Carotid artery disease
A major cause of stroke
Around 110 000 strokes and 20 000 transient ischaemic attacks (TIAs) occur in the UK alone every year, but because the importance of TIA symptoms might not be recognised by patients, this incidence could be a gross underestimate. About five per 1000 people aged 50-60 years and 10% of people older than 80 years have carotid stenosis greater than 50%.Carotid artery disease is a common but potentially treatable cause of TIAs and strokes. It is therefore important to be able to recognise the signs and manage patients appropriately.
In this article we discuss the investigation and management of carotid artery stenosis, which often occurs in the context of a stroke or TIA. The complete investigation and management of acute stroke are outside the scope of this article.
Anatomy of the carotid artery
The right common carotid artery arises from the brachiocephalic artery posterior to the right sternoclavicular joint, whereas the left common carotid artery arises from the aortic arch in the thorax and passes posterior to the left sternoclavicular joint.[F1]
In the neck, both common carotid arteries ascend in the carotid sheath alongside the internal jugular vein and vagus nerve. They divide into external and internal carotid arteries at the upper border of the thyroid cartilage at the vertebral level C4.
The external carotid artery supplies the head and neck outside the cranial cavity. The internal carotid artery enters through the carotid canal and terminates into anterior and middle cerebral arteries supplying the brain.
Carotid artery pathologies
Several pathological processes can affect the carotid artery. These include atherosclerosis, dissection, infection, connective tissue disease, and damage through trauma and radiotherapy.
Carotid dissection results from an intimal tear causing blood to track into the vessel wall. It can occur spontaneously or through trauma. Clinical presentations include sudden onset of neck pain, headache, and ipsilateral Horner’s syndrome. It can also cause neurological symptoms and is an important cause of TIAs and strokes in younger patients (aged 40-50 years). Atheromatous disease is the most common pathology affecting the carotid artery and will be the focus of this article.
Carotid artery disease is a major cause of ischaemic stroke—the risk increasing with the severity of the stenosis. Extracranial artery disease accounts for around 25% of ischaemic strokes. The cause of carotid stenosis is most often atherosclerosis, often including the bifurcation of the common carotid artery and the origin of the internal carotid artery. It is most serious within 2 cm of the bifurcation of the common carotid artery, and predominantly involves the posterior wall of the vessel. This is probably because of the higher turbulence of blood flow in the area.Blood travels through the stenosis with an increased velocity and pieces of plaque can break off into the bloodstream, blocking distal small arteries supplying the brain. When there is a break in the fibrous cap of the atheroma, contact between its lipid core and blood activates the coagulation cascade, promoting deposition of thrombi on to the surface of the plaque. Severe stenosis of the internal carotid artery increases the risk of ipsilateral transient ischaemic attacks or strokes.
Stenosis is considered mild if the artery is less than 50% blocked, moderate if 50% to 69% blocked, and severe if more than 70% blocked.
The risk factors for carotid artery disease are similar to other cardiovascular diseases. They include smoking, hypertension, hyperlipidaemia, and diabetes mellitus, as well as increasing age, sedentary lifestyle, and male sex  Peripheral vascular disease, history of ischaemic heart disease, and a family history of both cerebrovascular events and stroke predispose to carotid artery stenosis.
The prevalence of carotid artery stenosis in the general population is not high enough to justify screening programmes. However, a recent prospective study found the prevalence of substantial asymptomatic carotid artery stenosis to be higher among patients with severe peripheral vascular disease (16.7%), and that patient population may be a suitable subgroup to screen for asymptomatic carotid artery stenosis, especially if there is concomitant carotid bruit and hypercholesterolaemia.
Stenosis is asymptomatic when the patient has not had symptoms of ipsilateral retinal or cerebral ischaemia. Of the general population over 65 years, 5% to 10% have an asymptomatic stenosis of ≥50%. Asymptomatic stenosis is usually identified incidentally from auscultation of carotid bruits or screening by Doppler ultrasonography.
Amaurosis fugax is the sudden transient loss of vision. It is an ischaemic event often caused by emboli from the atherosclerotic carotid arteries lodging in the ophthalmic artery and is the most common ocular symptom. Patients experience an episode of transient monocular blindness often referred to as “a curtain coming down over one eye” lasting a few seconds to minutes, followed by full recovery of vision.
A TIA is a brief episode of neurological deficit resulting from focal cerebral ischaemia not associated with permanent cerebral infarction and which completely resolves within 24 hours of its onset. It can cause weakness in the contralateral limbs because emboli from the carotid circulation impact in smaller intracerebral vessels.
Crescendo TIAs refer to rapid successions of monocular or hemispheric symptoms that resolve within minutes after each episode, with two or more episodes a week. They correspond to multiple embolisations from active carotid plaques and are associated with a high risk of permanent neurological deficit.
Neurological symptoms lasting more than 24 hours are regarded as stroke. Cerebral infarction accounts for 80% cases of stroke. It is usually caused by atherosclerosis, embolism, or microangiopathy. Cartoid artery disease is an important cause of anterior circulation infarcts.
Anterior circulation infarcts—The anterior cerebral artery supplies the frontal lobe, the motor cortex controlling the leg, and the corpus callosum. Ischaemia in the territory of one anterior cerebral artery results in contralateral hemiplegia, incontinence, and mixed aphasia if the dominant lobe is affected and dyspraxia if the non-dominant lobe is affected.
The middle cerebral artery gives off branches to supply most areas of the motor and sensory cortex, the Wernicke’s area and Broca’s area of the dominant hemisphere, the internal capsule, and the optic radiation. If the inferior branch of the middle cerebral artery is affected, hemianopia will occur. If the superior branch of the middle cerebral artery is affected, hemiparesis will result. Specific signs of ischaemia of the dominant lobe include Wernicke’s aphasia (inferior branch of the middle cerebral artery) and Broca’s aphasia (expressive or receptive; superior branch of the middle cerebral artery), whereas ischaemia of the non-dominant lobe is manifested by constructional apraxia (inferior branch of the middle cerebral artery) and neglect (superior branch of the middle cerebral artery). A complete middle cerebral artery infarct will result in hemiparesis affecting the arm, face, and leg, and homonynous hemianopia.
Posterior circulation infarcts—Although the posterior circulation is not supplied by the carotid arteries, posterior infarcts are far more frequent in patients who also have carotid disease.
The posterior cerebral artery supplies the occipital lobes, the brain stem, and the cerebellum. Posterior cerebral artery infarcts will cause contralateral homonymous hemianopia and contralateral hemisensory loss. Interruption of the posterior circulation supplying the brainstem will result in dysarthria, nystagmus, and diplopia. Manifestations of cerebellar signs include ataxia, vertigo, dizziness, and drop attacks.
Investigation and diagnosis
Clinically, carotid artery stenosis may be diagnosed from bruits heard over the carotid artery on examination or investigation after a TIA or stroke. Carotid bruits, however, are an unreliable guide to the severity of stenosis. Complete occlusion of carotids does not have any bruit, and severely stenosed carotids may not have an associated bruit.
Investigations that should be carried out for patients presenting with a TIA or stroke include: urinalysis to detect the presence of glucose; fasting serum glucose level to detect diabetes; fasting serum lipid profile to detect hypercholesterolaemia; electrocardiography to look for changes due to myocardial infarction, atrial fibrillation, or ischaemia; echocardiography if mural thrombus is suspected; and erythrocyte sedimentation rate to rule out temporal arteritis. Studies have shown the risk of stroke after a TIA to be particularly high in the first few days, with most studies finding that more than a quarter of the strokes occur within 48 hours of the initial event. Therefore patients who have had a TIA need urgent assessment and treatment. UK national stroke guidelines recommend that all patients with a suspected TIA should be assessed and investigated within a week.
The ABCD2 scoring system (see box) is used to predict the short term risk of stroke in patients presenting acutely after a TIA on the basis of clinical findings. The risk of stroke identifies patients at particularly high risk who require immediate investigation and management. The urgency of referring patients for carotid imaging depends on the individual’s risk of stroke.
ABCD2 scoring system to assess stroke risk
- Age ≥ 60 years—1 point
- Blood pressure ≥140/90 mm Hg—1 point
- Clinical symptoms of unilateral weakness—2 points
- Clinical symptoms of speech impairment without weakness—1 point
- Duration of symptoms <60 minutes—1 point
- Duration of symptoms ≥60 minutes—2 points
- Diabetes mellitus —1 point
Early investigation is essential to detect the presence and extent of carotid stenosis to identify patients who can be considered for carotid endarterectomy.
Duplex ultrasonography is the initial screening test for carotid disease and its role in imaging of extracranial carotid stenotic disease is well established. It is a non-invasive means of investigation that uses high frequency sound waves to create images of the arterial anatomy and allows assessment of flow at the stenosis. It has a sensitivity of 90% and specificity of 94%. Treatment of carotid lesions is often given on the basis of duplex ultrasonography results alone.
Magnetic resonance angiography and computed tomography angiography
With the use of intravenous contrast, magnetic resonance angiography or computed tomography angiography allow carotid artery stenosis to be seen non-invasively. They are highly sensitive, can generate 3D images, and show the morphology of plaques.[F2] Patients with renal disease, however, might not tolerate intravenous contrast. Magnetic resonance angiography is contraindicated in patients who have cardiac pacemakers.
Digital subtraction angiography
Digital subtraction angiography is an invasive technique that delineates carotid vessels by subtracting a digitised background image from an image of the arteries injected with an intravascular contrast. Risks associated with its use include renal toxicity and contrast allergy. It also carries a <1% chance of causing a stroke during the process and is therefore rarely used. It is reserved only for difficult cases where duplex ultrasound results are technically inadequate and other non-invasive options have been exhausted.
The main aim of managing carotid artery disease is to minimise the risk of a stroke, aid recovery from a stroke, and prevent the recurrence and future complications of a stroke. The two key strategies in managing carotid stenosis involve risk factor modification and elimination of carotid stenosis by surgery if stenosis is severe.
Patients who presented with a TIA or amaurosis fugax
Referral urgency after a TIA is determined by risk of stroke, estimated by the ABCD2 score.
Patients with an ABCD2 score of <4—According to current guidelines from the National Institute for Health and Clinical Excellence (NICE) and the Royal College of Physicians, patients with an ABCD2 score of <4 should be started on 75-150 mg aspirin and referred for specialist assessment within a week.
Patients with an ABCD2 score of ≥4—These patients are considered high risk and should be given 75-150 mg aspirin immediately and referred for specialist assessment within 24 hours. Patients with two TIAs in a week (crescendo TIAs) are regarded as high risk, whatever their ABCD2 score.
Combined aspirin and dipyridamole (200 mg/12 hours) has shown additional benefit in prevention of stroke and other vascular events after a TIA compared with aspirin monotherapy.
Patients who presented with a stroke
Stroke units and thrombolysis have revolutionised the acute management of stroke. Patients should be admitted to a stroke unit for initial care and treatment. They should be kept on nil by mouth until their ability to swallow is assessed. Blood pressure should be managed closely. Urgent computed tomography or magnetic resonance imaging should be arranged to rule out a diagnosis of primary cerebral haemorrhage if thrombolysis is considered.
Intravenous thrombolytic treatment (recombinant tissue plasminogen activator) should be given to patients who present within three hours of stroke onset and have no contraindications. Thrombolysis has to be given in a narrow time window so campaigns are in place to raise the public awareness of the time crucial nature of recognising an acute stroke through the FAST test (facial weakness, arm weakness, speech problems, time to call 999).
Once haemorrhagic stroke is excluded, 300 mg/day aspirin should be given as soon as possible for two weeks and then continued at a dosage of 75 mg/day indefinitely. If a patient is aspirin intolerant, clopidogrel can be given instead. For immobile patients, graded pressure stockings should be prescribed to prevent deep vein thrombosis.
Lifestyle modification and medical treatment
Every effort should be made to modify risk factors to prevent progression of carotid artery disease for primary and secondary prevention of stroke. Hypertension is the most important treatable risk factor for stroke, and therefore tight control of blood pressure forms a vital part of management. The importance of smoking cessation should also be emphasised. Appropriate pharmacological and lifestyle measures should be taken for glycaemic control in diabetic patients. Statins (40 mg by mouth) are effective at reducing the risk of stroke and have a relative reduction of 17% in stroke risk per 1 mmol/L reduction in low density lipoprotein cholesterol.
Specialist assessment entails confirmation of the diagnosis of a TIA and carotid and brain imaging. Patients who have symptomatic carotid stenosis of <70% should not undergo surgery. NICE guidelines recommend that patients with symptomatic carotid stenosis of ≥70% should be referred for carotid endarterectomy within a week of onset of stroke or TIA symptoms. Surgery should ideally be performed within two weeks of the occurrence of a TIA or stroke. Asymptomatic patients would normally be considered for surgery if stenosis is found to be ≥70%.
Surgical management aims at clearing atheroma and improving brain perfusion. Carotid endarterectomy is currently the most effective and definitive treatment for stroke prevention in patients with symptomatic carotid stenosis. The absolute risk reduction of stroke from this treatment is 17%.
Doppler ultrasound should be repeated preoperatively to exclude complete occlusion in the interval between initial diagnosis and admission for surgery. A follow-up duplex scan should be planned for six weeks after the operation. Patients undergoing carotid endarterectomy should receive aspirin preoperatively, with this discontinued a week before surgery; be given systemic heparin intraoperatively; and then receive aspirin immediately postoperatively. Carotid endarterectomy carries a risk of cranial nerve palsy and perioperative stroke (1-3%). Follow-up in a carotid clinic should also be arranged a few weeks after surgery.
Percutaneous transluminal carotid artery stenting entails passing a catheter with a balloon at its tip through the skin into the carotid artery. The balloon is then inflated at the point of arterial narrowing.
Carotid artery stenting is currently recommended only for patients who are not candidates for conventional surgical treatment because of medical comorbidities.Aida Lai, fourth year medical student1, Charles N McCollum, consultant vascular surgeon and professor of surgery2
1University of Manchester, UK, 2University Hospital of South Manchester
Correspondence to: email@example.com
Competing interests: None declared.
Provenance and peer review: Not commissioned; externally peer reviewed
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Cite this as: Student BMJ 2011;19:d2342