Carotid Artery Stenosis

Asymptomatic carotid stenosis

• Defined as a narrowing of 50% or more at the origin of the proximal internal carotid artery in patients with no ipsilateral neurological symptoms (stroke, TIA, or amaurosis fugax) within the last six months.
  
  
• Some studies apply a threshold of 60% or greater, while stenosis of 70% or more is regarded as severe.
  
  
• Plaques may remain stable or progress, but in some cases rupture and embolisation occur, leading to TIA, stroke, or transient monocular blindness.
  
  

In clinical classification

• Mild stenosis: <50% narrowing
• Moderate stenosis: 50–69% narrowing
• Severe stenosis: ≥70% narrowing (haemodynamically significant or high-grade)
• Near-occlusion: >95% narrowing, often with collapse of the internal carotid lumen (“string sign” or pseudo-occlusion)

Two categories are recognised

• Symptomatic disease: associated with recent ipsilateral neurological events (stroke, TIA, or amaurosis fugax) within six months.
• Asymptomatic disease: absence of such neurological symptoms within that timeframe.

Atherosclerosis as the primary cause

• Carotid artery stenosis most commonly results from systemic atherosclerotic disease.
• Atherosclerotic plaque formation is promoted by haemodynamic stresses at the carotid bifurcation, where turbulent and oscillating blood flow encourages lipid deposition and plaque growth.
• Risk factors include advanced age, male sex, smoking, hypertension, hyperlipidaemia, diabetes, and genetic predispositions.
• Plaques may remain stable but can also rupture, leading to embolisation of thrombus or cholesterol-laden debris into intracranial or retinal arteries, causing transient ischaemic attack (TIA), ischaemic stroke, or transient monocular blindness (amaurosis fugax).
• Less commonly, luminal narrowing leads to cerebral hypoperfusion, particularly in the presence of poor collateral circulation.

Fibromuscular dysplasia (FMD)

• A significant non-atherosclerotic cause, particularly in young females.
• FMD is a non-inflammatory condition affecting medium-sized arteries, especially the renal and carotid arteries.
• Typically involves the mid-to-distal internal carotid artery and may extend into the intracranial circulation.
• Associated with aneurysm formation and dissection risk.
• The condition predisposes to stenosis independent of traditional vascular risk factors.

Other less common causes

Radiation arteritis

• Accelerated atherosclerosis and fibrosis following neck irradiation.

Spontaneous or traumatic dissection

• Intimal tears leading to intramural haematoma and stenosis.

Restenosis

• Recurrent narrowing after previous carotid endarterectomy or stenting, often due to neointimal hyperplasia.

Congenital and structural abnormalities

• Examples include carotid webs, considered a variant of fibromuscular dysplasia.

Sites of plaque formation

• Atherosclerotic plaques preferentially form at arterial branch points and curved segments.
• The outer wall of the carotid bifurcation and bulb is particularly susceptible because of disturbed flow patterns, turbulent haemodynamics, and oscillatory shear stress.
• These haemodynamic forces promote intima-media thickening and progression of atherosclerosis.

Plaque development and instability

• Plaques begin as fatty streaks which evolve into lipid-rich cores.
• Fibrous tissue accumulation creates a fibroatheroma with a fibrous cap.
• Unstable plaques exhibit a large lipid core, intraplaque haemorrhage, cap thinning, rupture, ulceration, and superimposed thrombosis.
• These features are strongly associated with atheroembolic events and are typically found in plaques from symptomatic patients.
• Stable plaques, in contrast, often contain small, deep lipid cores and thick fibrous caps, more frequently seen in asymptomatic disease.

Mechanisms of cerebral ischaemia

Embolisation

• The most common mechanism of ischaemia in carotid stenosis.
• Involves release of thrombus or cholesterol debris, leading to TIAs, retinal ischaemia, or cerebral infarction.

Haemodynamic compromise

• Less common but occurs in cases of severe stenosis with inadequate collateral circulation.
• Systemic factors such as hypotension, orthostatic changes, low cardiac output, or volume depletion may precipitate ischaemic symptoms.

Local thrombosis

• Disruption of the fibrous cap exposes atherosclerotic debris to circulating blood, resulting in thrombus formation.
• Local thrombosis can occlude the artery completely, compounding the risk of stroke.

Plaque characteristics linked to stroke risk

• Echolucent or heterogeneous plaques contain high lipid and haemorrhagic content, making them prone to ulceration and rupture.
• Symptomatic carotid stenosis is associated with echolucent plaques in approximately 70% of cases, compared with 20–30% in asymptomatic disease.
• Echolucent plaques confer a two- to four-fold higher risk of cerebral infarction than echogenic plaques.

Progression to occlusion

• Total internal carotid artery occlusion often arises from thrombosis superimposed on chronic stenosis.
• Cardioembolic events (e.g., atrial fibrillation, valvular disease) or carotid dissection may also cause occlusion.
• Chronic occlusions may remain asymptomatic but later manifest symptoms via embolic events from collaterals or through haemodynamic insufficiency in the setting of contralateral carotid disease or systemic hypotension.

Role of imaging

• Duplex ultrasound, computed tomography angiography (CTA), and magnetic resonance angiography (MRA) permit assessment of plaque morphology, echolucency, ulceration, and haemorrhage.
• These imaging markers help stratify risk and identify lesions prone to rupture, refining patient selection for intervention.

Prevalence and age-related trends

• The estimated prevalence of severe asymptomatic carotid stenosis (≥70%) ranges from 0.1% to 3.1%, with prevalence increasing with advancing age.
• A global meta-analysis estimated the prevalence of carotid stenosis among individuals aged 30–79 years in 2020 to be 1.5%. The prevalence of increased carotid intima-media thickness and carotid plaque was considerably higher, at 27.6% and 21.1%, respectively.
• Compared with 2000, the prevalence of carotid stenosis rose by nearly 60%, with the most significant increase seen in those aged 50–59 years.
• Asymptomatic carotid stenosis >50% is estimated to occur in 7.5% of men and 5% of women, while among those aged over 70 years, the prevalence is around 12% in men and 7% in women.
• In the United States, high-grade asymptomatic carotid stenosis (≥70%) has been reported in 1.0% of men and 0.6% of women aged ≥75 years.

Contribution to stroke

• Between 10% and 20% of ischaemic strokes are attributed to carotid artery stenosis, most often due to embolic events from atherosclerotic plaques.
• Carotid-related strokes are disproportionately disabling or fatal, reflecting the size and vascular distribution affected.
• The incidence of carotid stenosis among patients presenting with ischaemic stroke is estimated at 13 per 100,000 annually.

Regional and population differences

• In the Northern Manhattan Study, stroke attributable to carotid stenosis occurred at rates of 17 per 100,000 in Black individuals, 9 per 100,000 in Hispanic individuals, and 5 per 100,000 in White individuals.
• In Germany, pooled data from stroke centres found that 20.9% of ischaemic strokes were related to carotid stenosis.
• A London-based study reported carotid stenosis as the cause of ischaemic stroke or TIA in 7.9% of hospitalised patients, with an additional 11% having asymptomatic carotid stenosis.
• Although Black and Hispanic populations have a higher overall stroke risk, they exhibit lower rates of severe carotid stenosis (>70%) compared with White individuals. Conversely, Native American populations show a higher rate of severe stenosis.
• Male sex is consistently associated with a higher prevalence of carotid stenosis compared to females across studies.

Stroke burden

• Stroke is one of the leading causes of death and long-term disability worldwide.
• In the United States, approximately 795,000 strokes occur annually, including 610,000 first events and 185,000 recurrences.
• In 2021, there were 162,890 stroke-related deaths in the US.
• In the United Kingdom, over 100,000 strokes occur each year.
• The global population-attributable stroke risk from severe asymptomatic carotid stenosis (≥70%) is estimated to be 0.7%.

Vascular risk factors

• Advanced age: risk rises significantly after 55 years, with stroke incidence doubling with each additional decade.
• Male sex: higher prevalence compared with females.
• Smoking: an independent predictor of carotid stenosis, increasing the risk of atheroembolic stroke by up to 50%.
• Hypertension: high systolic blood pressure (>160/95 mmHg) triples the risk of stroke in men and nearly triples it in women compared with normotensive individuals.
• Hyperlipidaemia: elevated cholesterol is a strong independent risk factor for carotid atherosclerosis.
• Diabetes mellitus: contributes to both the development and progression of carotid disease.
• Family history of vascular disease: reflects underlying genetic predisposition.
• Obesity and sedentary lifestyle: accelerate atherosclerosis and are commonly seen in affected patients.
• Pre-existing cardiovascular or peripheral vascular disease: patients with coronary artery disease or peripheral arterial disease have an approximate 20% prevalence of high-grade carotid stenosis.

Neurological history

Transient ischaemic attack (TIA)

• Stereotypical, temporary loss of motor, sensory, or visual function.
• Usually lasts less than 60 minutes but may persist for up to 24 hours.
• High-grade stenoses may produce multiple very brief TIAs, often termed “crescendo TIAs”.

Stroke

• Focal neurological deficits lasting more than 24 hours.
• Presents with sudden visual field loss, weakness, sensory changes, dysarthria, or aphasia.
• Carotid stenosis predisposes particularly to watershed infarcts in cerebral border zones.

Amaurosis fugax

• Transient, ipsilateral monocular blindness caused by embolisation to the ophthalmic or retinal arteries.
• May present as intermittent retinal blindness on exposure to bright light.
• Rarely, complete blindness may occur due to ischaemic optic neuropathy.

Stroke-in-evolution or cerebral infarction

• Progressive neurological deficits resulting from ongoing embolic or thrombotic occlusion.

Presentation pattern

• Many individuals remain asymptomatic, with carotid stenosis often detected incidentally in the context of other atherosclerotic disease.
• A history of TIA is found in at least half of patients who later present with stroke attributable to carotid disease.
• Asymptomatic retinal artery emboli may be identified on fundoscopy, often during diabetic retinopathy screening, and commonly arise from an ipsilateral carotid lesion.

Asymptomatic findings

• Many patients with carotid stenosis have no clinical signs.
• Suspicion is often raised in those with established atherosclerotic risk factors such as peripheral arterial disease, coronary artery disease, hypertension, diabetes, or active smoking.

Cervical bruit

• A bruit on auscultation of the carotid arteries may suggest turbulent flow from underlying stenosis.
• It is not a sensitive or specific finding: associated with carotid stenosis in ~47% of patients, but high-grade stenosis is present in fewer than 2% of individuals with a bruit.
• Its detection usually prompts further vascular evaluation.

Focal neurological deficit lasting >24 hours (Stroke)

• Ischaemic stroke may present with sudden onset of visual loss or visual field deficit, weakness, aphasia, altered sensation, or dysarthria.
• Carotid stenosis predisposes particularly to watershed infarction in border-zone territories, where cerebral perfusion is most vulnerable.

Focal neurological deficit lasting <24 hours (Transient ischaemic attack – TIA)

• Temporary neurological deficits, with full return to baseline after resolution.
• Deficits generally last less than 60 minutes, though may persist up to 24 hours.
• High-grade stenosis can cause multiple very brief recurrent TIAs (“crescendo TIAs”).

Transient visual symptoms

• Transient monocular blindness (amaurosis fugax) due to emboli from the ipsilateral carotid.
• Homonymous hemianopia from embolic events affecting optic radiation.
• Intermittent retinal blindness, sometimes triggered by bright light exposure.
• Rarely, complete blindness due to ischaemic optic neuropathy.
• Neovascularisation of the iris may occur from ophthalmic artery ischaemia.
• Retinal artery emboli may be noted incidentally during fundoscopy, particularly in diabetic eye screening.

Additional systemic and neurological findings

• Blood pressure measurement in both arms and orthostatic readings may reveal haemodynamic compromise, especially in older patients.
• Neurological assessment should include cranial nerves, motor and sensory systems, and visual field testing.
• Cardiac examination may reveal arrhythmias (e.g., atrial fibrillation) or murmurs suggesting a cardioembolic source.
• Peripheral examination may show features of chronic vascular insufficiency such as cool extremities, loss of distal pulses, skin discolouration, or hair loss.

Laboratory studies

Complete blood count (CBC)

• Evaluates for anaemia or polycythaemia, which may influence cerebral perfusion and surgical risk.

Electrolytes, urea, and creatinine

• Establishes baseline renal function, crucial prior to contrast-enhanced imaging or operative procedures.

Lipid profile

• Detects hyperlipidaemia, an important modifiable cardiovascular risk factor.

Coagulation studies (PT, aPTT)

• Required preoperatively, particularly since heparin is administered during carotid endarterectomy (CEA).

Ultrasonography

Carotid duplex ultrasonography

• First-line, non-invasive diagnostic tool for suspected stenosis.
• Provides haemodynamic data, degree of stenosis, plaque characteristics, and contralateral vessel status.
• Sensitivity for ≥70% stenosis ~99%, specificity 86%, accuracy 95%.
• Quantification commonly based on NASCET criteria.
• Echolucent or ulcerated plaques indicate higher embolic risk.
• Three-dimensional duplex can measure plaque volume and texture, predictive of future vascular events.

Computed Tomography Angiography (CTA)

CTA of head, neck, and chest

• Offers detailed anatomical assessment of the carotid arteries, bifurcation, and aortic arch.
• Indicated when duplex is inconclusive or shows moderate stenosis (50–69%).
• Sensitivity ~85%, specificity ~93% for ≥70% stenosis.
• Determines lesion length, plaque burden, and suitability for stenting versus surgery.
• Limitations: radiation exposure and risk of contrast nephropathy.

Magnetic Resonance Angiography (MRA)

MRA of head, neck, and chest

• Alternative to CTA in patients with renal insufficiency (avoiding iodinated contrast) or when radiation avoidance is preferable.
• Sensitivity ~88%, specificity ~84% for ≥70% stenosis, though it often overestimates severity.
• Provides information on plaque composition, such as lipid core or intraplaque haemorrhage.
• Contraindications: ferromagnetic implants; gadolinium use limited in advanced renal dysfunction.

Digital Subtraction Angiography (DSA)

Arteriography

• Historic gold standard; used in landmark trials including NASCET.
• Precisely quantifies stenosis but carries a 1–2% risk of procedure-related stroke.
• Now reserved for cases where intervention is planned or non-invasive imaging is inconclusive.

Brain imaging

CT brain

• Performed in symptomatic patients to exclude haemorrhage or stroke mimics.
• Identifies infarction through hypo-attenuation, sulcal effacement, and grey–white matter loss.
• Useful when MRI is unavailable or contraindicated.

MRI brain

• More sensitive than CT for acute ischaemia; diffusion-weighted imaging detects infarcts within minutes.
• Identifies both acute and chronic infarction and prior haemorrhage.
• Susceptibility-weighted sequences highlight microhaemorrhages.

Ancillary cardiac investigations

Electrocardiogram (ECG)

• Detects arrhythmias, especially atrial fibrillation, as well as prior myocardial infarction or ischaemia.

Echocardiography

• Identifies potential cardioembolic sources, such as valvular disease or patent foramen ovale.
• Differentiates carotid-related from cardiac-related embolic disease.

Risk stratification with imaging

Transcranial Doppler

• Detects microembolic signals in intracranial arteries, predictive of stroke risk.

Ultrasound plaque echolucency

• Echolucent plaques suggest lipid-rich and unstable morphology prone to embolisation.

CT/MRI brain (silent infarcts)

• Presence of silent infarcts increases long-term risk of symptomatic stroke.

MRI plaque imaging

• Identifies intraplaque haemorrhage, ulceration, and fibrous cap thinning—markers of high embolic potential.

Cerebrovascular reserve studies

• Reduced cerebrovascular reserve indicates impaired compensatory flow and higher risk of ischaemic events.

Carotid dissection or subintimal haematoma

• More common in patients under 50 years of age.
• Often linked to trauma, vigorous exercise, or sudden neck movement (e.g., motor vehicle accident, roller coaster ride).
• Symptoms may include neck pain, Horner’s syndrome, or history of connective tissue disease.
• Duplex ultrasound, CT angiography, or MR angiography can show an intimal flap or crescent-shaped intramural haematoma with thrombus.

Thrombotic occlusion of the carotid artery

• Usually follows plaque rupture with superimposed thrombosis.
• Clinical features may be indistinguishable from high-grade stenosis.
• Involvement of the common carotid may result in absent carotid pulsation.
• Imaging with duplex ultrasonography, CTA, or MRA demonstrates a thrombosed occluded artery.

Fibromuscular dysplasia (FMD)

• Typically affects women under 50 years of age and is more frequent in those of Asian ancestry.
• May be associated with other occlusive arterial disease (e.g., subclavian artery involvement with absent radial pulses).
• Duplex ultrasound reveals smooth, non-calcified stenoses.
• CTA or MRA shows the characteristic “string-of-beads” appearance in the distal carotid artery.

Carotid web

• Considered a variant of fibromuscular dysplasia.
• Rare, but more common in young patients presenting with cryptogenic stroke.
• Seen as a shelf-like projection into the lumen on CTA, typically at the posterior carotid bulb.

Other differentials

• Valvular heart disease and atrial fibrillation (alternative embolic sources).
• Mural thrombosis not due to atherosclerosis.
• Vasculitides such as Takayasu arteritis and giant cell arteritis.
• Complicated migraine, which may mimic transient neurological events.

Deterrence and Patient Education

Lifestyle modification

• Aim for body mass index <25 kg/m².
• Blood pressure control with a target <120/80 mmHg.
• Total cholesterol <200 mg/dL.
• Fasting blood glucose <100 mg/dL.
• Absolute cessation of smoking.

Medical therapy

• Statins to reduce LDL cholesterol and stabilise plaque.
• Low-dose aspirin for antiplatelet therapy in secondary prevention.

Patient counselling

• Education on symptoms of stroke and TIA (e.g., sudden weakness, speech disturbance, facial droop, or transient visual loss).
• Clear instructions to seek urgent medical attention if neurological symptoms develop.

Risk communication

• Patients should understand that even asymptomatic carotid stenosis indicates systemic atherosclerosis and elevated cardiovascular risk.
• Adherence to medical therapy and routine follow-up is essential to reduce long-term morbidity and mortality.

General Approach

• Management aims to prevent stroke using a combination of intensive medical therapy and, in selected patients, revascularisation.
• Decisions are stratified by clinical presentation (asymptomatic vs symptomatic), degree of stenosis (NASCET criteria), patient-specific risk, life expectancy, and local operator outcomes.
• Contemporary trials comparing revascularisation versus intensive medical therapy are ongoing and may further refine indications.

Principles and current trial landscape

• Several randomised controlled trials over the past three decades underpin current recommendations for pharmacological therapy, carotid endarterectomy (CEA), and carotid artery stenting (CAS).
• Ongoing/recent trials (e.g., CREST-2, ACTRIS, ECST-2) compare carotid intervention with intensive medical management in asymptomatic disease and may alter thresholds and selection.

Asymptomatic carotid artery stenosis

• Intensive medical therapy is first-line. Most patients derive limited absolute benefit from revascularisation in the modern era of risk-factor control.
• Selection for intervention considers stenosis severity, perioperative risk (stroke/MI/death ≤3%), life expectancy (>5 years), and high-risk plaque/physiology (e.g., microembolic signals on transcranial Doppler, plaque echolucency or ulceration, silent embolic infarcts, intraplaque haemorrhage, progression of stenosis, reduced cerebrovascular reserve).
• Guideline examples:
  • CEA can be considered for ≥60–99% asymptomatic stenosis when perioperative risk is low and high-risk features are present.
  • CAS is a reasonable alternative when surgical risk is high or anatomy favours stenting.
• Large plaque ulceration generally accompanies high-grade stenosis and supports CEA; isolated large ulcers with <50% stenosis remain a grey area and warrant multi-disciplinary discussion.

Antiplatelet therapy

• Initiate at diagnosis and continue indefinitely.
• Aspirin preferred; clopidogrel if aspirin-intolerant; dual antiplatelet therapy (DAPT) for at least 4 weeks after stenting, then single-agent long-term.
• Avoid adding antiplatelet therapy to therapeutic anticoagulation unless a stent is present or a compelling indication exists.

Lipid-lowering therapy

• High-intensity statin for all patients; add ezetimibe if targets unmet; consider PCSK9 inhibitors in statin-intolerant patients or if LDL targets remain above goal despite maximal therapy.

Risk factor modification

• Treat smoking, hypercholesterolaemia, diabetes, and hypertension per guidelines.
• Lifestyle modification (healthy diet, weight optimisation, regular exercise) for all patients.

Symptomatic carotid artery stenosis

• CEA is recommended for ipsilateral ≥50% stenosis when neurological symptoms have stabilised; early revascularisation (within 2 weeks) reduces recurrent stroke.
• CAS has a higher periprocedural stroke risk in older patients; it can be considered in younger patients (≤65 years) in experienced centres or when surgical risk is high (e.g., hostile neck, prior radiation, restenosis).
• Start antiplatelet therapy after intracranial haemorrhage has been excluded and continue indefinitely.
• High-intensity statin with LDL-cholesterol target <1.8 mmol/L (<70 mg/dL); escalate with ezetimibe/PCSK9 as needed.

Concurrent carotid and coronary artery disease

• Combined CEA and coronary bypass carries ~9–12% perioperative stroke/MI/death and is usually reserved for patients with symptomatic carotid stenosis plus critical coronary disease.
• Staged or synchronous approaches depend on symptom status, bilateral disease, and centre expertise; routine coronary screening before CEA is not recommended in asymptomatic CAD.

Bilateral carotid artery stenosis

• In asymptomatic bilateral ≥70% stenoses, address the higher-grade side first; with equal stenoses, consider handedness and vascular territory risk.
• In symptomatic patients with contralateral asymptomatic disease, manage the symptomatic side urgently; treat the contralateral lesion electively based on its own merits.
• Antiplatelet therapy and risk-factor control as above; DAPT for stented patients for ≥4 weeks, then monotherapy.

Carotid restenosis

• Occurs in ~6% at 2 years after CEA/CAS.
• Early (<2 years) restenosis often reflects neointimal hyperplasia with low embolic risk—medical therapy is typical for asymptomatic cases.
• Revascularisation (often CAS to avoid redo CEA morbidity) is reserved for symptomatic patients or rapid progression.
• Post-stenting DAPT 1–3 months, then aspirin indefinitely; continue intensive risk-factor modification.

Chronic carotid artery occlusion

• Medical management preferred for chronic total ICA occlusion.
• Selected scenarios for procedural consideration (case-by-case):
  • Ipsilateral haemodynamic symptoms with contralateral ICA stenosis → consider contralateral ICA revascularisation.
  • Ipsilateral embolic symptoms with ipsilateral ECA stenosis → consider ECA revascularisation or ipsilateral ICA ligation to eliminate an embolic source via collaterals.

Procedural options

Carotid endarterectomy (CEA)

• Clear benefit for symptomatic 70–99% stenosis; modest benefit for 50–69% (greater in men).
• No benefit for <50% stenosis.
• Perioperative stroke/MI/death must be low; antiplatelet therapy pre- and post-procedure is recommended.

Carotid angioplasty and stenting (CAS)

• Viable alternative to CEA in high-surgical-risk anatomy or comorbidity; similar long-term protection from stroke in major trials, but higher periprocedural non-disabling stroke, and CEA has higher periprocedural MI.
• Post-procedure DAPT ≥4 weeks, then single antiplatelet indefinitely.
• Anatomical factors (e.g., long lesions, heavy calcification, tortuous arch) increase CAS risk and should influence selection.

Transcarotid artery revascularisation (TCAR)

• Alternative to transfemoral CAS for high-risk CEA candidates; direct carotid access with flow reversal provides embolic protection and avoids arch manipulation.
• Observational data suggest lower stroke rates compared with transfemoral CAS in high-risk cohorts; selection depends on anatomy (e.g., adequate CCA diameter and access distance).

Stroke

• Patients with asymptomatic carotid artery stenosis have an annual ipsilateral stroke risk of about 0.9%, which has progressively decreased with modern best medical therapy.
• In symptomatic patients, prognosis differs by initial presentation: those with TIA have an annual ipsilateral stroke risk of 1–2%, while those with prior stroke have a higher risk of 2–3%.

Pharmacotherapy versus intervention

• In NASCET, the 2-year stroke risk was 1.6% after CEA compared with 12.2% after medical therapy. Five-year cumulative ipsilateral stroke risk was 9% with surgery versus 26% with medical management.
• In ACAS, the 5-year risk of ipsilateral stroke was 5.1% in the surgical group versus 11% in the medical group; 1.2% of surgical patients had procedure-related strokes from arteriography.
  
  

Endarterectomy versus stenting

• EVA-3S reported higher perioperative stroke and death rates with CAS, though protection devices and dual antiplatelet therapy were not consistently used.
• A meta-analysis showed protected CAS had a 30-day stroke/death rate of 8.2% compared with 6.2% for CEA, but disabling stroke or death rates were similar.
• Systematic reviews confirm CEA has lower perioperative stroke risk, while CAS has lower risks of myocardial infarction and cranial nerve injury. Long-term stroke/death rates converge between the two.
• CREST found no overall difference between CEA and CAS in combined stroke, MI, or death. Periprocedural stroke was more frequent with CAS, while MI was more frequent with CEA; stroke had a greater long-term impact on quality of life. Cranial nerve injury occurred in 4.6% of CEA patients, with 80% resolving within one year.
• Pooled analyses (EVA-3S, SPACE, ICSS, CREST) showed CEA had lower combined periprocedural and postprocedural risks, but postprocedural stroke rates were similar between CAS and CEA, indicating improvements in CAS safety may narrow differences further.
• Cranial nerve injuries occur in 2–7% of patients after carotid endarterectomy, most commonly recurrent laryngeal or hypoglossal nerve dysfunction. Postoperative stroke occurs in 1–5%, perioperative mortality in 0.5–1.8%, and restenosis in 1–20%, with reoperation required in 1–3%.

Transcarotid artery revascularisation (TCAR)

• Provides direct carotid access with flow reversal to avoid navigating the diseased aortic arch.
• ROADSTER 1 and 2 trials demonstrated high technical success (96.5%) and low 30-day ipsilateral stroke (1.4%) and 1-year stroke rates (0.4%).
• Comparative registry studies show TCAR has outcomes comparable to CEA despite patients having higher comorbidities, and superior in-hospital outcomes compared with transfemoral CAS, with reduced risk of stroke or death.

Long-term outlook

• Prognosis correlates with stenosis severity. Patients with ≤70% asymptomatic stenosis progress to severe stenosis at a modest rate of up to 5% per year.
• Carotid endarterectomy and stenting reduce annual ipsilateral stroke risk to ~1%. Both are durable, with restenosis rates of ~6% over 2 years.
• Annual clinical and duplex ultrasound surveillance is recommended in many centres, though not universally.
• Carotid stenosis signals systemic atherosclerotic disease; lifelong risk factor modification (blood pressure, lipid management, smoking cessation) is critical to reduce long-term morbidity and mortality.

Overall

• The main natural complication of carotid artery stenosis is transient ischaemic attack or stroke, with progression to symptomatic disease occurring at an estimated rate of 0.9% per year.
• In patients with asymptomatic 70–99% stenosis, the 5-year ipsilateral stroke rate is approximately 4.7%.
• Asymptomatic carotid stenosis is also a strong marker of generalised atherosclerotic disease, conferring an increased risk of coronary artery disease and overall mortality.
• Following revascularisation, complications vary depending on patient comorbidity, severity of disease, and the technique used (endarterectomy vs stenting).

Stroke after carotid endarterectomy

• Usually due to thrombosis at the operative site with intracranial embolisation or release of atheromatous debris.
• Neurological deficits occurring immediately postoperatively may signal technical error and should prompt urgent re-exploration.
• Preventive strategies include intraoperative heparinisation and meticulous surgical technique.
• Rescue options may include thrombectomy or thrombolysis.

Stroke after carotid artery stenting

• Typically caused by thrombosis within the stent or embolisation during deployment.
• Risk is minimised by preoperative dual antiplatelet therapy (aspirin plus clopidogrel) and intraoperative heparinisation to maintain adequate activated clotting time.
• DAPT is generally continued for 1–3 months post-stenting before switching to single antiplatelet therapy.

Myocardial infarction after CEA or CAS

• Periprocedural myocardial infarction risk is about 2.3% following CEA and 1.1% after CAS, usually within the first few days.
• Preoperative aspirin for CEA, and aspirin plus clopidogrel for CAS, are protective.

Haematomas and access site bleeding

• Incisional haematomas after CEA or puncture site bleeding after CAS are uncommon and usually self-limiting.
• Expanding haematomas may require urgent surgical evacuation and transfusion.

Cranial nerve injuries after carotid endarterectomy

• Hypoglossal, vagus, and glossopharyngeal nerves are most frequently affected.
• Occurs in approximately 6% of patients, usually from traction rather than transection.
• Most cases recover spontaneously within six months.

Cerebral hyperperfusion syndrome

• Rare complication, more common after revascularisation of very tight stenoses or with contralateral carotid occlusion.
• Symptoms include headache, seizure, or neurological deficit, usually within hours to days.
• Imaging may demonstrate cerebral oedema, with or without haemorrhage.
• Management includes strict blood pressure control, head elevation, reduction of anticoagulation, and surgical decompression for severe cases.

Post-operative cerebral haemorrhage

• May occur after both CEA and CAS, often related to aggressive antiplatelet/anticoagulant therapy or uncontrolled hypertension.
• May overlap with cerebral hyperperfusion syndrome.
• Treatment is supportive with blood pressure control, head elevation, and decompression if required.

Ischaemic stroke

• In asymptomatic carotid stenosis, annual stroke risk is estimated between 1–5%, rising to nearly 10% if prior TIA or stroke has occurred.
• Pathogenesis is most often plaque rupture with embolisation and cerebral infarction.
• In stenoses <70%, pharmacological therapy is first-line; revascularisation is reserved for selected patients with high-grade disease.

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