Introduction. Clinical manifestations

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1 Carotid bruit Seemant Chaturvedi MD (Dr. Chaturvedi of Wayne State University received grant support from Boehringer Ingelheim and consulting fees from Merck.) Steven R Levine MD, editor. (Dr. Levine of the SUNY Health Science Center at Brooklyn has received honorariums from Genentech for service on a scientific advisory committee and a research grant from Genentech as a principal investigator.) Originally released April 24, 1995; last updated September 4, 2015; expires September 4, 2018 Introduction This article includes discussion of carotid bruit, cervical murmur, asymptomatic bruits, and symptomatic bruits. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations. Overview The author summarizes new information on management of patients with asymptomatic carotid bruits. Information regarding risk stratification for patients with asymptomatic carotid stenosis is presented. The recommendation against screening for asymptomatic carotid stenosis is provided. Comparative data on carotid endarterectomy and stenting are also provided. Finally, clinical trials that have been launched for this patient population are described. Key points Asymptomatic carotid stenosis is present in 4% to 6% of subjects age 65 years and older. Asymptomatic carotid stenosis increases the stroke risk to a slight degree, but the risk is much lower compared to symptomatic patients. Carotid endarterectomy can be useful for highly select patients if the major complication rate is low (less than 3%) and if the patient has at least a 5-year life expectancy. Intensive medical therapy is needed for all patients with carotid stenosis. Historical note and terminology The earliest report linking carotid artery disease with stroke is credited to Savory, who, in 1856, described a young woman with left monocular symptoms in combination with a right hemiplegia. Postmortem examination revealed an occlusion of the cervical portion of the left internal carotid artery. In 1914, Hunt emphasized the connection between obstructive lesions of the carotid artery and the development of neurologic symptoms. In 1957, Fisher brought attention to the relationship between carotid artery bruit and cerebrovascular disease when he described a 69-year-old woman with carotid artery bruits bilaterally who had sudden onset of weakness in her right leg (Fisher 1957). He also pointed out that lesions could result in either stenosis or total occlusion. In the following decade, these observations were confirmed, and a carotid bruit localized to the carotid bifurcation was considered to be indicative of carotid atherosclerosis. Clinical manifestations Presentation and course Localized bruits in the mid- and upper-regions of the neck, below the angle of the jaw, correlate well with underlying occlusive disease at the carotid bifurcation. The bruit is typically systolic in timing but varies in intensity. Bruits usually appear when the diameter stenosis is 50% or greater (corresponding to a 75% reduction in cross-sectional area) and may actually disappear at a diameter stenosis of greater than 90%. As the stenosis progresses from 50% to 90%, the bruit becomes louder and higher-pitched. A diastolic component is suggestive of more than 90% luminal narrowing with associated reduction in blood flow. A bruit over the carotid artery found in conjunction with a history of a hemispheric transient ischemic attack or retinal transient ischemic attack (amaurosis fugax) is likely to reflect a clinically significant, correctable carotid stenosis. Hemispheric symptoms include contralateral hemiparesis, contralateral paresthesia or hemisensory changes, visual field defects, and aphasia (dominant hemisphere) or neglect

2 (nondominant hemisphere). Prognosis and complications Patients with asymptomatic carotid bruits are approximately 3 times more likely to have an ischemic stroke than an age- and sex-matched population without carotid bruits. When patients with asymptomatic bruits from Framingham, Massachusetts, and Evans County, Georgia, were followed prospectively, the annual stroke rates were 1.9% (Wolf et al 1981) and 2.4% (Heyman et al 1980), respectively; the strokes were often contralateral to the bruit. In a prospective study among 566 patients with asymptomatic carotid bruits, the annual stroke rate was 1.5% compared to 0.5% in a population-based cohort of 428 patients (Wiebers et al 1982). Some investigators have suggested that a history of contralateral TIAs and renal dysfunction indicate increased stroke risk in patients with asymptomatic stenosis (Nicolaides et al 2005). Subsequent cerebral ischemic events were not significantly different in patients with localized versus diffuse bruits. Prognostic information from randomized trials is provided below. A systematic review found that with improvements in medical therapy, there has been a decrease in the stroke rate with asymptomatic carotid stenosis over the past 25 years (Abbott 2009). In the past decade, the annual rate of stroke has fallen below 1.5% per year, in the range where it overlaps with the stroke rate in patients treated surgically. Patients with asymptomatic carotid stenosis may be at increased risk for cognitive decline. A study followed 210 patients with greater than 70% stenosis with no previous history of stroke and 109 healthy control subjects (Balestrini et al 2013). Patients with carotid stenosis, especially those with impaired hemodynamic response to breath holding, were at increased risk for cognitive worsening over a 3 year follow-up period (odds ratio 4.16). Patients with asymptomatic stenosis need to live several years after carotid endarterectomy in order to benefit from the procedure and offset the upfront stroke risk from carotid endarterectomy. A study from Sweden showed that mortality among asymptomatic patients who undergo carotid endarterectomy is substantial (Kragsterman et al 2006). The 5-year survival in this series was 78.2% after 5 years and 45.5% after 10 years. Previous vascular surgery, cardiac disease, diabetes, and increasing age were predictors of decreased survival. Using transcranial Doppler to assess for microemboli can be useful in risk stratification. Two studies found that the occurrence of active microemboli is fairly low in subjects with asymptomatic carotid stenosis (Markus et al 2010; Spence et al 2010). In the Asymptomatic Carotid Emboli Study (ACES), 77 of 467 (16%) patients had evidence for microemboli at baseline. At 2 years, the risk of ipsilateral stroke was 3.6% in patients with microemboli and 0.7% in patients without microemboli (Markus et al 2010). Patients with progression of stenosis on serial duplex ultrasound (DUS) studies by 2 or more stenosis categories have an increased risk of TIA or stroke (Hirt 2014). Clinical vignette A 49-year-old man was referred to the neurology clinic with an asymptomatic left carotid bruit. The patient had a history of hypertension, diabetes, hypercholesterolemia, and mild obesity. The patient denied previous symptoms such as monocular visual loss, right-sided weakness or numbness, or speech difficulty. He had a carotid ultrasound that revealed 50% to 79% left carotid stenosis, shown to be 70% on angiography. He was placed on aspirin, simvastatin, an angiotensin-converting enzyme inhibitor, and continued on his regimen for diabetes. An exercise and weight loss regimen was encouraged. The patient was followed with serial ultrasound exams and the carotid stenosis remained stable over the next 5 years; he remains asymptomatic. The patient also remains free of ischemic heart disease. Biological basis Etiology and pathogenesis Atherosclerosis causing a stenosis of more than 50% of the carotid diameter is the most common cause of this bruit. A bruit may also be caused by conditions that increase turbulent flow. This may be anatomical (eg, vessel kinking) or rheological (eg, lowered viscosity with anemia). The velocity profile of circulating blood is laminar and, therefore, motion is soundless. Murmurs are created when laminar flow is disturbed by alterations in biophysical characteristics such as velocity, viscosity, and vessel wall anatomy. Experimental work has shown that for any degree of stenosis there is a given blood flow rate that produces jet instability with associated turbulence that will produce a bruit (Sacks et al 1971). Increasing the degree of stenosis

3 increases both the amount of turbulence and the likelihood of detecting a bruit. Carotid bruits have been described with a residual lumen diameter of 0.8 mm to 3.0 mm (normal mean carotid artery diameter 5.1 mm mm). It is, therefore, possible to hear a bruit with stenoses as low as 25% or even lower in high blood flow conditions. Theoretically, when the artery is occluded there should be no turbulence and, thus, no bruit. However, bruits are still audible in as many as 21% of patients with occluded internal carotid arteries (Ingall et al 1989). The most likely mechanism of bruit production with an occluded internal carotid artery is flow disturbance in a stenotic external carotid artery. Epidemiology" The number of patients with asymptomatic carotid bruits is large; approximately 12.6% of the population older than 45 years of age have been noted to have some type of cervical murmur (Sandok et al 1982). Approximately one third of these murmurs are localized carotid bifurcation bruits, and about three fourths of the persons with localized bruits have had neither hemispheric nor retinal ischemic symptoms. The number of patients with actual asymptomatic carotid stenosis is estimated at 4% to 6% in patients age 65 and above. After a systematic review of the literature, the United States Preventive Services Task Force recommended that the general population should not be screened for asymptomatic carotid stenosis, primarily due to concerns that clinical trials of carotid endarterectomy may not be reproduced in clinical practice (LeFevre and U.S. Preventive Services Task Force 2014). Prevention All patients with carotid bruits should be evaluated for the presence of atherosclerotic risk factors, such as smoking, lipid disorders, hypertension, and diabetes mellitus. Atherosclerosis involving the cerebrovasculature is associated with the same risk factors as atherosclerosis elsewhere, particularly hypertension. A comprehensive approach to risk factor reduction including hypertension control, cessation of smoking, normalization of the lipid profile, attainment of ideal body weight, and regular exercise is appropriate in all patients with cerebrovascular disease. The presence of carotid bifurcation disease is also a strong clinical marker for coronary atherosclerosis. In 2003, the American Stroke Association published a statement on coronary risk evaluation in patients with TIA or ischemic stroke (Adams et al 2003). Due to the fact that 30% to 50% of patients with carotid atherosclerosis will have underlying coronary heart disease, the statement comments that clinicians should consider coronary heart disease testing when the workup reveals carotid or other large-vessel atherosclerosis. The evaluation and management of patients with combined carotid and coronary occlusive disease are controversial and must be individualized based on symptoms, anatomy, and hemodynamic considerations. Differential diagnosis Cervical murmurs can be classified by their location and acoustic characteristics (Sandok et al 1982). Venous cervical murmurs ("hums") are common in children but may occur in up to 27% of normal adults. Venous hums are usually heard at the base of the neck and their sound is low-pitched, roaring, usually continuous, maximal during diastole, loudest in the upright position, and decreased or abolished by the Valsalva maneuver. Arterial bruits in the neck can be divided into supraclavicular, vertebral, and carotid. Supraclavicular bruits are diffuse and can be heard along the length of the carotid artery. They are frequently bilateral and systolic in timing. These murmurs are commonly due to transmission of heart sounds (aortic stenosis and other aortic outflow murmurs, mitral insufficiency, coarctation of the aorta, and patent ductus arteriosus), structural changes affecting the vessels at the base of the neck (atherosclerosis, subclavian tortuosity, Takayasu disease, or conditions associated with thoracic outlet syndrome), or a hyperdynamic state (hemodialysis, fever, anemia, and hyperthyroidism). Vertebral bruits are heard from the supraclavicular fossa to the mastoid region, along the posterior border of the sternocleidomastoid muscle. The sound is usually systolic but may extend into diastole. Vertebral bruits are associated with stenoses of the origin of the vertebral artery, bilateral carotid artery occlusion, reversal of blood flow in the vertebral artery, and hemangioma of the brainstem. Localized bruits in the mid- and upper-regions of the neck are, in most instances, due to atherosclerotic lesions in the proximal internal carotid artery. However, systolic bruits having identical acoustic characteristics may result from external carotid artery stenoses and may be heard with nonatherosclerotic lesions such as fibromuscular dysplasia or buckling and tortuosity of the carotid arteries.

4 Diagnostic workup Although the clinical implications of neck auscultation remain uncertain, invasive diagnostic tests are not indicated in every patient with a carotid bruit. Noninvasive carotid evaluation by duplex scanning facilitates accurate correlation of cervical bruits with extracranial arterial anatomy. Combining ultrasound imaging and Doppler assessment of blood flow, the duplex scan provides relevant information regarding the carotid bifurcation. Doppler techniques measure the frequency of the sound reflected from red blood cells. The faster the speed of the red cells, the higher the frequency of the reflected sound. An increasing stenosis produces a smaller lumen leading to a higher flow velocity. The ability of duplex imaging to distinguish between severe stenoses and mild stenoses is excellent, with a reported specificity of 84% and sensitivity of 99% (Roederer et al 1984). Some centers recommend surgery based on duplex scanning alone. In some centers, however, preoperative, confirmatory contrast arteriography is recommended. Contrast angiography, however, remains the gold standard for the diagnosis of carotid artery stenosis. Either conventional or digital subtraction techniques provide excellent images of the head and neck and the intracranial circulation. Computed tomography of the brain and MRI are used to identify prior infarcts as well as to exclude other intracranial lesions. Magnetic resonance angiography may provide an appropriate alternative to conventional contrast angiography in some patients, and some centers perform carotid surgery on the basis of a combined battery of duplex ultrasound and MRA, reserving angiography for discordant cases. Contrast-enhanced MRA may improve the accuracy of conventional MRA imaging and can be used in a noninvasive battery of carotid stenosis tests (U-King-Im et al 2004). CT angiography is also increasingly being performed in some centers. An overview of the pros and cons of different imaging modalities has been reviewed (Romero et al 2005). The hemodynamic significance of a carotid bruit (sufficiency of distal flow preservation or collateralization) can be evaluated by ocular pneumoplethysmography (systolic pressure reduction in the ophthalmic artery reflects a hemodynamically significant lesion) or transcranial Doppler. Transcranial Doppler also allows the assessment of microemboli in patients with extracranial carotid stenosis. A study of 319 patients who had greater than 60% asymptomatic carotid stenosis and transcranial Doppler exams with subsequent clinical follow-up indicated that patients with microemboli were at significantly higher risk for stroke at 1 year (15.6%) compared to patients without microemboli (1%) (Spence et al 2005). Ninety percent of these patients did not have microemboli at baseline, suggesting that the majority of patients are at low risk. With newer imaging modalities, there is the potential to investigate vascular inflammation. A report described MRI with a contrast agent, an ultrasmall superparamagnetic iron oxide (USPIO), in the asymptomatic carotid artery contralateral to a symptomatic stenosis (Tang et al 2006). In a preliminary study with 20 patients, 57% of regions analyzed on the asymptomatic side had inflammatory activity compared to 71% on the symptomatic side (p=0.007). Further studies are needed to see whether this is a useful marker for risk stratification. Management The detection of an asymptomatic carotid bruit invariably engenders considerable debate and uncertainty about proper evaluation and management. Which noninvasive tests should be performed? Should angiography be performed if the noninvasive tests suggest a moderate or severe stenosis? Should brain imaging be performed to search for asymptomatic infarcts? When is carotid endarterectomy or carotid stenting indicated for asymptomatic stenosis? All patients with cervical bruits, whether or not they are symptomatic, should be evaluated by noninvasive Doppler ultrasound to determine if the bruit reflects a significant internal carotid artery stenosis. Some centers recommend CT scans or MRI of the brain on all patients to either delineate old strokes in asymptomatic patients or exclude other intracranial lesions in symptomatic patients. However, routine CT scans on all patients with carotid stenoses may not be cost effective. Asymptomatic bruits. If, based on a thorough history, the patient is truly asymptomatic and Doppler studies demonstrate a stenosis of less than 80%, then conservative management with antiplatelet therapy such as aspirin and risk factor modification is appropriate for most patients. Anticoagulation with warfarin is not recommended. Patients with greater than 60% stenosis should be treated for hyperlipidemia, and the LDL level should be targeted for less than 100 mg/dl. If the patient has extensive vascular disease or a strong risk factor profile, a LDL of less than 70 mg/dl can be considered. Statin treatment will be useful in many patients. In carotid endarterectomy specimens, use of statins has been associated with reduced macrophage infiltration and matrix metalloproteinase 9 area, suggesting that

5 statins can be useful in stabilizing carotid plaques (Kunte et al 2008). Smoking cessation should be strongly encouraged. Asymptomatic patients with stenoses between 60% and 79% should be re-evaluated every 6 to 12 months with noninvasive studies to determine if there has been progression of stenosis. If, during follow-up, the patient becomes symptomatic or the lesion progresses, then further evaluation is warranted. Plaque morphology, as it becomes better defined and classified, may significantly influence clinical decision making in the future. Asymptomatic patients with high-grade (greater than 80%) stenoses by Doppler ultrasound who are good operative risks with excellent 5-year life expectancies should receive further evaluation with either MRA or contrast angiography. The Asymptomatic Carotid Atherosclerosis Study evaluated patients with 60% to 99% asymptomatic carotid stenosis and found a modest reduction in ipsilateral stroke with carotid endarterectomy (CEA) (Anonymous 1995). At 5 years, the projected rate of ipsilateral stroke was 11.0% in the medically treated patients and 5.1% in the surgery group. The annual absolute risk reduction of 1.2% per year is small, and some vascular neurologists have argued that it is not clinically meaningful. In addition, concerns have been raised about whether the low perioperative stroke rate in the Asymptomatic Carotid Atherosclerosis Study can be reproduced routinely in the community. Current recommendations are that for asymptomatic patients, the perioperative stroke rate should be less than 3% (Biller et al 1998), yet the stroke rate for asymptomatic patients was 4.6% in the Aspirin and Carotid Endarterectomy trial, which featured experienced surgeons at stroke centers. In addition, in up to 45% of patients with asymptomatic carotid stenosis, the future cause of an ipsilateral stroke may not be related to the carotid stenosis, with the cause being either cardioembolism or small vessel occlusive disease (Inzitari et al 2000). If a practitioner is confident that the perioperative stroke rate is less than 3% at their institution and if the patient is otherwise healthy and with a 5-year life expectancy, then there may be a small benefit for performing carotid endarterectomy in patients with 60% to 99% stenosis. This position was articulated in the American Academy of Neurology carotid endarterectomy guidelines (Chaturvedi et al 2005). The Asymptomatic Carotid Surgery Trial (ACST) results have been published (MRC ACST Collaborative Group 2004). This was a multicenter international study in which patients with more than 60% stenosis were randomized to immediate carotid endarterectomy or deferred carotid endarterectomy. Patients in the deferred carotid endarterectomy group were treated medically. Approximately 90% of patients were on antiplatelet therapy, 70% were on antihypertensive agents, and 40% were on lipid lowering medication. Enrolled were 3120 patients who were followed for a mean period of 3.3 years. The 5-year projected rates of total ischemic stroke were 11.8% in the deferred carotid endarterectomy group and 6.4% in the immediate carotid endarterectomy group. About half of strokes in both groups were disabling. The benefit was smaller in women compared to men. Patients younger than 75 years of age demonstrated benefit, but it was unclear if patients older than 75 years of age derived benefit because their death rate was higher during the follow-up period. The overall perioperative morbidity and mortality rate was 3.1% in the ACST. The ACST results resonate fairly well with Asymptomatic Carotid Atherosclerosis Study. The overall results show that the stroke rate can be reduced from approximately 2% per year to 1% per year. However, this is predicated on careful patient selection and excellent surgical results. As pointed out in an editorial by Barnett, real world surgical results do not always match clinical trial performance, and the benefits shown in the ACST could be obliterated if the perioperative complication rate exceeds the trial results (Barnett 2004). In addition, one would need to operate on approximately 40 patients to prevent 1 disabling stroke, which raises questions about the cost effectiveness of this approach for the health care system. The ACST investigators have also reported 10-year results (Halliday 2010). At 10 years, there was still a benefit for carotid endarterectomy, but it was lower in absolute terms. The immediate carotid endarterectomy group had a 10- year stroke risk of 13.4% compared to 17.9% in the deferred carotid endarterectomy group (absolute gain 4.6%). Patients ages 75 years and older once again did not show clear benefit. Stroke risk in both the carotid endarterectomy and medical therapy group were substantially lower in the patients who received lipid-lowering treatment. In a combined analysis of Asymptomatic Carotid Atherosclerosis Study and ACST, it was noted that there was no clear benefit for carotid endarterectomy in asymptomatic women (Rothwell and Goldstein 2004). One of the potential reasons for this finding is that women seem to do better with medical therapy. In a study evaluating endarterectomy specimens, women had more features of stable plaques such as low macrophage staining and strong smooth muscle staining (Hellings et al 2007).

6 Carotid artery stenting (CAS) is increasingly being considered as an alternative to carotid endarterectomy and in fact, most carotid stenting is being performed in asymptomatic patients. The SAPPHIRE trial found that patients at high medical risk for endarterectomy who were subsequently randomized to stenting or endarterectomy had a lower risk of stroke, myocardial infarction, or death with stenting (12.2% at 1 year) compared to surgery (20.1%) (Yadav et al 2004). However, the study did not include a control group who were treated medically and it remains unclear as to whether stenting is superior to intensive medical therapy in patients considered high risk for endarterectomy. In the 3- year results of the SAPPHIRE study, there was not a clear difference between carotid endarterectomy and carotid artery stenosis (Gurm et al 2008). The relatively high death rate in both groups raises questions about whether either procedure is necessary in high risk for carotid endarterectomy asymptomatic patients. The Carotid Revascularization Endarterectomy versus Stenting Trial (CREST) was reported in 2010 (Brott et al 2010). This study enrolled conventional risk patients and subjects were assigned to either carotid endarterectomy or carotid artery stenting. The study originally included symptomatic patients only, but asymptomatic patients with more than 60% stenosis on angiography or more than 70% stenosis on ultrasound were included in The study was not powered to detect a difference in the 1176 asymptomatic patients, however. The primary endpoint of stroke, myocardial infarction, or death within 30 days or ipsilateral stroke after 30 days did not differ between the 2 groups (carotid artery stenting 3.5%, carotid endarterectomy 3.6%) (Brott et al 2010). At 4 years, there was a trend favoring carotid endarterectomy if periprocedure myocardial infarction events are not included (carotid artery stenting 4.5%, carotid endarterectomy 2.7%, p=0.07). Carotid artery stenting is not currently approved for conventional risk patients. In the interim other studies are ongoing, including the Asymptomatic Carotid Trial 1 (ACT-1), which is randomizing conventional risk patients to endarterectomy or stenting. In community practice, carotid endarterectomy appears to have better outcomes than carotid stenting. In an analysis of over 20,000 patients treated at 186 hospitals in the United States, the in-hospital stroke and death rate was 4.0% with carotid stenting and 1.5% with carotid endarterectomy (Choi et al 2015). This difference remained statistically significant (p<0.001) after adjustment for baseline characteristics. A systematic analysis found that results of carotid endarterectomy are improving. Registry and clinical trial showed an average 6% reduction in major complications during the period 1991 to 2010 (Munster et al 2015). The authors proposed that the new benchmarks for an asymptomatic patient should be stroke/death less than 1.2% and a periprocedural mortality rate of less than 0.4%. Evidence is accumulating that improvements in medical therapy have led to a reduction in stroke risk for patients with asymptomatic carotid stenosis. In the Oxford Vascular Study, 101 patients with greater than 50% carotid stenosis were treated medically (Marquardt et al 2010). During a mean of 3 years follow-up, only one minor stroke and 5 transient ischemic attacks occurred. The annual stroke risk was 0.34%. A study from the Netherlands followed 293 patients with asymptomatic stenosis of 50 to 99% for a mean period of 6.2 years. The any territory risk of stroke was 0.4% in patients with 50 to 99% stenosis and 0.5% in patients with 70 to 99% stenosis (den Hartog et al 2013). This study, along with the transcranial Doppler studies mentioned above, suggests that carotid revascularization may not be necessary in the majority of patients with asymptomatic carotid stenosis. Due to the advances in medical therapy, some have advocated multi-center clinical trials to compare aggressive medical therapy (AMT) alone versus AMT plus carotid revascularization (Chaturvedi 2003). Funding was announced for the CREST 2 study. The CREST 2 study was launched to compare AMT alone versus either AMT plus carotid endarterectomy or AMT plus carotid stenting (Chaturvedi and Sacco 2015). AMT consists of aspirin, high dose statin therapy with a LDL goal of less than 70 mg/dl, blood pressure reduction targeted to national guidelines, and lifestyle modification. This North American study will have 2 parallel trials comparing AMT alone versus AMT plus carotid endarterectomy and AMT alone versus AMT plus carotid stenting. Similar trials are being conducted in Europe. Symptomatic bruits. Patients with hemispheric transient ischemic attacks or amaurosis fugax associated with lesions of less than 50% by ultrasound should be treated with aspirin and risk factor modification. If the patient has had recent symptoms (in the previous 6 months) and if there is severe (greater than 70%) stenosis, then carotid endarterectomy will be of benefit in reducing the stroke rate if the patient is an otherwise stable surgical candidate and the surgery can be performed with a less than 6% stroke rate (North American Symptomatic Carotid Endarterectomy Study Group 1991). For patients with 50% to 69% stenosis, carotid endarterectomy is likely to be of a greater benefit in patients with hemispheric as opposed to retinal symptoms, patients with ulcerated lesions as opposed to smooth lesions, and men compared to women (Barnett et al 1998; Chaturvedi et al 2005).

7 Special considerations Pregnancy Little information is available. Carotid bruits, like cardiac outflow murmurs, may be more frequent in pregnant women. This may be related to an increased cardiac output (increased flow) or decreased blood viscosity (decreased hematocrit) associated with pregnancy. Anesthesia All patients during carotid endarterectomy should at least have continuous monitoring of blood pressure (by intraarterial catheter) and ECG. The most commonly used regional techniques include superficial cervical plexus block, local infiltration, and deep interscalene block. The advocates of regional techniques claim a better ability to assess the patient's neurologic status, a lower incidence of perioperative myocardial infarction (Zuccarello et al 1988), a decreased incidence of blood pressure fluctuations in the perioperative period, and a hospital cost savings related to a decrease in intensive care unit requirements (Gableman et al 1983). The evaluation of neurologic status under regional anesthesia allows for a rapid and accurate decision regarding the need for intraluminal shunting during carotid endarterectomy. General anesthesia with EEG monitoring, on the other hand, has the advantage of reducing the cerebral metabolic demand of the brain while increasing cerebral blood flow and provides for good airway control, reduced patient anxiety, and a quiet surgical field. The reliability of EEG monitoring in predicting which patients will require shunts has, however, been questioned (Pruitt 1983). A trial of 3526 patients in which patients were randomly assigned to treatment with general or local anesthesia found no difference in the rate of stroke, death, or myocardial infarction within 30 days of surgery (GALA Trial Collaborative Group et al 2008). Regardless of the anesthesia technique chosen, 2 objectives must be met in all patients undergoing carotid endarterectomy: (1) to provide a safe approach in patients with multisystem vascular disease, and (2) to allow for reliable, continuous neurologic monitoring. References cited Abbott AL. Medical (nonsurgical) intervention alone is now best for prevention of stroke associated with asymptomatic severe carotid stenosis: results of a systematic review and analysis. Stroke 2009;40(10):e PMID Adams RJ, Chimowitz MI, Alpert JS, et al. Coronary risk evaluation in patients with transient ischemic attack and ischemic stroke: a scientific statement for healthcare professionals from the Stroke Council and the Council on Clinical Cardiology of the American Heart Association/American Stroke Association. Stroke 2003;34(9): PMID Anonymous. Endarterectomy for asymptomatic carotid artery stenosis. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. JAMA 1995;273(18): PMID Balestrini S, Perozzi C, Altamura C, et al. Severe carotid stenosis and impaired hemodynamics can influence cognitive deterioration. Neurology 2013;80(23): PMID Barnett HJ. Carotid endarterectomy. Lancet 2004;363(9420): PMID Barnett HJ, Taylor DW, Eliasziw M, et al. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis: North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med 1998;339(20): PMID Biller J, Feinberg WM, Castaldo JE, et al. Guidelines for carotid endarterectomy: a statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke 1998;29(2): PMID Brott TG, Hobson RW 2nd, Howard G, et al. Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med 2010;363: PMID Chaturvedi S. Should the multicenter carotid endarterectomy trials be repeated. Arch Neurol 2003;60(5): PMID

8 Chaturvedi S, Bruno A, Feasby T, et al. Carotid endarterectomy-an evidence-based review: Report of the TTA Subcommittee of the AAN. Neurology 2005;65: PMID Chaturvedi S, Sacco RL. How recent data have impacted the treatment of internal carotid artery stenosis. J Am Coll Cardiol 2015;65(11): PMID Choi JC, Johnston SC, Kim AS. Early outcomes after carotid artery stenting compared with endarterectomy for asymptomatic carotid stenosis. Stroke 2015;46(1): PMID den Hartog AG, Achterberg S, Moll FL, et al. Asymptomatic carotid artery stenosis and the risk of ischemic stroke according to subtype in patients with clinical manifest arterial disease. Stroke 2013;44(4): PMID Fisher CM. Cranial bruit associated with occlusion of the internal carotid artery. Neurology 1957;7: PMID Gableman CG, Gann DS, Ashworth CJ, Carney WI. One hundred consecutive reconstructions: local vs. general anesthesia. Am J Surg 1983;145: GALA Trial Collaborative Group, Lewis SC, Warlow CP, et al. General anesthesia versus local anaesthesia for carotid surgery (GALA): a multicentre, randomised controlled trial. Lancet 2008;372(9656): PMID Gurm H, Yadav JS, Fayad P, et al. Long-term results of carotid stenting versus endarterectomy in high-risk patients. N Engl J Med 2008;358(15): PMID Halliday A, Harrison M, Hayter E, et al. 10-year stroke prevention after successful carotid endarterectomy for asymptomatic stenosis (ACST-1): a multicenter randomized trial. Lancet 2010;376: PMID Hellings WE, Pasterkamp G, Verhoeven BA, et al. Gender associated differences in plaque phenotype of patients undergoing carotid endarterectomy. J Vasc Surg 2007;45(2): PMID Heyman A, Wilkinson W, Heyden S, et al. Risk of stroke in asymptomatic persons with cervical arterial bruits: a population study in Evans County, Georgia. N Engl J Med 1980;302:838. PMID Hirt LS. Progression rate and ipsilateral neurological events in asymptomatic carotid stenosis. Stroke 2014;45(3): PMID Ingall T Homer D, Whisnant J, Baker H, O'Fallon W. Predictive value of carotid bruit for carotid atherosclerosis. Arch Neurol 1989;46:418. PMID Inzitari D, Eliasziw M, Gates P, et al. The causes and risk of stroke in patients with asymptomatic internal-carotid-artery stenosis: North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med 2000;342(23): PMID Kragsterman B, Bjorck M, Lindeback J, Berggvist D, Parsson H; Swedish Vascular Registry (Swedvasc.). Long-term survival after carotid endarterectomy for asymptomatic stenosis. Stroke 2006;37: PMID Kunte H, Amberger N, Busch MA, Ruckert RI, Meiners S, Harms L. Markers of instability in high-risk carotid plaques are reduced by statins. J Vasc Surg 2008;47(3): PMID LeFevre ML, U.S. Preventive Services Task Force. Screening for asymptomatic carotid artery stenosis: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med 2014;161(5): PMID Markus H, King A, Shipley M, et al. Asymptomatic embolization for the prediction of stroke in the Asymptomatic Carotid Emboli Study (ACES): A prospective observational study. Lancet Neurol 2010;9: PMID Marquardt L, Geraghty OC, Mehta Z, Rothwell PM. Low risk of ipsilateral stroke in patients with asymptomatic carotid stenosis on best medical treatment. Stroke 2010;41:e11-7. PMID

9 MRC Asymptomatic Carotid Surgery Trial (ACST) Collaborative Group. Prevention of disabling and fatal strokes by successful carotid endarterectomy in patients without recent neurological symptoms: randomized controlled trial. Lancet 2004;363: Munster AB, Franchini AJ, Qureshi MI, Thapar A, Davies. Temporal trends in safety of carotid endarterectomy in asymptomatic patients: systematic review. Neurology 2015;85(4): PMID Nicolaides A, Kakkos S, Griffin M, Geroulakos G, Ioannidou E. Severity of asymptomatic carotid stenosis and risk of ipsilateral hemispheric ischaemic events: Results from the ACSRS study. Eur J Vasc Endovasc Surg 2005;30: PMID North American Symptomatic Carotid Endarterectomy Study Group. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991;325: PMID Pruitt JC consecutive carotid endarterectomies using local anesthesia, EEG, and selective shunting with Pruitt- Inahara carotid shunt. Contemp Surg 1983;23: Roederer G, Langlois Y, Jager K, et al. The natural history of carotid arterial disease in asymptomatic patients with cervical bruits. Stroke 1984;15(4):605. PMID Romero JM, Ackerman RH, Dault NA, Lev MH. Noninvasive evaluation of carotid artery stenosis: indications, strategies, and accuracy. Neuroimaging Clin N Am 2005;15: PMID Rothwell PM, Goldstein LB. Carotid endarterectomy for asymptomatic stenosis: asymptomatic carotid surgery trial. Stroke 2004;35(10): PMID Sacks AH, Tickner EG, Macdonald IB. Criteria for the onset of vascular murmurs. Circ Res 1971;29(3): PMID Sandok B, Whisnant J, Furlan A, Mickell J. Carotid artery bruits: prevalence survey and differential diagnosis. Mayo Clin Proc 1982;57:227. PMID Spence JD, Tamayo A, Lownie SP, Ng WP, Ferguson GG. Absence of microemboli on transcranial Doppler identifies lowrisk patients with asymptomatic carotid stenosis. Stroke 2005;36: PMID Spence JD, Coates V, Li H, et al. Effects of intensive medical therapy on microemboli and cardiovascular risk in asymptomatic carotid stenosis. Arch Neurol 2010; 67: PMID Tang T, Howarth SP, Miller SR, et al. Assessment of inflammatory burden contralateral to the symptomatic carotid stenosis using high-resolution ultrasmall, superparamagnetic iron oxide-enhanced MRI. Stroke 2006;37: PMID U-King-Im JM, Trivedi RA, Graves MJ, et al. Contrast-enhanced MR angiography for carotid disease. Neurology 2004;62(8): PMID Wiebers D, Folger W, Forbes G, Younge B, O'Fallon W. Ophthalmodynamometry and ocular pneumoplethysmography for detection of carotid occlusive disease. Arch Neurol 1982;39:690. PMID Wolf PA, Kannel WB, Sorlie P, McNamara P. Asymptomatic carotid bruit and risk of stroke: the Framingham study. JAMA 1981;245: PMID Yadav JS, Wholey MH, Kuntz RE, et al. Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med 2004;351: PMID Zuccarello M, Yeh H, Tew JM. Morbidity and mortality of carotid endarterectomy under local anesthesia: a retrospective study. Neurosurgery 1988;23: PMID **References especially recommended by the author or editor for general reading.

10 Former authors Richard Gusberg MD ICD and OMIM codes ICD codes ICD-9: Occlusion and stenosis of carotid artery: ICD-10: Occlusion and stenosis of carotid artery: I65.2 Profile Age range of presentation years years 65+ years Sex preponderance male=female Family history none Heredity none Population groups selectively affected none selectively affected Occupation groups selectively affected none selectively affected Differential diagnosis list venous cervical murmurs venous hums arterial bruits supraclavicular bruits vertebral bruits localized bruits systolic bruits fibromuscular dysplasia Associated disorders Amaurosis fugax Cardiovascular disease Hemispheric stroke Intracranial stenosis Thromboembolic stroke

11 Transient ischemic attacks Vertebrobasilar disease Other topics to consider Carotid transient ischemic attacks Ischemic stroke Neurologic complications of cardiovascular procedures Objective tinnitus Copyright MedLink Corporation. All rights reserved.