Carotid Artery Disease
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.
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 stensosis:
Degree of Stenosis
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.
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
- This may include transient visual loss (termed amaurosis fugax)
- 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.
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.
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:
|Partial Anterior Circulation Stroke (PACS) (35%)||Cortical stroke in middle or anterior cerebral artery areas.
|Will present with either:
|Lacunar Stroke (LACS) (20%)||Occlusion of the deep penetrating arteries.||Will present with any of:
|Posterior Circulation Stroke (POCS) (25%)||Occlusion of vertebrobasilar or PCA circulation, affecting brainstem, cerebellum, or occipital lobe.||Variety of presentation can occur, typically:
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
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:
Bloods, including FBC, U&Es, clotting, lipid profile, and glucose
- ECG (checking for any potential source of clot)
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.
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
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.
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
- Recent data is now suggesting a benefit of up to 16 hours in selected cases for thrombectomy
- Haemorrhagic stroke – referral to neurosurgery (for potential clot evacuation*) and correction of any coagulopathy
*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 atorvastatin 80mg OD
- Aggressive management of any 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). Timely referral is important, aiming for revascularisation as soon as possible, with current targets within 2 weeks for patients with stabilised neurology and fit for surgical intervention.
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.
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.
*A recent study noted that CEA was a superior option to carotid stenting, the latter option associated with an early and sustained approximately 55% increased hazard for 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
Mortality of a stroke at 7 days is 12% and at 30 days is 19%.
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.
- 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