Prepared By: Jasleen Saini, BSc. (Hons), MD candidate (2022) – Senior Blog Manager; email@example.com
Reviewed by: S. Uzair Ahmed, MD – Endovascular Neurosurgery Fellow
Division of Neurosurgery, Department of Surgery, College of Medicine
University of Saskatchewan, Saskatoon, SK, Canada
Atherosclerotic lesions of the carotid artery bifurcation are a common cause of stroke. In patients with extracranial carotid artery disease, the degree of internal carotid artery stenosis is the most important predictor of cerebral infarction (1). The risk of stroke is closely related to the severity of carotid artery bifurcation stenosis. Carotid endarterectomy (CEA) improves cerebral blood flow and minimizes the risk of stroke by removal of the atherosclerotic plaques.
The North American Symptomatic Carotid Endarterectomy Trial (NASCET) was a randomized, controlled study that evaluated the utility of CEA in 659 patients with symptomatic carotid artery stenosis. It was first published in the New England Journal of Medicine (NEJM) in 1991. The study was aimed at providing definitive evidence to support or refute the use of CEA as a prophylactic treatment against stroke.
Patients were randomized to either medical therapy alone (i.e., antiplatelet, antihypertensive, anti-lipid, and antidiabetic therapy, as needed) or medical therapy with CEA in 50 centres across the United States and Canada. Enrolling centers had to demonstrate expertise and low rates of procedural complications. Patients were eligible for the trial if they provided informed consent, were less than 80 years old, and had a cerebrovascular event (i.e., transient ischemic attack, monocular blindness, non-disabling stroke) in the previous 120 days with ipsilateral carotid stenosis of 30-99% (as per selective carotid angiography). A uniform and strict technique for measuring carotid artery stenosis from an arteriogram was used in the trial (percentage of stenosis = [1 − minimum residual lumen/normal distal cervical internal carotid artery diameter] × 100). In neurological follow-up, patients were assessed at 1, 3, 6, 9, and 12 months, then every 4 months for death or stroke.
The monitoring and executive committees agreed to prematurely terminate the study in patients with high-grade stenosis (70-99%) because of evidence demonstrating the efficacy of CEA in these patients. the parallel study dealing with symptomatic patients with medium-grade stenosis (30-69%) continued as planned.
The estimates of the cumulative risk of ipsilateral stroke at two years were 26% in the 331 medical patients and 9% in the 328 surgical patients. There was a significant reduction in the absolute risk of ipsilateral stroke by 17% (±3.5%, P<0.001). For a major or fatal ipsilateral stroke, the corresponding estimates were 13.1% and 2.5%, reducing the absolute risk of major or fatal ipsilateral stroke by 10.6% (±2.6%, P<0.001) (1). The number needed to treat for the NASCET study can be calculated by using the formula NNT = 1/ARR. Therefore, 5.88 patients with severe stenosis would need to be treated with CEA to prevent one ipsilateral stroke.
Procedural complication rates were low in the study. Perioperative (within 30 days of the procedure) stroke or death occurred in 5.8% of patients in the surgical cohort. Other complications included cranial nerve injury, myocardial infarction (MI), congestive heart failure (CHF), and other cardiovascular problems, of which 81% were mild.
Results from the NASCET study were consistent with the findings from the European Carotid Stenosis Trial. However, the benefits of CEA in patients with asymptomatic carotid stenosis were still being explored in subsequent trials at the time. In conclusion, CEA in addition to medical therapy significantly reduces the absolute risk of ipsilateral stroke and major or fatal ipsilateral stroke in patients with symptomatic, high-grade (70-99%) carotid artery stenosis. This well-designed and well-executed trial was successful in providing definitive evidence to support the use of CEA.