Management of Extracranial Carotid Artery Stenosis

Management of Extracranial Carotid Artery Stenosis Pathogenesis and definitions

Atherosclerosis is the commonest arterial disorder in developed countries and, when complicated by thrombosis and embolism, causes ischaemic stroke, myocardial infarction and peripheral arterial disease.

Plaque forms where there is endothelial injury and haemodynamic stress — in the cerebral circulation this is at sites of arterial branching, especially the bifurcation of the common carotid artery. LDL cholesterol enters the subendothelium, is oxidised by macrophages and smooth muscle cells, and growth factors and cytokines drive foam cell accumulation and smooth muscle proliferation.

Plaques with a fatty core and fibrous cap narrow the lumen and stiffen the wall. A defect in the fibrous cap from rupture or erosion predisposes to thrombosis — platelets adhere and are activated, which is the site of action of antiplatelet drugs.

Most strokes and TIAs secondary to carotid stenosis occur by thromboembolism; haemodynamic hypoperfusion is a relatively rare cause because of collateral supply through the circle of Willis.

Risk factors: cigarette smoking, diabetes mellitus, age, dyslipidaemia, hypertension and genetic predisposition. Arterial dissection is a rare cause in the elderly (common in the young), usually after minor neck or head trauma with sudden neck rotation.

Symptomatic stenosis = ipsilateral TIA, ischaemic stroke or amaurosis fugax within the preceding six months.

The degree of carotid stenosis should be reported using the NASCET method, in which the diameter at the stenosis is compared with the diameter of the distal internal carotid artery. ECST used a different denominator, so the two are not interchangeable.

Doppler ultrasound is the usual first-line non-invasive test (70–79% stenosis corresponds to peak systolic velocity >230 cm/s and end-diastolic velocity 110–140 cm/s).

CT angiography is increasingly replacing MRA and duplex because it is often combined with the initial stroke CT; limitations are contrast toxicity in renal impairment, contrast allergy and poor visualisation with heavy plaque calcification. MRA is limited by tolerability, metallic implants and misinterpretation of swallowing artefact or turbulent flow as stenosis.

Catheter angiography is the gold standard but carries a 0.5–2% risk of stroke or TIA from plaque dislodgement, dissection or catheter thrombus — it should be preceded by non-invasive imaging and performed only in experienced neurovascular units.

Antiplatelet therapy — aspirin, clopidogrel, or aspirin with extended-release dipyridamole; short-course dual antiplatelet therapy after minor stroke or high-risk TIA.

High-intensity statin — SPARCL showed atorvastatin 80 mg reduced recurrent ischaemic stroke by around 20%; treat cholesterol above 3.5 mmol/L, with dietetic input.

Blood pressure control (PROGRESS: perindopril-based regimen); target ≤130/80 mmHg in diabetic patients; plus glycaemic control, smoking cessation and lifestyle advice.

Anticoagulation is not indicated for carotid stenosis itself — it is reserved for atrial fibrillation, prosthetic valves or another specific indication. Heparin in acute stroke gives no net benefit.

All patients with suspected non-disabling stroke or TIA who, after specialist assessment, are considered candidates for carotid endarterectomy should have carotid imaging within 24 hours of symptom onset.

Symptomatic stenosis of 50–99% (NASCET) with stable neurological symptoms: assess and refer for carotid endarterectomy as soon as possible, within seven days of symptom onset, in a vascular surgical centre, plus optimum medical treatment.

Symptomatic stenosis <50% (NASCET): should not undergo carotid intervention; best medical treatment only.

Evidence (pooled ECST and NASCET, Rothwell, Lancet 2003): the absolute risk reduction of ipsilateral ischaemic stroke or death with CEA for 70–99% NASCET stenosis was 16% (p<0.001). Patients with 50–69% stenosis benefited by a slimmer margin, and below that threshold there was overall harm. Benefit requires a perioperative stroke or death risk of no more than 5%.

Subgroups deriving additional benefit: male sex, advancing age and recent symptoms. Near-occlusion derives no benefit.

ACAS: CEA reduced the 5-year risk of ipsilateral stroke or perioperative stroke/death from 11% to 5.1%, but not the risk of major stroke. ACST: immediate CEA reduced the 5-year risk of all strokes and perioperative death from 11.8% to 6.4%. The 30-day stroke or death rate after CEA in both trials was around 3%.

ACST subgroup analysis showed no evidence of benefit in patients older than 75 or in women. These trials predate widespread statin use, good blood pressure control and routine dual antiplatelet therapy, so with modern medical management the stroke rate in asymptomatic stenosis (already only ~2% per annum) would be lower still, potentially negating any benefit of surgery.

Conclusion from the textbook: patients over 75 with asymptomatic stenosis and those with less than 60% stenosis should not be offered surgery. Those managed medically must be educated about TIA and stroke symptoms and told to present urgently.

Advantages: performed under local anaesthesia, avoiding general anaesthesia; faster recovery and shorter stay; no neck incision, so less haematoma, infection and cranial nerve injury. Disadvantages: distal embolisation during catheter passage and during stent deployment and post-dilatation, greater restenosis, and the cost of the stent and cerebral protection device.

Pooled analysis of four trials (Bonati, Lancet 2010): stroke or death within 120 days was 8.9% after stenting vs 5.8% after endarterectomy (RR 1.53). CEA carries a small excess of myocardial infarction (<1%) and cranial nerve injury.

Age is the key modifier (Howard, Lancet 2016): in symptomatic patients, procedural stroke or death was identical below age 70, and all the excess risk of stenting was in older patients. Long-term effectiveness at preventing recurrence is similar at all ages.

Textbook/NICE indication for stenting: patients who meet criteria for intervention but are unsuitable for surgery — inaccessible or high cervical bifurcation, restenosis after endarterectomy, radiotherapy-associated stenosis, fibromuscular dysplasia and dissection.

Vertebral and intracranial disease: vertebral artery origin stenting is relatively safe but has not been shown superior to medical management (VIST); intracranial stenting carries risks of dissection, rupture and plaque embolisation and is reserved for recurrent symptoms despite medical therapy.

Geriatric decision-making: benefit accrues over years, so weigh frailty, cognition, comorbidity and life expectancy. A frail patient with limited life expectancy should be managed medically.