Symptoms of extracranial carotid disease are most often caused by embolization. Arterial emboli account for approximately one-quarter of strokes in Europe and North America, and 80% of these originate from atherosclerotic lesions in a surgically accessible artery in the neck. The most common lesion is at the bifurcation of the carotid artery. Lesions of atherosclerosis in the internal carotid artery occur along the wall of the carotid bulb opposite to the origin of the external carotid artery. Enlarging the bulb just distal to this major branch point creates a low wall shear stress area, resulting in flow separation and loss of unidirectional flow. This allows for greater interaction between atherogenic particles and the vessel walls at this site, accounting for the localized plaque at the carotid bifurcation. Transcranial Doppler (TCD) studies have shown that emboli are observed in approximately 20% of patients with moderate (>50% stenosis) lesions at the carotid bifurcation, and even higher rates are seen with more than 70% stenosis. The incidence and frequency of emboli are increased in patients who have recently become symptomatic. The neurologic dysfunction associated with microemboli may appear as sudden or transient neurologic symptoms, including unilateral motor and sensory loss, aphasia (difficulty finding words), or dysarthria (difficulty speaking due to motor dysfunction). These are referred to as transient ischemic attacks (TIA). Most TIAs are brief, lasting only a few minutes. By convention, 24 hours is the arbitrary limit of a TIA. If the symptoms persist, it is a stroke or cerebrovascular accident (CVA). An embolus to the ophthalmic artery, the first branch of the internal carotid artery, can produce a temporary monocular vision loss, known as amaurosis fugax, or permanent blindness.  The prevalence of significant carotid artery stenosis (defined as≥50% narrowing) is approximately 1.2% to 1.8% globally. The annual occurrence rate ranges from 2% to 6%. The cumulative risk of stroke may be as high as 15% in the first year and 30% within 5 years. Moreover, as high as one-fourth of patients harbor a risk of recurrent stroke within 5 years. Stroke results from thromboembolism originating from vulnerable plaques and low-flow states, inducing hypoxic-inducible factor 3A. A large lipid-rich necrotic core, intra-plaque hemorrhage, surface fissures, minimal calcification, and a thin fibrous cap are hallmarks of vulnerable plaques.  The study of lesion biology through contrast-enhanced ultrasound and vessel wall imaging is more critical than assessing luminal narrowing through angiography alone, as applied in the North American Symptomatic Carotid Endarterectomy Trial (NASCET) and European Carotid Surgery Trial (ECST) trials. There is also an emerging role of proteomic analysis, artificial intelligence, and machine learning in determining the same. The accessibility of this localized atheroma enables the effective removal of the plaque and a significant reduction in stroke risk. Without treatment, 26% of patients with TIAs and more than 70% with carotid artery stenosis will develop permanent neurological impairment from continued embolization at 2 years. The risk of CVA can be reduced to 9% with plaque removal, and is typically lower for patients presenting with amaurosis fugax.  Carotid revascularization procedures comprise: Carotid endarterectomy (CEA). Carotid artery stenting (CAS) . Transcarotid artery revascularization (TCAR) . CEA was first reported by Eascott et al in 1954 and described in 1975 by DeBakey. Annually, 150,000 patients undergo CEA globally. In the United States, the annual usage of the procedure decreased from 51.6 to 22.5 cases per 100,000 population from 2006 to 2020. Carotid revascularization procedures have profound benefits if performed within 2 weeks of the index event. Surgery is usually deferred in the initial 48 hours (except in crescendo TIAs or stroke in evolution), owing to increased risk of periprocedural thromboembolic events from plaque instability and vulnerability.  Revascularization is not recommended for cohorts with diminished consciousness, disabling strokes (modified Rankin Scale score ≥3), and infarctions involving >30% of the middle cerebral artery region. ECST, NASCET, and Veteran Affairs Cooperative Study (VACS) proved the superiority of CEA plus medical therapy over medical therapy among symptomatic individuals with >70% carotid stenosis. The 5-year risk reduction of 16% with 1-month stroke and mortality risk of 7.1% was observed. The risk reduction was a mere 4.6% for cohorts with 50% to 69% stenosis, with no benefits observed if the stenosis was less than 50%.  CEA is superior to CAS in symptomatic CAS. CEA has also been shown to ameliorate carotid artery stenosis-induced cognitive dysfunction. Only CEA improves visual acuity. The endarterectomy versus stenting in patients with symptomatic severe carotid stenosis (EVA-3S) trial and International Carotid Stenting Study (ICSS) reported a higher risk (2- to 3-fold) of stroke or death associated with stenting. The North American carotid revascularization endarterectomy versus stenting (CREST) trial revealed a high risk of stroke in CAS and myocardial infarction in CEA. The European Stroke Organization (ESO) does not advocate stenting for patients older than 70.