Symptomatic Carotid Artery Stenosis

Book
In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan.
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Excerpt

Stroke is the third leading cause of death in developed countries and the leading cause of morbidity. The majority of strokes (85%) are ischemic in nature, and the most common source of occlusion is thought to be intracranial embolic disease from the ipsilateral carotid artery. Recurrent strokes are a significant concern as these often occur in the same vascular territory as the initial stroke and are associated with 65% mortality.

Determining the difference between hemodynamic and embolic causes in the presence of internal carotid artery stenosis is important to determine the source of ischemia—usually presenting as classic stroke or transient ischemic attack (TIA). Symptoms may include contralateral motor or sensory deficits, as well as amaurosis fugax. Hemodynamic compromise may cause a presentation similar to a classic stroke or TIA but may also be less predictable and atypical. Patients have reported symptoms such as limb shaking, retinal claudication, headache from large pulsatile external carotid artery collaterals, syncope, and generalized fatigue. One-third of all strokes are related to cervical carotid disease. The mechanism of cervical carotid stroke is usually embolization from the carotid bifurcation plaque, but hemodynamic compromise from stenosis may also play a role. The risks of embolization and hemodynamic compromise increase the greater the degree of carotid artery stenosis.

The benefit of carotid endarterectomy (CEA) depends on the degree of stenosis, with greater benefit associated with higher levels of stenosis. CEA is not a benign procedure, with an estimated 4% to 7% risk of stroke and death within the first 30 days of surgery. This is related to many factors but primarily to manipulation of intraluminal plaque. Periprocedural morbidity can also be difficult to quantify accurately because the natural history of stroke and TIA also results in a certain percentage of recurrent stroke and death. Therefore, it is important to determine levels of stenosis at which the risk of CEA is outweighed by the benefit versus medical management alone. Optimal medical management should be applied to all patients and includes lipid-lowering agents, hypertension control, and diabetes management.

Timing of Carotid Endarterectomy

The timing of intervention for carotid stenosis is controversial because there is conflicting evidence about the risks and benefits of intervention performed at various time periods. The landmark trials North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the European Carotid Surgery Trial (ECST), both published in 1991, showed that CEA for symptomatic carotid stenosis performed within 6 months of a symptomatic event reduces the rate of recurrent stroke, and most of the benefit was realized when CEA was performed within 2 weeks of the ischemic event. This led to recommendations that CEA be performed within 14 days of an ischemic event, with some guidelines using even stricter guidelines of CEA within 48 hours of the referring event. Another study from the Swedish Vascular Registry (Swedvasc), published in 2012, suggested an increased risk of perioperative complications when CEA was performed within 48 hours of the ischemic event compared to CEA performed 3 to 7 days after the event (11.5% versus 3.6%). There was also no increased risk of embolic events in CEA performed at 8 to 14 days after the event. More recent guidelines favor first classifying the index event as either a TIA or stroke—then considering CEA within 48 hours if the initial event is a TIA. If the initial event is a stroke, intervention between 3 to 7 days can be considered. An exception to waiting 48 hours after the initial event would be patients who have repetitive or worsening TIAs, also called crescendo TIAs. These patients likely benefit from early intervention to avoid further neurologic compromise. Multiple patient-specific factors play into the decision of optimal timing for a CEA.

Asymptomatic Carotid Artery Stenosis

Another area of contention is the presence of significant carotid artery stenosis in asymptomatic patients (patients without neurologic symptoms for the last six months.) Three randomized control trials studied whether CEA could reduce stroke risk in patients with asymptomatic carotid stenosis (usually >50% stenosis), comparing CEA with optimal medical management. These studies were the Veterans Affairs Cooperative Study Group (VA), the Asymptomatic Carotid Atherosclerosis Study (ACAS), and the Asymptomatic Carotid Surgery Trial-1 (ACST-1). In general, these studies found that stroke risk was significantly decreased in patients with asymptotic carotid stenosis, but there were limitations to these studies, including the following: there was a low incidence of ischemic stroke in both study groups; only surgeons with low complication rates were allowed to participate in two of these studies; and advances have been made in medical management of carotid stenosis since these studies were performed.

Carotid Artery Stenosis and Coronary Artery Disease

Given that carotid stenosis is an atherosclerotic process, it is not surprising that a significant portion of patients with severe carotid stenosis have concurrent coronary artery disease (CAD). In patients who need coronary artery bypass graft surgery (CABG) and who are known to have severe (>70%) but asymptomatic carotid stenosis, the question arises regarding performing CEA before or at the same time as the CABG. A randomized control trial of 185 patients showed significant benefit for CEA either prior to or at the same time as CABG compared to patients who underwent CEA 1 to 3 months after CABG. The delayed CEA group had a significantly increased risk of perioperative or delayed stroke.

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