Carotid Artery Disease

Original Author: Aimee Rowe
Last Updated: March 12, 2019
Revisions: 39

Carotid artery disease refers to the build-up of atherosclerotic plaque in one or both common and internal carotid arteries, resulting in stenosis or occlusion.

The majority of carotid artery disease is asymptomatic, but it is also responsible for approximately 10-15% of ischaemic strokes, due to plaque rupture and/or atheroembolism.

In this article, we shall look at the clinical features, investigations and management of a patient with carotid artery disease.

Fig 1 - Atherosclerotic plaque from a carotid endarterectomy specimen

Figure 1 – Atherosclerotic plaque from a carotid endarterectomy specimen.


The pathophysiology of carotid artery disease is as for atheroma elsewhere, starting with a fatty streak, accumulating a lipid core and formation of a fibrous cap. The turbulent flow at the bifurcation of the carotid artery predisposes to this process specifically at this region.

Carotid artery disease is usually classified radiologically by the degree of stenosis:

Degree of Stenosis

Diameter Reduction







Total Occlusion



Risk Factors

The major risk factors for carotid artery disease are age (≥65 years), smoking, hypertension, hypercholesterolaemia, obesity, diabetes mellitus, history of cardiovascular disease, and a family history of cardiovascular disease.

Clinical Features

Carotid artery disease will often be asymptomatic, however may present as a focal neurological deficit. This can take one of two forms:

  • Transient ischaemic attack (TIA) – lasts less than 24 hours before full resolution*
  • Stroke – lasts for more than 24 hours without full resolution

Much of the detailed initial assessment for a patient presenting with a stroke is typically beyond the scope of a vascular surgeon. The Oxford Stroke (Bamford) Classification provides a system to classify stroke symptoms in relation to the arterial regions involved (see Appendix).

On examination, a carotid bruit may be auscultated in the neck, however this is associated with carotid stenosis in less than half of cases.

Other than the clinical features from stroke, carotid stenosis (even with complete occlusion) is likely to be asymptomatic if unilateral. This is due to collateral supply from the contralateral internal carotid artery and the vertebral arteries, via the Circle of Willis.

*This may include transient visual loss, termed amaurosis fugax

Differential Diagnoses

Atherosclerosis is the most common form of carotid artery disease. However, there can be other pathologies involved:

  • Carotid Dissection – Patients are often younger (<50yrs) and have an underlying connective tissue disease, with the event potentially precipitated by trauma or sudden neck movement
  • Thrombotic Occlusion of Carotid Artery – Thrombus can only be differentiated from atheromatous plaque on imaging and will present clinically as for atheroma
  • Fibromuscular Dysplasia – This is non-atheromatous stenotic angiopathy causing hypertrophy of the vessel wall, predominantly affecting young (<50yrs) females and, whilst most commonly in the renal arteries, the carotid arteries can be affected, presenting clinically with focal neurological deficit
  • Vasculitis – Various great vessel vasculitidies, such as Giant Cell Arteritis or Takayasu’s Arteritis, can cause carotid stenoses, however patients typically have systemic symptoms and other vessels may be affected

In addition, non-cerebrovascular conditions that manifest neurologically should be considered. These include hypoglycaemia, Todd’s paresis*, subdural haematoma, space-occupying lesion, venous sinus thrombosis, post-ictal state, and multiple sclerosis.

*Todd’s Paresis = Unilateral motor paralysis following a seizure


Initial Investigations

Any patient suspected of ischaemic (or haemorrhagic) stroke should have an urgent CT head scan (Fig. 2) to check for infarction potentially amenable to thrombolytic treatment.

Other investigations for a patient admitted with a stroke include:

  • Fig 2 - CT scan. Hyperdense artery sign in a patient with middle cerebral artery infarction.

    Figure 2 – CT head scan showing hyperdense artery sign in a patient with middle cerebral artery infarction

    Bloods, including FBC, U&Es, clotting, lipid profile, and glucose

  • ECG (checking for any potential source of clot)

Follow-up Investigations

Once a diagnosis of ischaemic stroke or TIA is made, it is important to screen the carotid arteries for disease precipitating the presentation. This can be done initially with Duplex ultrasound scans*, which gives a good estimate as to the degree of stenosis, as well as excluding any other possible differentials.

Lesions within the carotid artery should then be further characterised with CT angiography (CTA) which gives a more accurate percentage stenosis and characterises the diseased portion of the vessels for potential surgery if the USS scan shows a greater than 50% stenosis.

*As this investigation is cheap, non-invasive and readily available, it is ideal for use in screening asymptomatic patients with risk factors or investigating symptomatic patients who may warrant prophylactic surgical intervention


Acute Management

All patients admitted with a suspected stroke should be started on high flow oxygen and blood glucose optimised (target 4-11mmol); a swallowing screen assessment should also be made on admission.

Initial management depends on the nature of the stroke:

  • Ischaemic stroke –  IV alteplase (r-tPA), if patients are admitted within 4.5hrs of symptom onset and meet inclusion criteria. 300mg aspirin OD should then be started as an inpatient for 14 days
    • Select patients may instead be suitable for thrombectomy
  • Haemorrhagic stroke – correction of any coagulopathy and referral to neurosurgery (for potential clot evacuation*)

*Neurosurgery is often not advised for a haemorrhagic stroke, unless superficial lobar bleed or ventricular bleed, yet this will be at the neurosurgeon’s discretion

Long Term Management

All patients with a known stroke or TIA should also be started on cardiovascular risk factor management:

  • Anti-platelet therapy long term, typically aspirin 300mg OD for two weeks, then clopidogrel 75mg OD
    • If not tolerated, trial combination therapy aspirin and dipyradimole
  • Statin therapy, ideally high-dose atorvastatin
  • Aggressive management of hypertension and/or diabetes mellitus
  • Smoking cessation
  • Regular cardiovascular exercise and active lifestyle with weight loss

Patients presenting with symptomatic carotid artery stenosis ≥50% should be referred for surgical revascularisation (see below). Patients with asymptomatic carotid artery stenosis of >70% are very rarely surgical treated at present unless they are young and have had a symptomatic contralateral stenosis.

A referral to the Speech and Language Therapy (SALT) team is advised for any dysphagia or dysphasia. Physiotherapy and Occupational Therapy input is advised for any ongoing mobility issues, with many stroke patients requiring rehabilitation.

Carotid Endarterectomy

The mainstay of surgical treatment for ischaemic stroke prevention is via a carotid endarterectomy (CEA)*. A CEA involves removing the atheroma and associated damaged intima, thereby reducing the risk of future strokes or TIAs.

*Data has shown that CEA is a superior option to carotid stenting, with the latter option associated with an increased risk of long-term major adverse events

The Carotid Endartectomy

Initially the artery is isolated and clamped, before an arteriotomy is created and often a temporary bypass shunt placed for the duration of the procedure. Shunting is especially important for any contralateral occlusive disease to minimise any cerebral hypoperfusion.

The plaque and diseased intima are carefully dissected from within the artery, with careful attention not to create any free edge that could result in dissection. The arteriotomy is closed with a patch graft to prevent iatrogenic stenosis and reduce the risk of re-stenosis.

The main risks of CEA surgery are stroke (2-3%), nerve damage to the hypoglossal, glossopharngeal, or vagus nerve, myocardial infarction, local bleeding, or infection

Fig 3 - Carotid endarterectomy, the mainstay of surgical intervention in carotid artery disease.

Figure 3 – Carotid endarterectomy, the mainstay of surgical intervention in carotid artery disease.


Mortality of a stroke is 12% at 7 days and 19% at 30 days.

The most significant improvement from rehabilitation occurs between 4-6 weeks, yet 50% of survivors will remain dependent at 1 year. This is significantly less in patients that are fit for carotid endarterectomy, however this is a preselected cohort, and those with a high mortality post-stroke will not be candidates for CEA.

Other complications of a stroke include dysphagia, seizures, ongoing spasticity, bladder or bowel incontinence, and depression, anxiety, or cognitive decline.

Key Points

  • Most cases of carotid artery stenosis are asymptomatic, however the major sequela of the condition is ischaemic stroke
  • First line investigation is via carotid US Doppler, with confirmed cases being further assessed with CT angiography
  • Selected cases will be offered carotid endartectomy (CEA) for risk reduction management of ischaemic stroke

Appendix – The Oxford Stroke Classification

Classification Description Signs and Symptoms
Total Anterior Circulation Stroke (TACS) (20%) Large cortical stroke in middle or anterior cerebral artery areas Must have all of:

  • Motor weakness or sensory deficit of ≥2/3 areas (face, arm, leg)
  • Homonymous hemianopia
  • High cortical dysfunction (dysphagia, dyspraxia, or neglect)
Partial Anterior Circulation Stroke (PACS) (35%) Cortical stroke in middle or anterior cerebral artery areas Will present with either:

  • 2/3 TACS criteria
  • Limited motor or sensory deficit (1 of leg, arm or face)
  • High cortical dysfunction alone
Lacunar Stroke (LACS) (20%) Occlusion of the deep penetrating arteries Will present with any of:

  • Pure motor ≥2/3 areas (face, arm, leg)
  • Pure sensory ≥2/3 areas (face, arm, leg)
  • Pure sensorimotor ≥2/3 areas (face, arm, leg)
  • Ataxic hemiparesis
Posterior Circulation Stroke (POCS) (25%) Occlusion of vertebrobasilar or PCA circulation, affecting brainstem, cerebellum, or occipital lobe Variety of presentations can occur, typically:

  • Ipsilateral CN palsy with contralateral motor or sensory defects
  • Bilateral motor or sensory deficits
  • Isolated homonymous hemianopia
  • Cerebellar dysfunction


Question 1 / 3
Which of the following is NOT a risk factor for carotid stenosis?


Question 2 / 3
Pharmacological and lifestyle management for carotid stenosis include all except?


Question 3 / 3
A patient presents with motor loss affecting their right arm only. An ischaemic stroke is suspected. Where has the occlusion occurred?


Further Reading

Thrombectomy for Stroke at 6 to 16 Hours with Selection by Perfusion Imaging
Albers GW et al., NEJM

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