Carotid Artery Stenosis
Narrowing of the main blood vessels to the brain due to plaque buildup, significantly increasing the risk of a stroke.
Emergency Management: Acute ischemic stroke requires calling a stroke code, rapid CT Head non-contrast (to rule out hemorrhage), and administration of IV Tenecteplase 0.25 mg/kg if within 4.5 hours of symptom onset.
A narrowing of the extracranial carotid arteries, most commonly at the bifurcation of the common carotid artery into the internal and external carotid arteries, primarily caused by atherosclerosis. It is a major risk factor for ischemic stroke and transient ischemic attacks (TIAs).
Detailed Overview
Atherosclerotic plaque accumulation in the internal carotid artery (ICA) compromises cerebral blood flow and poses a high risk for atheroembolism. Emboli from unstable plaques can travel to the brain via the middle cerebral artery, causing an ipsilateral ischemic stroke, or to the ophthalmic artery, causing amaurosis fugax. Management depends on whether the stenosis is symptomatic or asymptomatic and the degree of narrowing.
Epidemiology & Demographics
Prevalence is roughly 75% in men and 62% in women >65 years old for any degree of plaque. High-grade stenosis (>70%) is found in 2-3% of adults >65. It accounts for approximately 15-20% of all ischemic strokes.
Etiological Mechanism
The primary cause is atherosclerosis. Rare causes include fibromuscular dysplasia (FMD), carotid artery dissection, and radiation-induced arteriopathy.
Primary Causes
["Atherosclerosis (plaque formation)", "Fibromuscular dysplasia (in younger females)", "Prior neck radiation for head/neck cancers"]
Endothelial injury allows LDL to enter the intima, where it is oxidized and engulfed by macrophages to form foam cells. This fatty streak progresses to a fibrous plaque containing a necrotic lipid core. Inflammatory factors can cause the fibrous cap to thin and rupture. Upon rupture, platelet aggregation and thrombosis occur. Emboli from this thrombus dislodge and travel distally to occlude cerebral or retinal vessels.
Diagnostic Criteria & Guidelines
Diagnosis is initially made with Duplex Ultrasound showing elevated peak systolic velocities (>125 cm/s corresponds to >50% stenosis; >230 cm/s corresponds to >70% stenosis). Confirmed with CTA or MRA of the neck prior to surgical intervention.
For all patients (symptomatic or asymptomatic): High-intensity statin (Atorvastatin 80 mg or Rosuvastatin 40 mg daily), Antiplatelet therapy (Aspirin 81 mg daily or Clopidogrel 75 mg daily), strict blood pressure control (target <130/80), and smoking cessation.
Second-Line & Adjunctive Therapy
Addition of a second antiplatelet agent (e.g., Aspirin + Clopidogrel for 21 days) only immediately following a minor ischemic stroke or high-risk TIA. Addition of Ezetimibe 10 mg or PCSK9 inhibitor if LDL remains >70 mg/dL.
Surgical & Procedural Management
Carotid Endarterectomy (CEA) is indicated for symptomatic patients with 50-99% stenosis (highest benefit in 70-99%) to be performed within 14 days of symptom onset. Carotid Artery Stenting (CAS) or Transcarotid Artery Revascularization (TCAR) is an alternative for patients at high surgical risk or those with prior neck radiation.
Patient Counseling & Advice
Counsel the patient that transient symptoms (like a 5-minute loss of vision) are a medical emergency ('mini-stroke') and portend a high risk of a massive stroke in the following 48 hours. They must call 911 immediately if symptoms occur.
Follow-Up & Monitoring Schedule
Serial Carotid Duplex US annually for moderate asymptomatic stenosis. Post-CEA/CAS surveillance ultrasound at 6 weeks, then annually to check for restenosis.
Preventive Strategies
Aggressive management of cardiovascular risk factors in mid-life. Routine screening with US is *not* recommended for the general population but may be considered in patients with multiple risk factors.
Patients with symptomatic severe stenosis have a 25-30% risk of stroke within 2 years if unoperated. CEA reduces this risk to <10%. Perioperative stroke/death rate for CEA is 2-3%.