Elsevier

Neurologic Clinics

Volume 33, Issue 2, May 2015, Pages 443-457
Neurologic Clinics

Management of Asymptomatic Carotid Stenosis

https://doi.org/10.1016/j.ncl.2014.12.008Get rights and content

Section snippets

Key points

  • With intensive medical therapy, the risk of stroke or death in patients with asymptomatic carotid stenosis (ACS) is now below the risk of carotid endarterectomy or stenting.

  • Most ACS patients (∼90%) would be better off with medical therapy than with either intervention.

  • The few patients who could benefit from intervention can be identified by transcranial Doppler embolus detection, reduced cerebral blood flow reserve, carotid ulceration on 3-dimensional ultrasound, intraplaque hemorrhage on MRI,

Disease Description

Asymptomatic carotid stenosis (ACS) refers to narrowing of the carotid artery caused by atherosclerosis in patients who have not experienced a stroke or transient ischemic attack in the territory of that artery. Patients with vague symptoms such as lightheadedness, or symptoms in the vertebrobasilar territory should not be regarded as symptomatic, for the purpose of managing their carotid stenosis.

The term is sometimes applied to patients who may have experienced a transient ischemic attack

Cardiovascular risk of patients with asymptomatic carotid stenosis

Patients with ACS are at a high risk of myocardial infarction, so they warrant intensive medical therapy. Indeed, in the Veterans Affairs study in 1994,8 the risk of myocardial infarction among patients with ACS was 33% over 4 years, similar to the risk of patients with known coronary disease. Among patients with ACS and no known coronary disease, their first event was myocardial infarction in 56% of cases. It is therefore axiomatic that all patients with asymptomatic stenosis should receive

Management of patients with asymptomatic carotid stenosis

As described by Spence and Hackam in 2010,15 and illustrated in the Stenting Versus Aggressive Medical Therapy for Intracranial Arterial Stenosis (SAMPRISS) trial,16 in which the risk of stroke was higher with stenting of intracranial arteries than with intensive medical therapy, there is much more to intensive medical therapy than aspirin and a small dose of statin drugs. Comprehensive management of ACS should include lifestyle modification, effective blood pressure control, antiplatelet

Metabolic vitamin B12 deficiency

Metabolic B12 deficiency is common (30% of patients over age 71 attending a stroke prevention clinic)43 and frequently missed, because serum B12 measures total B12, not active B12. To ascertain adequacy of functional B12, it is necessary to measure holotranscobalamin, or to assess the function of B12 by measuring methylmalonic acid, or in folate-replete patients, total homocysteine (tHcy). High levels of tHcy increase the risk fourfold among patients with atrial fibrillation,44 and are

Current Guidelines

A PubMed search on the terms “asymptomatic carotid stenosis” and “guideline” (publication type) or “consensus development conference” (publication type) yielded 4 references.48, 49, 50, 51 Of these, one was a paper about research priorities of the Society for Vascular Surgery, with no guideline provided51; two were Italian national guidelines from 200648 and 2009,49 and one was an Australasian guideline from 2010.50 In addition, there is a guideline from the American Academy of Neurology,52 a

Summary

Patients with ACS are at high risk of myocardial infarction and require intensive medical therapy; such therapy has reduced the risk of stroke to well below the risk of carotid endarterectomy or stenting. Most patients with ACS should be treated only with intensive medical therapy including lifestyle change. The few patients who could benefit from revascularization can be identified by procedures such as microembolus detection on TCD, and most of these should be offered endarterectomy in

Disclosures

Dr J.D. Spence has received grants from the Canadian Institutes for Heath Research, Heart & Stroke Foundation of Canada (HSF), and the National Institute of Health/National Institute of Neurologic Disorders and Stroke. Lecture honoraria/travel support/consulting fees were provided by Sanofi-Synthelabo, Bayer, Merck and Boehringer Ingelheim. Research support for investigator-initiated projects was provided by Pfizer (substantial donation in kind of study medication to support HSF grant for

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