Carotid endarterectomy

Carotid Stenosis and Endarterectomy

Neurovascular Intensive Course

24-29 March 2008

Carotid Stenosis• The prevalence of hemodynamically significant carotid stenosis varies with

age and other risk factors. • Estimates indicate that 5 per 1000 persons aged 50-60 years and

approximately 10% of persons older than 80 years have carotid stenosis greater than 50%.

• Patients with carotid artery stenosis are at increased risk for subsequent stroke, myocardial infarction (MI), and death.

• The proportion of all strokes attributable to previously asymptomatic carotid stenosis is small; however in patients older than 60 years who have cerebral infarction, approximately 15% have ipsilateral carotid stenosis of 70% or greater.

• The frequency of hemodynamically significant carotid artery stenosis is higher in symptomatic patients than in asymptomatic patients.

• In 40-50% of those with a complete stroke, the primary etiology of the stroke is related to extracranial carotid disease (stenosis).

Carotid Stenosis• Unlike other cerebral vessels, the internal carotid artery is not an end

vessel. In most individuals it is in continuity with the vessels of the circle of Willis and those of the orbit, and no part of the brain is completely dependent on it.

• Therefore occlusion, which occurs most frequently in the first part of the internal carotid artery (immediately beyond the carotid bifurcation), is often silent (30 to 40 percent of cases).

• The syndromes caused by common carotid occlusion are identical to those of its internal branch, the internal carotid artery.

• The clinical manifestations of atherosclerotic thrombotic disease of this artery are among the most variable of any cerebrovascular syndrome.

• If the bifurcation is patent, few if any symptoms may result, in some cases because retrograde flow from the external carotid maintains internal carotid flow and perfusion of the brain.

Sites of Stenosis• Stenotic changes are most prominent along the posterior wall of the

common and internal carotid arteries. Thus the lateral projection often best depicts the severity of the narrowing.

• The region of the common carotid bifurcation and proximal internal carotid artery is by far the most common site of involvement.

• At this location, stenosis greater than 50 per cent is about two to three times more common than complete arterial occlusion.

• Common carotid occlusion accounts for less than 1 percent of cases of carotid artery syndrome—the remainder being due to disease of the internal carotid artery itself

• The common carotid can be occluded by an atheromatous plaque at its origin, more often on the left side.

• The second most frequent site of involvement is the vertebral artery. Unlike the carotid system, stenosis and occlusion are about equal in occurrence.

• Intracranial arterial stenosis or occlusion is uncommon. Individually, the basilar, intracranial carotid, and proximal circle of Willis arteries are each involved in 1 to 4 per cent of patients.

Stroke Syndromes• Ischemia involving individual vascular territories causes specific

clinical stroke syndromes.• Acute Management :objective of treatment is to restore blood flow to

the brain.– Thrombolytic agents such as recombinant tissue plasminogen activator

have been used to break up the occlusive intracranial emboli and restore blood flow.

– Antiplatelet and anticoagulation with warfarin is begun for patients with clots outside of the carotid system, artificial cardiac valves, atrial myxoma, endocarditits, or atrial fibrillation.

• Prevention:– Treatment of the risk factors includes reduction of blood pressure and

cholesterol, control of blood sugar, and cessation of smoking.– Surgical removal of an atherosclerotic plaque from the carotid artery

( carotid endarterectomy), has been shown to reduce the incidence of stroke in selected patients.

Mechanisms of Stroke• There are two mechanisms by which strokes arise from atherosclerosis and

superimposed thrombotic occlusion of the internal carotid artery. – Occlusion of the carotid may give rise to an embolus that passes distally

in the territory of its tributary vessels, downstream from the internal carotid artery (middle and anterior cerebral arteries and their branches). This has been termed artery-to-artery embolism.

– Occlusion of the carotid artery may lead to ischemia in the distal field (watershed or border zone) in the region of lowest perfusion between its major branch vessels. (less often)

Atherogenesis and StrokeDevelopment of fatty streaks, small subendothelial deposits of lipid.

Plaque consisting of a central lipid core bounded on its lumen side by an endothelialized fibrous cap containing vascular smooth muscle cells (VSMC), and connective tissue

As the plaque grows, due to the process of positive remodelling, the vessel may expand, so that initially lumen diameter is not compromised (large volume atherosclerotic plaques may coexist without significant luminal stenosis and not be readily apparent on purely angiographic imaging modalities)

Clinical events are caused by rupture of the fibrous cap and by exposure of the highly thrombogenic lipid core to the circulation, resulting in the rapid formation of thrombus

Vessel expansion when the plaque grows

Vessel stenosis

Rupture of fibrous cap and Thrombus formation

Plaque neovascularization, intraluminal hemorrhage

Fibrous cap Formation

Cellular LevelCombination of high levels of circulating low-density lipoproteins (LDL) and endothelial dysfunction (smoking, hypercholesterolemia, hypertension and diabetes have all been associated with endothelial dysfunction and increased permeability)

Dysfunctional endothelium expresses adhesion molecules which allow recruitment of monocytes within the vessel wall(e.g. vascular cell adhesion molecule, VCAM-1)

Monocytes mature into macrophages, which then ingest oxidized LDLs via scavenger receptors, becoming foam cells and contributing to atheroma expansion.

Accumulation of foam cells and their subsequent death within the atheroma via oncosis and/or apoptosis lead to the development of the acellular lipid core composed of cholesterol esters and cell debris

The vasa vasorum or plaque neovascularization is thought to be particularly important in the recruitment and adhesion of monocytes within the plaque, which can promote atheroma growth.

Cellular LevelVSMC migrate from the medial layer of the vessel wall and synthesize extracellular matrix components such as elastin and collagen, which are essential to the formation and integrity of the fibrous cap

The fibrous cap contains inflammatory cells, predominantly macrophages, which produce a number of proteases such as metalloproteinases and cathepsins, which break down the matrix proteins in the fibrous cap

Dynamic imbalances in the enzymatic action of macrophages and the protective activity of VSCMCs may eventually lead to rupture of the fibrous cap and clinical events.

The fragile immature vascular endothelium associated with angiogenic microvessels increase the likelihood of intraplaque haemorrhage and of subsequent complications

Pathological Feature

• Atheromatous ulceration was first recognized surgically during carotid endarterectomy, with platelet thrombi being seen within the base of ulcer craters.

• Ulcer-related debris was invoked as a cause of embolic stroke, even in the absence of significant stenosis.

Predisposing Factors for Atherosclerosis

• Low blood levels of high-density-lipoprotein (HDL) cholesterol • High levels of low-density-lipoprotein (LDL) cholesterol• Long-duration cigarette smoking (decrease CBF and HDL)• Excess of homocystine• Speculative role for chronic inflammation or and intracellular infection of

uncertain origin within plaques (Chlamydia pneumoniae has been implicated in some studies)

• Familial• Obesity• It is affected in 50 to 80 per cent of patients presenting with cerebrovascular

disease.• Atherosclerotic stenosis or occlusion of the midportion of the common

carotid may also occur years after radiation therapy for laryngeal or other head and neck cancer.

Common Clinical Features of Carotid Stenosis

• Symptoms:– Transient ischaemic attack.– Amaurosis fugax.– Cerebral infarction.

• Signs:– Carotid bruit: 80%.– Upper motor neuron lesions following cerebral infarction.– Retinal infarctions/cholesterol emboli.

Classification

• Internal carotid stenosis is generally classified as – severe (70 to 90 per cent)– moderate (30 to 69 per cent)– mild (less than 30 per cent).

• Markedly severe stenosis causes slowing of internal carotid blood flow, resulting in delayed filling of intracranial branches as compared with extracranial ones

Radiological investigations

• Duplex ultrasound.• CTA• Magnetic resonance angiography (MRA).• Digital subtraction angiogram.

Doppler ultrasound• Doppler ultrasound is a major diagnostic technique for evaluation of carotid

stenosis. • It is noninvasive, rapid and relatively low cost and is reasonably sensitive

and accurate in the evaluation of the degree of carotid bifurcation stenosis. • However, the technique does not provide anatomical detail of the vessels

within the neck. • The Doppler signal frequency spectrum is a complex waveform generated

by a Fourier analysis of reflected signals obtained from an intravascular sample on ultrasound. This frequency signal corresponds with the actual flow velocity analysis of the vessel.

• Localization of this signal is aided by the ultrasound probe, which shows the outlines of the vessel

Ultrasound image of the carotid artery bifurcation with the ultrasound probe located in the proximal internal carotid artery.

Doppler ultrasound• It may be analyzed for pulsatility of the flow with periodical increases and

decreases in velocity and for the turbulence of the flow, which shows red blood cells accelerating and decelerating when an obstruction is encountered.

• When turbulence is noted, the red blood cells may actually reverse their direction and certainly decelerate, resulting in a wide variety of speeds.

• The Doppler signal then spreads out—a process described as "filling in the window beneath the curve"

• Turbulent currents are seen at obstructions within the vessel, such as at an atherosclerotic plaque.

• A sudden increase in velocity along the course of a vessel would also correlate with the increased velocity of flow seen at a stenosis in an attempt to maintain constant flow.

• Eventually, as stenosis worsens, flow volume cannot be maintained even with increases in flow velocity. Such changes in velocity may be correlated with angiographic measurements of per cent stenosis.

Normal internal carotid artery Doppler study with pulsatile flow and uniform systolic acceleration in flow creating a window under the frequency figure. Grossly abnormal high peak frequency internal carotid Doppler study with no clear window caused by a variety of frequencies recorded from a stenotic and turbulent region.

Doppler ultrasound

• It has a limited area of coverage and thus cannot see tandem lesions or even isolated lesions within the distal internal carotid artery near the skull base.

• Thus, while Doppler ultrasound is valuable in screening patients with carotid vessel disease, its limitations require complementary studies to provide information in instances where Doppler ultrasound has major limitations.

Color Flow Duplex Scanning• Previous duplex scanners used ultrasound and Doppler analysis of their

signals separately. • Now, more technologically advanced computers can produce spectral

patterns of Doppler signals returning from multiple areas and project them directly on the ultrasound monitor's screen.

• Flow direction through an individual pixel may be displayed as a color. • Typically, red is used to depict blood flow towards the brain and blue is used

to depict blood flow away from the brain. • White usually denotes very high blood velocity at a stenosis. • Increasing velocity may be displayed by a variation in colors. • With this combination of Doppler and ultrasound techniques, real-time

noninvasive depiction of flowing blood within a vessel is possible

Color flow duplex study of a high-grade stenosis with white signal intravascularly denoting high velocity of flow at the stenosis .

Indication For Ultrasound Doppler

1. A screening test for a carotid artery flow stenosis in a patient presenting with • an ipsilateral transient ischemic attack or completed stroke. • the potential of multiple causes for these events.

2. In the postoperative follow-up of patients to detect evidence of subclinical restenosis of an operative vessel.

3. Identify different components within atherosclerotic plaque. – Low echogenicity may be seen in areas of thrombus or excessive deposition of

lipid. – Calcium is particularly reflective. Small amounts of calcium within a plaque are

seen as a bright signal return.4. The intraoperative assessment of carotid endarterectomy patients.

– Confirmation of resumption of flow after unclamping of the carotid artery and the search for lumen irregularities or intimal flaps before wound closure.

CTA• In most cases, a diagnostic evaluation for cerebral

vascular disease can be performed by using either MRA or CTA.

• The immediate availability of CTA in many critical hospitals on a 24-hour basis makes CTA attractive in the care of patients who present after hours in the emergency department.

• CTA requires iodinated contrast agents to be injected at a relatively high flow rate.

• Patients with renal disease may not tolerate intravenous contrast agents.

• Motion artifacts remain a problem if the examination is performed by using older CT equipment

MR Angiography

• Magnetic resonance angiography (MRA) is a medical imaging modality used to reveal the shape of vessels for diagnosis and therapeutic purposes.

• It is non-invasive and provides three-dimensional (3D) data sets as opposed to the planar or two-dimensional (2D) projections of conventional x-ray digital subtraction angiography (DSA)

• Contrast-enhanced MRA (CE MRA) uses contrast agents to enhance the vascular lumen.

• The most widely available methods for post-processing MRA data sets are multiplanar reformatting (MPR), maximum-intensity projection (MIP), subvolume MIP, surface-rendering (SR), volume rendering (VR) and virtual intraluminal endoscopy (VIE).

• When a flow void at the carotid bifurcation was present on 2D TOF MRA this generally was associated with a stenosis of 70 % or greater, thus indicating the potential need for carotid endarterectomy.

CE MRA

• In order to obtain high quality images with arterial- phase CE MRA the timing of the contrast bolus and the rate of injection is crucial. The period of preferential carotid enhancement is typically brief (e.g. as short as 5 seconds).

• Imaging too late can result in significant jugular venous contamination of the images and poor carotid visualization.

• The optimal rate of contrast media injection has been shown to be approximately 2 mL per second

• Injection of this 18-20 mL bolus of Gd-chelate contrast agent is followed immediately by a 20 mL bolus of normal saline injected at the same rate (2 mL/sec) in order to flush the contrast agent rapidly through the arm veins and superior vena cava.

• This helps to ensure that the full dose of contrast reaches the cervical vessels in a uniform bolus.

Coronal source image from the 3D CE MRA acquisition reveals a right carotid artery dissection (arrow)

The MIP reconstruction (a) clearly demonstrates acarotid artery stenosis. However, quantification of stenosis is best performed on MPR images (b, c) perpendicular to the vessel axis (arrow in c, stenosis of internal carotid artery in the axial plane)

CE MRA demonstrates overlap between arterial and venousphases.

Normal contrast enhanced 3D MRA. a-c Direct coronal view of the first pass 3D MRA acquired with elliptical centric phase encodingtechnique. Note good visualization of all of the major vessels as well as many smaller vessels within the neck. Also note good separationof arteries and veins, the latter not being visible. b and c The 3D MRA can be rotated in different projections as illustrated

Volume Rendering• VR is a technique that displays all of the 3D data at once• It reveals internal structures that would normally be hidden or omitted when

using surface rendering techniques. • Frequently, 3D VR image displays of vascular anatomy provides excellent

anatomic information for surgical planning.

Volume rendered view of the aortic arch and branches

Virtual Intraluminal Endoscopy

• Virtual intraluminal endoscopy (VIE) is a recently developed technique for assessing the inside of the vascular wall

• It combines the features of endoscopic viewing and cross-sectional volumetric imaging and involves the generation of a sequence of perspective views calculated from points (flight path) located within the vascular lumen.

Virtual endoscopy of the abdominal aorta guided by the vessel centerline (red line)

Vascular Analysis

• The purpose of vascular analysis is to allow the clinician to perform quantitative assessment of vessel morphology in order:

– 1) to decide on the appropriate approach to treatment (surgical or pharmacological) according to the degree of stenosis

– 2) to monitor the progress of the disease.

• Intraluminal diameters and cross-sectional areas are needed to accurately quantify the degree of stenosis.

• For non-elliptic or amorphous stenoses, estimation of the smallest (as well as of the largest) diameter is not clear.

• In this case, cross-sectional area reduction better correlates with the hemodynamic impact of the stenosis than diameter reduction.

• For these reasons, vessel cross-sectional area has been proposed as a more accurate parameter for stenosis calculation

Automatic quantification along the vessel centerline

MRA - Pitfall• In the case of 2D TOF the major discrepancy is that of overestimation of

vessel stenosis, increasing possibility of miscategorizing the lesion. • Miscategorizing a lesion due to overestimation could result in a patient

undergoing invasive endarterectomy when in actuality the degree of stenosis was somewhat less than 70% if evaluated by catheter angiography

• In patients with severe high grade stenosis that result in a flow void on the MRA that is misdiagnosed as total vessel occlusion when in reality the vessel is patent

• MRA is contraindicated in patients who have cardiac pacemakers or cerebral aneurysm clips or in those who have undergone certain other medical procedures.

• In addition, MRA is highly motion sensitive. Many patients require sedation.

Post-Treatment Surveillance• MRA is often used to evaluate patients following treatment for vascular

disease (carotid atherosclerotic disease). • Determination of possible restenosis after carotid endarterectomy is an

indication for cervical carotid MRA. • Techniques for this type of study are identical with those for preoperative

carotid vascular evaluation. • Images can detect and quantify restenosis and help determine the need

for further interventional therapy.

DSA• Role of cervical-cerebral angiography is evolving as less invasive alternative

tests have become available. • Many experienced vascular surgeons are more comfortable with cervical-

cerebral catheter angiography than with other studies. • Clinicians perform carotid angiography routinely, and cerebral angiography

or digital subtraction angiography (DSA) is reserved for patients who are likely candidates for surgery or for patients who may benefit from angiographically based carotid intervention.

• Cerebral angiography also involves the injection of iodinated contrast agents. The overall contrast dose is similar to that required for CTA.

• The performance of catheter-based cervical-cerebral angiography depends on the skill and experience of the angiographer.

• Overall major morbidity rates are 0.1-1%.

DSA• Injury may occur in the form of iatrogenic stroke or bleeding around the

catheter introduction site. • Angiograms do not provide much information concerning the nature of the

plaque lesion. • Cerebral angiography is the most costly means of carotid stenosis

evaluation. • If cases are selected carefully, the overall risk of diagnostic angiography

together with the morbidity related to carotid surgery is less than the risk of stroke for the untreated patient

MRA Vs catheter angiography

• Catheter angiography provides the reference gold standard

• Catheter angiography is an invasive procedure there are measurable risks and complications associated with it.

– Clinical series have shown that reversible complications occur in 1 – 14% of catheter angiograms and that significant and often irreversible complications with severe morbidity or mortality occur in between 0.5 and 1% of cases

• Evaluation of carotid stenosis using 3D TOF MRA technique shows better correlation with catheter angiography (the sensitivity and specificity for quantification of stenosis with 3D TOF is in the range of 90% or better when compared with carotid catheter angiography).

MRA vs CTA

MRA CTA

Lumen stenosis Accurate quantitation of vessel lumen stenosis

Dense calcium deposits are present within an atherosclerotic plaque at the carotid bifurcation this may limit accurate quantitation of vessel lumen stenosis

Post-traumatic vessel injury or dissection

MRA has the advantage of being more specific for traumatic vessel dissection since it detects the presence of intramural hematoma.

Unable to detect the presence of intramural hematoma.

Satefy in Trauma

Since many trauma patients may be unable to give a proper history, MR safety considerations may preclude use of MRA in the acute situation.

There are not the critical safety concerns with CTA.

Availability Less rapidly available More rapidly available in many emergency

How should the degree of stenosis be assessed?

• If CDU suggests carotid stenosis, then MRA is the best non invasive confirmatory test, whereas CTA should be used when CDU detects carotid occlusion.

• Iodine contrast may limit CTA in patients with renal insufficiency or cardiac failure.

• Conventional angiography remains the gold standard, although most centres will recommend surgery on the basis of duplex ultrasound findings alone.

• The argument against the routine use of angiography is the low but recognized complication rate. In patients with asymptomatic stenosis, the risk is approximately 1%.

• Doppler carotid ultrasound has very rarely reported to cause stroke, presumably because of dislodgement of plaque by the transducer.

• A practical approach to assess the degree of carotid stenosis would be CDU combined with either CTA or MRA.

• Rather than using catheter or conventional angiography as the first test, it could be used to resolve equivocal findings, especially to resolve occlusion versus near-occlusion.

How should the degree of stenosis be assessed?

• NASCET and ECST used conventional cerebral angiography, whereas the Asymptomatic Carotid Atherosclerosis Study (ACAS) and the Asymptomatic Carotid Surgery Trial (ACST) used carotid duplex ultrasound.

• The results of meta-analyses of computerized tomographic angiography (CTA), magnetic resonance angiography (MRA) and colour duplex ultrasound (CDU) are shown

Carotid Endarterectomy• The most common vascular or neurosurgical procedures done to prevent

stroke.• In symptomatic patients with TIA or RIND, carotid endarterectomy has

been shown to be more effective in preventing stroke and death than medical management alone in patients with more than 70% stenosis

• However, its superiority over medical therapy alone is yet to be proven in those patients with mild (0–29%) or moderate (30–69%) symptomatic carotid stenosis

• Advances in catheter-based technology have made angioplasty of the carotid artery with or without stent placement an option for certain patients unable or unwilling to undergo carotid endarterectomy.

• The Asymptomatic Carotid Artery Study (ACAS), the European Carotid Surgery Trial (ECST), and the North American Symptomatic Carotid Endarterectomy Trial (NASCET) demonstrated the benefit of surgery for both asymptomatic and symptomatic carotid artery stenosis.

• Ulcerated lesions are associated with a higher than average risk in patients who undergo CEA

• Lesions of the high cervical carotid artery are easily reached via an endovascular route, but they are difficult to expose in an open surgical fashion

• The North American Symptomatic Carotid Endarterectomy Trial Collaboration (NASCET) (1991) and the European Carotid Surgery Trial (ECST) (European Carotid Surgery Trialists Collaborative Group 1991) established that surgery is efficacious for symptomatic patients with ipsilateral carotid stenosis greater >70%.

• In the NASCET, patients who underwent CEA had an absolute reduction of 17% in the risk of ipsilateral stroke at 2 years.

• In the ECST, surgery-allocated patients had an significant absolute risk reduction of 6.5% in ipsilateral stroke and a relative reduction of 39%.

• Carotid endarterectomy was only helpful in patients with greater than 50% narrowing of the internal carotid artery. The more severe the narrowing the greater the benefit in reducing further strokes. There is no benefit in having an operation once the artery is blocked. 1

• In patients with 50-69% narrowing the risks of stroke or death were reduced by 7-9% at 5 years after surgery. In patients with more severe narrowing greater than 70% the risks of stroke or death were reduced by 14-19% at 5 years after surgery. 1

Carotid endarterectomy

1. Neurosurg Focus 5 (6):Article 2, 1998 Carotid endarterectomy compared with angioplasty and stenting: the status of the debate Felipe C. Albuquerque, M.D., George P. Teitelbaum, M.D., Donald W. Larsen, M.D., and Steven L. Giannotta, M.D.

Carotid endarterectomyRecommendations1. CEA is indicated for symptomatic patients with stenosis of 70-99%, this is

valid only for centres with a perioperative complication rate (all strokes and death) less <6% (level I).

2. CEA may be indicated for some patients with stenosis of 50-69% without a severe neurologic deficit; this is valid only for centres with a perioperative complication rate (all strokes and death) less <6%; males with recent hemispheric symptoms are the subgroup of patients most likely to benefit from surgery (level I).

3. CEA is not recommended for patients with stenosis less <50% (level I).4. CEA should not be performed in centres not exhibiting equally low

complication rates like NASCET or ECST.5. CEA may be indicated for some patients with asymptomatic stenosis of 60

and 99%; only patients with a low surgical risk (<3%) and a life expectancy of at least 5 years are likely to benefit from surgery (level II).

European Stroke InitiativeRecommendations for Stroke Management, 2002

Potential complications of carotid surgery

• Because the operation is performed on a diseased artery carrying blood to the brain, there is a risk during the operation or shortly after (particularly the first 24 hours), that a further stroke may occur. (2% risk of intra-operative neurological deficit.)

• This is in fact uncommon and affects about 3-4% of patients • A smaller risk of death, but this is very low at around 1% or less. The

procedure-related risk of stroke of death should be less than 3% in asymptomatic patients and less than 6% in symptomatic patients.

• There are a number of nerves that run close to the operation site that can be injured. The commonest is a sensory nerve (greater auricular nerve) to the upper part of the neck. Injury to this nerve can lead to some tingling or numbness in the neck and earlobe, but it is not usually a significant problem.

• The other nerve commonly seen is the hypoglossal nerve. • It is occasionally injured and leads to deviation of the tongue to one side.

Usually these problems are temporary because the nerve is bruised and not actually cut.

1. Neurosurg Focus 5 (6):Article 2, 1998 Carotid endarterectomy compared with angioplasty and stenting: the status of the debate Felipe C. Albuquerque, M.D., George P. Teitelbaum, M.D., Donald W. Larsen, M.D., and Steven L. Giannotta, M.D.

Carotid Surgery for Asymptomatic Stenosis

• The results of trials assessing carotid endarterectomy (CEA) in asymptomatic patients are still a matter of controversy.

• The largest of these trials, the Asymptomatic Carotid Atherosclerosis Study (ACAS), reported that patients with an asymptomatic carotid stenosis greater than 60% had a 5-year relative risk reduction of 53% of ipsilateral stroke if CEA was performed (Executive Committee for the Asymptomatic Carotid Atherosclerosis Study (ACAS) 1995).

• However, the absolute risk reduction was small (5.9% in 5 years), as was the rate of ipsilateral stroke in the medically treated group (11.0% in five years, or 2.3% annually).

• Moreover, these results were achieved with a perioperative rate of complications (stroke or death) of only 2.3%.

• Finally, the 5-year results were calculated on the basis of a two follow-ups and extrapolated, which reduces largely the reliability of the effect size.

Recommendations : Surgery for asymptomatic carotid stenosis is not generally recommended (level II). It may be discussed on individual patient basis.

European Stroke InitiativeRecommendations for Stroke Management, 2002

NASCET

• Carotid endarterectomy decreased the risk of stroke over 2 years by 17% compared to medical management in symptomatic patients with 70–99% stenosis.

• With greater than 80% internal carotid stenosis, carotid endarterectomy provided an absolute risk reduction of 11.6% in stroke and death end points over a 3-year time period.

• A smaller benefit (6.5% absolute risk reduction over 5 years) was evident for carotid endarterectomy in symptomatic patients with 50– 69% stenosis

compared to medical management.

ACAS

• In asymptomatic individuals with high-grade stenosis (>70%), the relative risk reduction over 5 years was 53%, but the absolute risk reduction was only 1.2% per year. Thus, the number of strokes prevented by carotid endarterectomy in asymptomatic stenosis of >70% is similar to the benefit seen with symptomatic stenosis of 50–69%.

Preoperative Assessment

Cardiovascular Risk• Many patients presenting for carotid endarterectomy will have concomitant

coronary artery disease and up to 20% have a history of myocardial infarction.

• The annual long-term mortality rate from cardiac disease in these patients is 5%, similar to the 6% rate among patients with symptomatic triple vessel coronary artery disease and far exceeding the mortality rate from stroke.

• The cardiac risk is further increased by other associated medical conditions such as hypertension and obesity.

• The high prevalence of coronary artery disease, as determined by history, electrocardiography or cardiac catheterization present in over 55% of these patients, is responsible for the increased risk of postoperative myocardial infarction (5%) when compared to those patients without coronary artery disease (0.5%).

• Evidence of cardiac disease should be sought by careful history and thorough examination, noting the presence of angina and its severity, previous myocardial infarction and symptoms and signs of cardiac failure. The ECG should be examined for abnormalities of rhythm and evidence of previous infarction and ischaemia.

Cardiovascular Risk• When indicated, chest radiograph is examined for evidence of cardiac

failure. • Further cardiac work-up, including an exercise ECG, radionuclide studies or

coronary angiography, may be necessary and is best co-ordinated with a cardiologist.

• Hypertension, present in up to 70% of patients presenting for CEA, must be well controlled.

• Postoperative hypertension and transient neurological deficits are more frequent in patients with poor preoperative blood pressure control (BP> 170/95 mmHg).

• Sudden normalization of blood pressure should be avoided in order to reduce the risk of hypoperfusion and stroke.

• Elective surgery should be postponed in those patients with uncontrolled blood pressure, unstable angina, congestive cardiac failure or myocardial infarction in the previous six months, as the perioperative cardiac risk is greatly increased.

• In some unstable patients, combined coronary artery bypass and CEA may be necessary.

Grading of patients undergoing carotid endarterectomy

Neurological Risk• Evaluation of the cerebrovascular system should carefully document the

presence of transient or permanent neurological deficit. • This is essential for assessing postoperative progress as well as quantifying

perioperative risk of stroke. • Frequent daily TIAs, multiple neurologic deficits secondary to cerebral

infarctions or a progressive neurological deficit increases the risk of new postoperative neurological deficit.

• Results of tests assessing the cerebral vascular system, such as duplex ultrasound scan, cerebral angiography and CO2 reactivity, should be available.

Respiratory Risk• Chronic obstructive pulmonary disease is often present in these patients

and needs optimal medical treatment preoperatively, which may include bronchodilators, corticosteroids, physiotherapy and incentive spirometry.

• Cigarette smoking should be stopped 6–8 weeks preoperatively. • If necessary, preoperative pulmonary function tests like PEFR, FVC:FEV1

ratio and a baseline arterial blood gas analysis with the patient breathing air should be carried out to guide perioperative care of the patient.

Endocrine Risk• Diabetes mellitus has been shown to exist in about 20% of patients

presenting with CEA and most of these patients are insulin dependent. • Adequate blood glucose control with absence of ketoacidosis preoperatively

must be established. • In experimental studies, even modest elevations in blood glucose have

been shown to augment postischaemic cerebral injury.• Manifestations of diabetes mellitus such as renal failure, silent myocardial

infarction, autonomic and sensory neuropathy and ophthalmic complications must be looked for.

• It is very important that the patient's preoperative medication should be reviewed.

• These patients are often receiving cardiac and antihypertensive drugs, antiplatelet agents, antacids, steroids, insulin and anticoagulants. Most of the drugs should be continued except for the antiplatelet agents and anticoagulants.

What increases the risk of perioperative stroke and death?

• Most authorities accept that contralateral carotid occlusion and age >75 years increase the risk of perioperative stroke.

• In NASCET, medical complications such as myocardial infarction, arrhythmia, congestive heart failure and sudden death were 1.5 times more likely in patients with a history of myocardial infarction, angina or hypertension (P < 0.05)

Surgical Technique

• Anesthetic Considerations And Positioning

• Operative Procedure

• Intraoperative Monitoring And Shunt Use

• Patch Angioplasty

• Postoperative Care

• Complications Of Endarterectomy

ANESTHETIC CONSIDERATIONS AND POSITIONING

• Most surgeons perform carotid endarterectomy with the patient under general anesthesia

• The principal goals of anesthetic management are to maintain adequate cerebral and myocardial perfusion.

• The patient is placed in the supine position with the head turned away from the side of the operation

Outline of the procedure• Vertical incision at the anterior border of the sternocleidomastoid.• Common, internal and external carotid arteries are dissected free and

taped.• Carotid sinus is blocked with lignocaine.• Arteries above and below the diseased segment are clamped.• Arteriotomy is made through the diseased segment into the normal vessel

above and below.• Intraluminal Javid shunt is then inserted into the common carotid vessel and

internal carotid artery through the arteriotomy, to allow cerebral circulation to continue

• Plane between the plaque and arterial wall is developed with a Watson–Cheyne dissector.

• Full extent of the plaque is removed.• Distal intima is tacked down.• Clamps are reapplied and the shunt removed.• Arteriotomy is closed with a patch.

OPERATIVE PROCEDURE• The patient is placed in the supine

position with a small roll beneath the shoulder and the head turned away from the side of the operation.

• The incision runs along the anterior border of the sternocleidomastoid muscle and curves posteriorly 1 cm below the angle of the mandible to avoid injury to the facial nerve.

• The platysma is incised, and the dissection is carried along the medial border of the sternocleidomastoid muscle.

• Keep the medial blade of self-retaining retractors in the superficial layers of the wound (deeper placement can cause injury to the recurrent laryngeal or superior laryngeal nerve.)

•Beneath the sternocleidomastoid muscle, the internal jugular vein is encountered.

• The common facial branch of this vein, which courses medially, is doubly ligated and divided, and the vein is gently retracted laterally

• The carotid artery can be gently palpated, and the carotid sheath is visible.

• Care must be taken during dissection of the carotid sheath because, on rare occasions, the vagus nerve is located anterior to the artery.

• The carotid sheath is opened inferiorly along the anterior surface of the artery to the level of the omohyoid muscle.

• The superior thyroid artery, the first branch of the external carotid, was next isolated.

• Dissection is then completed around the external carotid artery and superior thyroid artery, which are isolated with vessel loops.

• Proximal control of the common carotid artery is obtained by careful dissection of the posterior wall from the underlying vagus nerve and passage of a vessel loop

• A Rumel tourniquet is fashioned by placing the umbilical tapes on the internal carotid and common carotid arteries through a segment of rubber tubing.

• The hypoglossal nerve was located by following the ansa hypoglossi upward across the carotid bifurcation

• The hypoglossal nerve early in the dissection, because it crosses the distal internal carotid artery.

• It can be mobilized and gently retracted medially for better distal exposure.

• All vessels were isolated and encircled with vessel loops.

• The area between internal and external carotid artery was not dissected, leaving the carotid sinus nerve intact.

• Before manipulation of the carotid artery in the region of the bifurcation, lidocaine (2 per cent Xylocaine) without epinephrine is instilled into the carotid sinus and along the course of the nerve of Hering to minimize bradycardia and hypotension resulting from stimulation of these structures.

• The carotid plaque can often be gently palpated to determine its distal end

• The patient was anticoagulated with IV heparin, 100 units/kg to achieve an activated clotting time twice baseline.

• The blood pressure is maintained at or slightly above awake baseline, and the electroencephalography results are examined

• The shunt tubing is filled with heparinized saline and clamped to ensure that there are no intraluminal bubbles, and it is compared with the internal carotid artery to ensure proper sizing.

• The internal carotid artery is clamped first; using an aneurysm clip because it is less traumatic to the vessel.

• The common carotid artery is then clamped with an angled or straight Fogarty Hydragrip clamp, and the external carotid artery and superior thyroid artery are clamped with aneurysm clips.

• An arteriotomy is started about 1 cm proximal to the bifurcation in the midline of the common carotid artery using a #11 blade

• The electroencephalogram is again examined to determine whether shunt placement is necessary

• If no changes have occurred, dissection is carried distally along the plaque with a no. 4 Penfield dissector, and the arteriotomy is completed with an angled Pott’s scissors (along the anterior midline of the internal carotid artery )

• Dissection must be carried to at least 1 cm distal to the end of the plaque to allow for posterior wall extension and placement of a shunt, if necessary

• The incision is carried through the arterial wall until plaque is encountered, and a smooth plane is developed between plaque and artery wall.

• The completed arteriotomy is shown. • A 5 French silastic tube with a silk tied at the

center was prepared as a shunt. • The shunt was inserted into the distal internal

carotid artery, taking care not to cause a dissection of the intima or embolization of debris distally.

• The proximal end of the shunt was placed in the common carotid artery and distal blood flow was reestablished.

• A Freer elevator was used to carefully separate the plaque from the media, starting proximally with circumferential dissection of the plaque.

• A curved clamp is placed between plaque and artery wall, and the plaque is sharply incised with a scalpel.

• Care must be taken to ensure that the remaining plaque in the common carotid artery has a smooth edge

• The plaque is then dissected free from the arterial wall with the Penfield dissector to the bifurcation and into the external carotid artery.

• It is often helpful to have the assistant temporarily release the external carotid artery clamp as dissection proceeds up that artery and the plaque is gently torn free from its distal attachment.

• An angled Pott's scissors was used to cleanly cut half way across the proximal plaque from the medial side.

• Division of the proximal plaque was completed from the lateral side.

• The plaque was separated from the vessel wall up to the bifurcation

• A small curved clamp was insinuated circumferentially between the plaque and the wall of the external carotid.

• A critical part of the dissection involves the distal attachment of the plaque to normal intima of the internal carotid artery.

• The plaque was dissected distally to normal intima.

• Note the manipulation of the shunt to allow clear visualization.

• By gentle dissection and proximal traction on the plaque (eversion endarterectomy), it will usually tear away from its distal attachment and leave a firm

• The orifice of the vessel was probed with a small clamp to remove any remaining plaque.

• If the intima at this site is not adherent, it should be further resected or, less commonly, tacked to the arterial wall with a 6-0 Prolene suture.

• The vessel is shown after removal of the plaque.

• Double armed 7-0 polypropylene sutures were used to tack the distal intima to the media and prevent distal dissection

• The surface of the exposed media was carefully washed with heparinized saline and inspected under 3.5X magnification to wash away debris and ensure that there were no wisps of loose material.

• A collagen impregnated dacron patch was sutured with 6-0 polypropylene to the edges of the arteriotomy starting at the distal corner.

• Suturing of the medial wall of the patch was completed.

• The lateral wall was closed, leaving a 4 mm gap through which the shunt could be extracted.

• Note the stabilization of the vessel wall in preparation for removal.

• The distal end of the shunt was removed first.• Just before final suturing at the proximal end of the

arteriotomy, the internal carotid artery clamp is briefly released

• The resulting backflow of blood ensures that the artery is patent and flushes any residual debris from the lumen.

• The lateral suture line was completed. • The superior thyroid artery clamp is removed as the

final suture is placed in order to have continuous backflow of blood.

• The clamps are then removed in the following order: – external carotid artery– common carotid artery– internal carotid artery

• This sequence ensures that any potential embolic material is flushed into the external artery circulation.

• Thrombin-soaked cellulose foam was applied to the vessel to seal any residual needle puncture sites, and gentle pressure is applied to the wound with a sponge for about 1 minute.

• Meticulous hemostasis is maintained during closure; occasionally, a small drain is placed in the superficial wound.

• The vagus nerve is seen posteriorly between the carotid and internal jugular vein.

• Ultrasound was standing by for intraoperative assessment of the repair.

• The sterily wrapped ultrasound head was applied to the distal internal carotid artery.

• Duplex scanning showed a good caliber vessel with good flow, normal velocity and no intimal flaps.

• A closed suction drain was placed for 24 hours.

• The closed incision is shown.

INTRAOPERATIVE MONITORING AND SHUNT USE

• Direct measurement of cerebral blood flow with diffusion techniques such as xenon-133 are require special operating room facilities.

• Electroencephalography correlates well with diminished hemispheric cerebral blood flow but may not reflect regional ischemia or embolic events

• Somatosensory evoked potential monitoring may be more sensitive• Transcranial Doppler ultrasound can demonstrate both embolic events and

diminished velocity in the middle cerebral artery during cross-clamping

PATCH ANGIOPLASTY• The routine use of vein or synthetic patch angioplasty in carotid

endarterectomy has been advocated• Angioplasty provides theoretical advantage compared with direct closure by

maintaining a larger lumen and improving flow patterns at the distal end of the arteriotomy, thus limiting acute occlusion or restenosis at this site

• Patch angioplasties require additional cross-clamping time and are susceptible to aneurysmal dilatation and rupture, especially patches from smaller veins

Postoperative Care• All patients should be observed in an intensive care unit for 24 to 48 hours

after the procedure with sequential neurological examinations by nursing staff.

• Blood pressure should be rigidly controlled in the approximate preoperative range with continuous monitoring by arterial catheter; hemodynamic parameters are similarly monitored by Swan-Ganz catheter in selected patients.

• Intravenous fluids, pressors, inotropes, and antihypertensive agents are routinely administered to optimize these indices.

• Postoperative electrocardiography and chest radiography should be performed for all patients.

• Urine output and serum electrolytes are monitored during the period of intensive care.

• The cervical wound is repeatedly examined for enlargement or superficial bleeding.

• Aspirin therapy is initiated immediately after surgery, and stable patients are usually discharged to home within 3 to 5 days.

Carotid Chemoreceptor and Baroreceptor Dysfunction

• Postoperative haemodynamic instability is common (incidence >40%) after CEA and is thought to be due to carotid baroreceptor dysfunction.

• It is postulated that the atheromatous plaques dampen the pressure wave reaching the carotid sinus baroreceptors and with the removal of these plaques, increased stimulation of baroreceptors may result in bradycardia and hypotension.

• The hypotension can be prevented or treated by blocking the carotid sinus nerve with a local anaesthetic, intravenous fluid administration or, if necessary, the administration of vasopressor drugs, such as phenylephrine.

• Hypertension after CEA is less well understood and has been reported to be more common in patients with preoperative hypertension, particularly if poorly controlled,and in patients who undergo CEA in which the carotid sinus is denervated.


• Hypertension after CEA in which the sinus nerve is preserved has been postulated to be due to temporary dysfunction of the baroreceptors or nerve, caused by intraoperative trauma.

• Mild increases in blood pressure are acceptable (up to about 20% above preoperative levels), but marked increases are treated with an infusion of antihypertensive drugs such as nitroglycerine or esmolol or repeated bolus doses of labetalol, depending on the patient's condition in the immediate postoperative period.

• Other causes of haemodynamic instability after CEA include myocardial ischaemia/infarction, dysarrhythmias, hypoxia, hypercarbia, pneumothorax, pain, confusion and bladder distension, which should be treated appropriately.

• Hypotension may lead to hypoperfusion and ischaemic infarction of the brain.


• Hypertension may increase the incidence of wound haematoma formation with possible airway obstruction.

• Similarly, myocardial ischaemia/infarction may occur as a result of either complication.

• Therefore, the blood pressure must be closely monitored and controlled in the immediate postoperative period.

• Regional anaesthesia appears to be associated with a higher incidence of postoperative hypotension while general anaesthesia is more often associated with postoperative hypertension.

• CEA may result in loss of carotid body function with reduced ventilatory response to hypoxemia and hypercarbia.

• This effect is further exaggerated in patients with coexisting pulmonary disease, especially in the presence of respiratory depressant drugs.

• Provision of supplemental oxygen and close monitoring of ventilatory status is particularly important in these patients and if necessary, they should be admitted to the high dependency / intensive care unit for observation.

Complications of Endarterectomy

• Cerebral infarction

• Intracerebral hemorrhage

• Cranial nerve injuries

• Myocardial infarction

• Wound hematoma

• Wound infection

• Recurrent carotid stenosis

Is there an upper age limit?• In a subgroup analysis of 409 patients 75 years or older from the North

American Symptomatic Carotid Endarterectomy trial (NASCET), the absolute risk reduction (ARR) for ipsilateral stroke was 28.9% (95% CI 12.9–44.9) at 2 years in patients with 70–99% stenosis and 17.3% (95% CI 6.6–28.0) in patients with 50–69% stenosis.

• The numbers needed to treat (NNT) were three and six, respectively. • Combined data from NASCET and ECST showed clear benefit in

symptomatic patients >75 years of age with NNT of five versus 18 for patients younger than 65 years

How quickly should and can surgery be carried out?

• Transient ischemic attacks preceded stroke in 23% of patients when the ECST, Oxford Vascular Study, Oxfordshire community stroke project and the UK TIA Aspirin Trial were analysed.

• 43% of these occur within 1 week, 17% on the day of stroke. • However, it is not clear if all these events related to severe carotid stenosis. • It is recommended that evaluation of patients with TIA should be undertaken

as a matter of urgency. There is nothing more disheartening than witnessing a severe stroke in a patient with known severe symptomatic carotid stenosis while they are waiting for investigations or are on the waiting list for surgery.

• In a small study of 143 patients, eight disabling strokes (5.6%) with carotid occlusion in four and asymptomatic carotid occlusion in eight patients occurred in the 19.6 days after the presenting event while awaiting surgery.

• In this study, carotid occlusion occurred in 12 patients (8.4%).• Surgery need not be delayed in patients with stroke as the morbidity and

mortality are no different in patients with and without a non-disabling hemisphere stroke operated on within 30 days as opposed >30 days.

How quickly should and can surgery be carried out?

• In non-operated patients in NASCET, the risk of fatal and non-fatal stroke within 32 days of randomization (not from the time of the initial ischaemic event) was low at 3.3% in NASCET

• Although some authors have carried out endarterectomy in patients with recent occlusion, this is not universally accepted.

• A combined analysis of ECST and NASCET showed that benefit from surgery was greatest for those randomized within 2 weeks after their last ischaemic event (NNT = 5) than for patients randomized after more than 12 weeks (NNT = 125).

• It would therefore seem appropriate to recommend that symptomatic patients with severe stenosis >70% be operated on as soon as possible, preferably within 1–2 days.

• Because the carotid occludes as a result of thrombosis, it may be reasonable to anticoagulate these patients with Heparin (Sanofi Aventis, Paris, France) or Clexane (Sanofi) while awaiting surgery despite the lack of proof of benefit.

What is the risk of recurrent stenosis?

• The cumulative risk of recurrent stenosis >50% has been estimated to be as high as 21.6% at 10 years in a study of 338 patients or as low as 0.1% of 1000 patients at 7.1 year follow up (70%).

• The explanation for this discrepancy is unclear. • Restenosis is more common after primary closure than patch closure (P <

0.0001).

How does carotid angioplasty compare?

• In the Endarterectomy Versus Angioplasty in Patients With Symptomatic Severe Carotid Stenosis trial, the 30- day rate of stroke with internal carotid artery stenting (CAS) without distal protection was 3.9 (0.9–16.7 95% CI) times higher than that of CAS with cerebral protection.

• 38 In the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS) the periprocedural risk of disabling stroke and death was 6.4%, almost identical tothe risk of endarterectomy (5.9%), with most deaths in the angioplasty group related to stroke.

• At 1 year, restenosis (70%) of the ipsilateral carotid artery was more common after endovascular treatment than after endarterectomy( 18.5vs 5.2%, P = 0.0001) and more common with angioplasty alone compared with angioplasty and stenting (74 vs 26%).

• Recurrent ipsilateral symptoms at 1 year (predominantly transient ischaemic attacks) were more common in endovascular patients with severe stenosis (15.6%) compared with those with lesser degrees of stenosis (7.8%, P = 0.02).

• Following the cessation of randomizing patients for CAVATAS in 1997, a new trial, CAVATAS 2 or International Carotid Stenting Study (ICSS), was launched. This trial randomizes patients with high grade stenoses (greater than 70%) to either endarterectomy or primary stenting.


• This differs from CAVATAS in which primary angioplasty was the main procedure used followed by stenting only if there were complications such as severe arterial dissection or when the angiographic results postangioplasty were not satisfactory.

• ICSS is ongoing and as of October 2005, 700 patients have been enrolled in 33 centres from 14 countries including several Australian centres.

• The Stenting and Angioplasty with Protection in Patients and High Risk for Endarterectomy study was a study of a highly selective group of patients with carotid stenosis (>50% symptomatic or >80% asymptomatic) deemed at high risk for carotid endarterectomy because of associated medical conditions.

• The study was stopped prematurely because of lack of enrolment and less than 50% of patients enrolled actually underwent randomization, somewhat invalidating the conclusions.

• The cumulative periprocedural (30 days) incidence of stroke (any severity or vascular territory), myocardial infarction or death was 4.8% in the stenting group and 9.8% (P = 0.09) in the endarterectomy group.


• This difference is largely explained by the increased risk of myocardial infarction in the carotid endarterectomy group.

• The risk of major ipsilateral stroke or death was 1.8 versus 3.7%.

• The risk of stroke or death was not significantly reduced in the stenting group at 1 year.

• In the ongoing Carotid Revascularization Endarterectomy versus Stent Trial, the periprocedural risk of stroke and death with carotid artery angioplasty increases with increasing age (P = .0006).

• Wholey et al. found that restenosis (>50%) at 3 years is more common with self expanding stents than balloon-mounted stents (16.3 vs 3.7%, P = 0.0422).

• It is anticipated that the evolution of stent technology will reduce the risk of restenosis.


• Among a high-risk subset (severe coronary artery disease, chronic obstructive lung disease or renal insufficiency), the composite end-point stroke/myocardial infarction/death was 7.4%, significantly greater than the corresponding rate of 2.9% in the low-risk subset (P < .0005).

• The subsequent risk of stroke after carotid endarterectomy is approximately 1% per year and the long-term results of angioplasty are not known.

• A recent Cochrane review has concluded that the current evidence does not support a widespread change in clinical practice away from recommending carotid endarterectomy and that there is a strong case to continue recruitment in randomized trials.

• The use of historical controls would seem inappropriate, as the complication rates of endarterectomy have lessened in recent years.

What should be recommendedto patients?

• There is no argument that patients with >70% symptomatic stenosis, particularly patients aged 75 years or older, benefit the most where the combined risk of angiography and subsequent surgery is of an acceptable low level (<6%).

• The benefit of carotid endarterectomy in patients with either symptomatic 50–70% stenosis or asymptomatic stenosis >70% is less marked and a recommendation could be made either way.

• It is not unreasonable to recommend a conservative approach to patients with asymptomatic stenosis, warning the patient of expected symptoms, and to intervene should the stenosis become symptomatic or more severely stenosed.

Conclusion• CEA reduces the incidence of stroke in patients with symptomatic high-

grade carotid artery stenosis. • This benefit is only seen if the perioperative complications, mainly stroke

and myocardial infarction, are kept to a minimum. • Therefore, to realize the potential surgical benefits of this increasingly

popular procedure, it is essential to provide the optimal physiological environment during surgery and this requires a thorough understanding of the pathophysiology of carotid artery disease and careful anaesthetic management.

• Research directed at areas of controversy, such as the application of neurological monitors, methods for the prevention and/or treatment of cerebral ischaemia and the development and evaluation of effective interventions to reduce the high cardiac morbidity and mortality associated with CEA are needed urgently.

Conclusion• Carotid endarterectomy remains the treatment of choice for patients with

symptomatic carotid stenosis >70%. • The benefit of carotid endarterectomy in patients with symptomatic 50–70%

stenosis or asymptomatic stenosis greater than 70% is less marked and each case will need to be assessed on the balance of risks and benefits.

• If carotid surgery is recommended for these patients, then the combined complication rate for preoperative angiography and subsequent surgery needs to be less than 6% for symptomatic and 3% for asymptomatic patients, otherwise the benefit is lost.

• Angioplasty and stenting remains an evolving technique.• The benefit of this technique over carotid endarterectomy for de novo

carotid lesions has not been proven by randomized controlled trials. • Therefore, we would recommend that it should not be considered for

general use except for participation in a randomized trial, patients with inaccessible stenosis, severe comorbidities precluding endarterectomy or combined symptomatic coronary and carotid artery disease as a prelude to coronary artery bypass surgery and in clinical trial situation.

Thank You

Health & Medicine

Carotid endarterectomy