially macrophages and T lymphocytes, accumulate at the shoulders of the plaque. Neovessels grow into the base and predispose to intraplaque haemorrhage. Calcification may be patchy or extensive.

A stable plaque has a thick fibrous cap and a small lipid core. A vulnerable plaque has a thin cap, a large core, active inflammation, and often intraplaque haemorrhage. These features are visible on high-resolution MRI and are increasingly used to refine risk beyond the stenosis percentage.^[1][4]

Figure 4. Vulnerable carotid plaque and its cerebral consequences on CT and MRI. Source: Wikimedia Commons (CC BY-SA).

Most people with carotid stenosis have no symptoms. The stenosis is found when a bruit is heard, when duplex is performed before cardiac surgery, or when imaging is done for another reason. Asymptomatic does not mean harmless: it identifies a person at increased vascular risk, even if the annual stroke risk is now low on modern treatment.

Amaurosis fugax is sudden, painless loss of vision in one eye. Patients often describe a shade or curtain descending over the visual field. It lasts minutes and then resolves. The cause is a transient embolus to the ophthalmic or central retinal artery. On fundoscopy, a Hollenhorst plaque may be visible in a retinal arteriole, but the examination is often normal between attacks.

Amaurosis fugax is a TIA of the retina. It carries the same urgency as a hemispheric TIA and should trigger immediate vascular imaging.

A TIA is a focal neurological deficit caused by ischaemia that resolves, with no persistent disability. Typical carotid symptoms are contralateral face and arm weakness or numbness, aphasia, neglect, and homonymous hemianopia. Symptoms may be brief, and the patient may look completely normal by the time you see them. That is precisely why the history matters.

A stroke is a persistent deficit with infarction on imaging. It may be minor and non-disabling, or major with dense hemiplegia, aphasia, neglect, and reduced consciousness. The size and location of the infarct determine whether revascularisation is safe and when it should be done.

A bruit is a rushing sound heard over the carotid bifurcation, usually with the bell of the stethoscope while the patient holds their breath. It is generated by turbulent flow at the stenosis. It is a useful clue when present, but it is neither sensitive nor specific: a tight stenosis can be silent, and a bruit can come from a tortuous or hyperdynamic artery. Absence of a bruit never excludes carotid stenosis, and presence of a bruit does not prove that the plaque is the cause of the symptoms.

Examine the neck and heart as in cardiac physical examination. Look for:

• a carotid bruit, and any radiation to the ear or jaw;
• blood pressure in both arms, because subclavian disease can alter the reading;
• an irregular pulse or a murmur, which raises the possibility of a cardioembolic source;
• absent or reduced peripheral pulses, which suggest widespread atherosclerosis;
• fundoscopy for retinal emboli or ischaemia;
• a full neurological examination, including language, neglect, visual fields, and gait.

Focal neurological symptoms have many causes. The history and the pattern of symptoms usually narrow the list before imaging; the table shows the features that separate the main mimics.

Two practical points follow. First, a patient can have both carotid and cardiac sources; finding a stenosis does not exclude AF. Second, a normal carotid duplex does not explain a stroke, so continue the search.

Duplex ultrasound combines B-mode imaging of the plaque with Doppler measurement of blood velocity. It is the first-line test because it is available, cheap, radiation-free, and gives both anatomical and functional information.^[1] It shows the stenosis, the plaque texture, and the flow velocity.

Its weakness is operator dependence and variability between laboratories.^[1] A single velocity should not be used in isolation; use a multiparametric approach that combines peak systolic velocity (PSV), end-diastolic velocity (EDV), the internal carotid to common carotid PSV ratio, and the appearance of the plaque.^[1]

The NASCET and ECST methods are not interchangeable. A 50% NASCET lesion is about 70% by ECST, a 70% NASCET lesion is about 82% by ECST, and an 80% NASCET lesion is about 88% by ECST.^[1] Modern trials and guidelines report NASCET percentages, so always ask which method the reporting laboratory used.

Figure 2. The NASCET and ECST methods of grading carotid stenosis. Source: Wikimedia Commons (CC BY-SA).

Figure 3. Duplex ultrasound showing a right internal carotid artery with severe stenosis. Source: Wikimedia Commons (CC BY-SA).

CTA gives a high-resolution anatomical map of the aortic arch, the carotid bifurcation, and the intracranial vessels. It measures the residual lumen directly, shows calcification and ulceration, and helps plan access for stenting. A residual lumen of 1.3 mm or less usually corresponds to a NASCET stenosis of 70% or more, with reported sensitivity of 88.2%, specificity of 92.4%, and a negative predictive value of 98%.^[1]

CTA is useful when duplex is equivocal, when the stenosis is near occlusion, or when the patient has a pacemaker or other contraindication to MRI. It exposes the patient to radiation and iodinated contrast, so check renal function and allergy status.

MRA, especially contrast-enhanced and time-of-flight sequences, gives accuracy comparable to CTA and avoids ionising radiation. It can also image the vessel wall and plaque, showing intraplaque haemorrhage, a lipid-rich core, and fibrous cap integrity.^[1] These features are increasingly used to identify vulnerable plaques. MRA is less suitable for uncooperative patients, those with claustrophobia, and those with some implanted devices; gadolinium carries a small risk in severe renal impairment.

Digital subtraction angiography (DSA) was the historical reference standard, but it is invasive and carries a small risk of stroke. It is now used mainly when non-invasive tests are discordant, for complex anatomy, or for planning an endovascular procedure.^[4]

• Brain imaging. CT or MRI separates ischaemic stroke from haemorrhage and shows the size and pattern of infarction. The infarct size influences the safety and timing of revascularisation.
• Cardiac evaluation. ECG, telemetry, and echocardiography look for atrial fibrillation, left ventricular thrombus, and valve disease. Use ECG interpretation and consider atrial fibrillation even when a carotid plaque is present.
• Laboratory tests. Check glucose and HbA1c, lipids, renal function, full blood count, and coagulation. These guide medical treatment and procedural safety.
• Disability assessment. The modified Rankin Scale (mRS) and the extent of infarction help decide whether early revascularisation is safe.

There is no single diagnostic score. The decision rests on four questions:

1. Is the stenosis real and how severe is it? Use NASCET grading, with duplex first and CTA or MRA for confirmation.
2. Is it symptomatic? An ipsilateral retinal or cerebral event within six months defines symptomatic disease.^[1][2]
3. Is the plaque vulnerable? Silent ipsilateral infarction, progression of 20% or more, intraplaque haemorrhage, impaired cerebrovascular reserve, microembolic signals, a large hypoechoic area, or a predominantly echolucent plaque all raise the risk in asymptomatic disease.^[1]
4. Can the patient tolerate treatment? Life expectancy, comorbidity, anatomy, and the expected procedural risk determine whether intervention can help.

The ESVS 2023 guideline formalises plaque features into the decision for asymptomatic disease, whereas the AHA/ASA 2021 recommendation for asymptomatic disease rests mainly on the degree of stenosis.^[1][5][6] That difference is one source of the variation in practice.

Every patient needs intensive medical treatment, whether or not they undergo a procedure. Revascularisation is added only when the estimated benefit exceeds the procedural risk. The two levers are the same in every case: stabilise the plaque and, in selected patients, remove or bypass the tightest lesion.

Medical treatment targets the plaque, the blood pressure, and the glucose. It also treats the rest of the vascular tree.

Antiplatelet choice is pragmatic. Aspirin is cheap and widely available; clopidogrel is used when aspirin fails or cannot be tolerated. Dual antiplatelet therapy is not a long-term strategy for stable carotid disease because it increases bleeding. It is used around stenting and, in some protocols, while a recently symptomatic patient waits for surgery.^[4]

Statins do more than lower LDL. They stabilise the plaque, reduce inflammation, and lower the risk of recurrent events. A patient who cannot tolerate a statin should be discussed with a lipid specialist rather than simply left untreated.

Blood-pressure control needs judgement. Very aggressive lowering can cause symptoms in a patient with bilateral severe stenosis and poor collateral flow, but uncontrolled hypertension accelerates plaque. Start treatment, monitor for postural and neurological symptoms, and individualise the target.

CEA removes the plaque through an incision in the neck. The artery is opened, the plaque is dissected free, and the arteriotomy is closed directly or with a patch. It is usually performed under general or local anaesthesia, with a shunt used selectively when cerebral perfusion is inadequate.

The indications are best remembered by the trial evidence:

• Symptomatic 70–99% stenosis. CEA reduces the risk of ipsilateral stroke when the perioperative stroke and death rate is low. The AHA/ASA 2021 guideline recommends CEA if the estimated perioperative morbidity and mortality is below 6% (Class I, Level A).^[4][6] In NASCET, the 2-year risk of ipsilateral stroke fell from 26% to 9%.^[4]
• Symptomatic 50–69% stenosis. The benefit is modest. In NASCET, the 5-year stroke risk fell from 22.2% to 15.7%, with an absolute risk reduction of 4.6% and a number needed to treat of 22 in the pooled analysis.^[4] Selection matters: age, sex, plaque appearance, comorbidity, and the patient's own values all influence the decision.
• Symptomatic less than 50% stenosis. Revascularisation is not routinely recommended.^[4] The ESVS 2023 guideline allows consideration of CEA in selected patients whose symptoms persist despite medical therapy, after multidisciplinary review.^[2]
• Asymptomatic stenosis. Discussed separately below.

CAS widens the stenosis with a balloon and a stent, usually through the femoral artery. An embolic protection device is used when the anatomy allows. The patient needs dual antiplatelet therapy before and for at least four weeks after the procedure.^[4]

CAS is an alternative to CEA in patients with cardiac comorbidity, unfavourable neck anatomy, previous neck irradiation, restenosis after CEA, or a high surgical risk.^[2][4] It avoids a neck incision and cranial nerve injury, but it carries a higher periprocedural stroke risk than CEA in many trials. EVA-3S reported a procedural stroke or death rate of 9.6% with CAS versus 3.9% with CEA; ICSS reported 7.4% versus 3.4%.^[4] CREST found no significant difference in the primary composite outcome (CAS 7.2% versus CEA 6.8%), but CAS had more periprocedural strokes and CEA had more myocardial infarctions.^[4]

Age is important. CAS is less favourable in older patients, especially those over 70, because of aortic arch atherosclerosis, tortuosity, and calcification. The European Stroke Organisation advises against stenting above 70 years unless surgery is contraindicated.^[4] Where available, transcarotid artery revascularisation (TCAR) with flow reversal is another option, but its evidence base is smaller and it is not a substitute for CEA in every patient.^[1]

Time is the most modifiable part of the decision. The benefit of CEA is greatest when it is performed soon after the index event. In a pooled analysis of NASCET and ECST, the number needed to treat to prevent one ipsilateral stroke at five years rose from about 5 when surgery was done within two weeks to 125 when it was delayed beyond 12 weeks.^[1]

The ESVS 2023 guideline recommends revascularisation within 14 days for appropriate patients (Class I, Level A).^[1][5] The AHA/ASA 2021 guideline recommends performing the procedure between 48 hours and two weeks of the index event (Class IIa, Level B).^[4][6] The small difference reflects uncertainty about the first 48 hours, when some data suggest a higher procedural risk. For severe (70–99%) stenosis, benefit may persist for up to 12 weeks, but earlier is better.^[4]

Do not operate on a patient with a large established infarct or a disabling deficit. Revascularisation is generally avoided when the mRS is 3 or more, the infarct exceeds 30% of the ipsilateral middle cerebral artery territory, or consciousness is reduced, because of the risk of haemorrhage into the infarcted brain. These patients can be reassessed after neurological recovery.^[1][4]

Asymptomatic disease is the hardest decision, because the absolute benefit is small and medical therapy has improved.

The historical trials showed a benefit. In ACAS, CEA reduced the 5-year risk of ipsilateral stroke or periprocedural stroke or death from 11.0% to 5.1%.^[1] ACST-1 showed an absolute benefit of 4.6% at 10 years.^[1] Those trials used medical therapy that would now be considered inadequate.

Contemporary medical treatment has changed the baseline. A meta-analysis of recent studies found an annual ipsilateral stroke risk of about 0.49% in asymptomatic patients on best medical treatment.^[3] With such a low risk, the procedural risk can easily outweigh the benefit.

Guidelines still offer intervention to selected patients:

• AHA/ASA 2021. CEA may be considered for asymptomatic stenosis greater than 70% when the risk of perioperative stroke, myocardial infarction, and death is low (Class IIa, Level C).^[4][6] Annual duplex surveillance is reasonable for known stenosis greater than 50% (Class IIa, Level C).^[4]
• ESVS 2023. For average-risk patients with 60–99% asymptomatic stenosis, CEA may be considered (Class IIa, Level B), and CAS may be considered (Class IIb, Level B), when high-risk plaque features are present and the 30-day procedural stroke or death rate is below 3% with a life expectancy greater than five years.^[1][5]

The 2025 CREST-2 trial has made this area more uncertain, not less. In the stent trial, adding CAS to optimal medical therapy reduced the 4-year composite of periprocedural stroke or death or later ipsilateral stroke from 6.0% to 2.8% (p = 0.02; number needed to treat 31). In the parallel endarterectomy trial, the reduction from 5.3% to 3.7% did not reach statistical significance (p = 0.24).^[1] The ECST-2 trial found no benefit of revascularisation over medical therapy at two years in asymptomatic or low-to-intermediate-risk symptomatic patients.^[1]

How should a clinician use these data? First, CREST-2 enrolled patients with high-grade asymptomatic stenosis and achieved excellent medical control; its results apply to that population, not to every plaque. Second, the benefit in the stent trial was driven by fewer late ipsilateral strokes, despite more periprocedural events. Third, the endarterectomy result did not show significant benefit, which argues for a careful, shared decision rather than routine surgery. Guidelines written before these trials may lag behind the evidence. The reasonable approach is to treat everyone medically, discuss the uncertainty, and reserve intervention for patients with a long life expectancy, low procedural risk, and features suggesting a vulnerable plaque.

The main risk of CEA or CAS is stroke or death around the procedure. The acceptable ceiling depends on the patient and the guideline: the AHA/ASA uses below 6% for symptomatic disease, and the ESVS uses below 3% for asymptomatic disease.^[4][1]

Other harms differ by procedure:

• CEA: myocardial infarction, cranial nerve injury (especially the hypoglossal, vagus, and glossopharyngeal nerves), neck haematoma, wound infection, and restenosis.
• CAS: access-site haematoma, contrast nephropathy, stent restenosis, and a higher periprocedural stroke rate in many trials.^[4]
• Both: bleeding, infection, and the consequences of a procedure that was not needed.

Restenosis is more frequent after stenting than after endarterectomy in some trials. In SPACE, restenosis was significantly more frequent after CAS than after CEA (10.4% versus 4.6%).^[4] Surveillance should follow the local protocol, and a rising velocity or new symptoms should prompt repeat imaging.

Follow-up has three aims: control risk factors, detect restenosis or progression, and recognise recurrent symptoms.

• Clinical review. Check blood pressure, lipids, glucose, smoking status, medication adherence, and any new neurological symptoms.
• Imaging after revascularisation. The AHA/ASA 2021 guideline does not recommend routine long-term duplex surveillance after symptomatic revascularisation (Class III, Level B), because the yield is low.^[4] Practice varies, and many centres perform a baseline scan and then interval scans. Repeat imaging is indicated for new symptoms or a concerning examination.
• Known asymptomatic stenosis. Annual duplex is reasonable when the stenosis is greater than 50% (Class IIa, Level C).^[4] Some protocols use six-monthly scans initially and then annual scans.^[4]
• Secondary prevention. Continue antiplatelet therapy, a statin, blood-pressure control, and glucose control indefinitely. Stopping treatment after a successful operation is a common and avoidable error.

Of the disease:

• TIA and ischaemic stroke, including disabling stroke.
• Retinal artery occlusion and chronic ocular ischaemic syndrome.
• Silent infarction and cognitive decline, especially with bilateral disease.
• Myocardial infarction and vascular death, because carotid disease marks systemic atherosclerosis.

Of treatment:

• Periprocedural stroke or death.
• Myocardial infarction, especially after CEA.
• Cranial nerve injury, neck haematoma, and wound infection after CEA.
• Access-site complications and contrast nephropathy after CAS.
• Restenosis, which is more common after CAS in some trials.
• Bleeding from antiplatelet therapy.

The prognosis depends on symptoms, stenosis severity, plaque behaviour, and treatment.

A recently symptomatic severe stenosis is dangerous. Without revascularisation, the early recurrence risk is high, and the 2-year risk of ipsilateral stroke in NASCET was 26%.^[4] CEA reduced that risk to 9% when performed with a low complication rate.^[4] For moderate stenosis, the benefit is smaller: a 5-year risk reduction from 22.2% to 15.7%, with a number needed to treat of 22.^[4]

Asymptomatic stenosis has a much lower annual risk on modern treatment, around 0.49% in a recent meta-analysis.^[3] That is why the decision to operate is driven by plaque features, life expectancy, and procedural risk rather than by the percentage alone.

After a TIA or stroke, the first year carries the highest risk. More recent registries suggest a risk of about 6% in the first year after a carotid-related TIA, compared with the much higher figures seen in older studies.^[1] The decline reflects better medical treatment and earlier revascularisation.

Primary prevention is the same as for any atherosclerotic disease: do not smoke, control blood pressure, treat dyslipidaemia and diabetes, stay active, and maintain a healthy weight.

Screening the general population for asymptomatic carotid stenosis is not recommended. The AHA/ASA 2021 guideline explicitly advises against screening low-risk populations (Class III, Level C).^[4][6] The yield is low, and the harms of unnecessary intervention are real. Case-finding is more reasonable in patients with known coronary or peripheral arterial disease, in whom the prevalence of carotid stenosis is higher, and in anyone with a carotid bruit or a compatible neurological symptom.^[1]

Secondary prevention after a TIA or stroke is the core of this topic: antiplatelet therapy, a statin, blood-pressure control, glucose control, smoking cessation, and timely revascularisation when indicated.

Older adults. Age increases both the risk of stroke and the risk of procedural complications. CAS is less favourable over 70, and CEA is generally preferred when surgery is feasible.^[4] Frailty, life expectancy, and the patient's own goals matter more than chronological age alone.

Women. Women have a lower prevalence of significant stenosis than men, and the benefit of CEA for moderate symptomatic stenosis is less clear. In pooled trial data, the number needed to treat for moderate stenosis is 36 in women and 9 in men.^[2] The AHA/ASA 2021 guideline suggests that there is no benefit of CEA in women with moderate stenosis, whereas the European Stroke Organisation concludes that the benefit does not differ significantly by sex.^[2] This is a genuine disagreement, not a failure to read the guideline. Discuss it explicitly with the patient.

Patients with atrial fibrillation. AF and carotid stenosis often coexist, and finding one does not exclude the other. If the infarct pattern is embolic in several territories, or the plaque is only moderate, the AF may be the more likely cause; if the plaque is severe and ulcerated in the symptomatic territory, it may be the source even when AF is present. The case needs joint stroke, cardiology, and vascular input, because the choice of treatment for one condition can affect the other.

Patients with bilateral disease or occlusion. A tight stenosis contralateral to an occlusion, or bilateral severe disease, reduces cerebral reserve. Correct anaemia, avoid unnecessary hypotension, and involve a vascular team early.

Carotid stenosis is a global problem, but the resources to treat it are not evenly distributed. Most stroke deaths occur in low- and middle-income countries.^[1] A practical approach:

• Start medical treatment immediately. Aspirin, a statin, and blood-pressure control are cheap, effective, and do not depend on vascular imaging. Do not wait for a duplex result to begin them.
• Use duplex if available. It is the most practical first test. If it is not available, CTA or MRA can confirm the diagnosis when the patient can access them.
• Do not guess the percentage from a bruit. A bruit cannot grade stenosis. If no imaging is available, treat the patient as having symptomatic atherosclerotic disease, optimise medical therapy, and refer for imaging when possible.
• Concentrate surgery. CEA should be performed in centres with audited outcomes and a stroke/death rate below the accepted ceiling. A low-volume surgeon without a team should not start carotid surgery for a single case.
• Stenting needs experience and support. CAS requires antiplatelet therapy, embolic protection where available, and a team that can manage complications. It is not the low-resource alternative to CEA unless the centre has the infrastructure and outcomes to support it.
• Refer early. A patient with a recent TIA or minor stroke and a severe stenosis should be referred to a stroke or vascular centre as soon as possible, because the benefit of revascularisation falls with delay.

• Stroke medicine and transient ischaemic attack
• Atrial fibrillation and flutter
• ECG interpretation
• Cardiac physical examination
• Heart failure
• Peripheral arterial disease and dyslipidaemia