Eversion Carotid Endarterectomy

Updated: Feb 01, 2016
  • Author: Jovan N Markovic, MD; Chief Editor: Vincent Lopez Rowe, MD  more...
  • Print


Eversion carotid endarterectomy (eCEA) involves oblique transection of the internal carotid artery (ICA) at its origin at the carotid bifurcation, followed by extirpation of the plaque by means of eversion and subsequent reimplantation of the ICA into the carotid bulb. It has been validated in randomized and nonrandomized prospective studies as a safe and effective surgical treatment for carotid stenosis. The efficacy of surgical treatment of atherosclerotic carotid stenosis in the prevention of stroke is well documented.

After coronary artery disease and cancer, stroke is the third leading cause of death overall in developed countries, with a 30-day mortality of up to 12%. [1] Worldwide, stroke is the second leading cause of mortality (6.5 million deaths in 2013 [1] ) and is an important cause of long-term disability. [2]

In the United States the annual incidences of stroke and transient ischemic attacks (TIAs) are approximately 800,000 and 300,000 cases, respectively. [1] Using data from the National Institute of Health (NIH), the Centers for Disease Control and Prevention (CDC), and other US government agencies, the American Stroke Statistics Committee estimated that stroke accounts for about 1 of every 20 deaths in the United States and that someone in the United States has a stroke as often as every 40 seconds. [1]

Only 29% of patients with nonfatal stroke recover with normal neurologic function. [3, 4] In the Framingham study, which prospectively followed 5184 men and women from the general population for 26 years, Sacco et al reported a very high incidence of recurrent cerebrovascular infarctions (9% per year) in patients who survived an initial stroke. In the same study, the cumulative 5-year recurrent stroke rate was 42% for men and 24% for women. [5]

In addition to high rates of death, recurrence, and long-term disability, [6, 7] management of stroke imposes a substantial economic burden on society. The annual health care expenditure related to stroke in the United States is approximately $33 billion. [1]



In routine clinical practice, indications for the treatment of patients with carotid stenosis are based on the presence of symptoms and the degree of stenosis. [8] In 2008, the Society for Vascular Surgery (SVS) formulated evidence-based clinical practice recommendations for the management of carotid stenosis. [9]

The SVS guidelines recommended carotid endarterectomy (CEA) as the treatment of choice for low-risk symptomatic patients with carotid artery stenosis greater than 50% and low-risk asymptomatic patients with carotid artery stenosis greater than 60%. [9] Generally, carotid surgery is performed if a patient’s perioperative stroke or mortality risk is less than 3% and the life expectancy is greater than 5 years. [10]

The reference standard for calculation of the degree of carotid artery stenosis is based on the North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria (see the image below). In this approach, the smallest residual lumen at the level of stenosis is compared with the normal distal ICA lumen by means of catheter-based arteriography.

North American Symptomatic Carotid Endarterectomy North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria. Convention for describing carotid stenosis is to compare lumen diameter at most narrow point to diameter of internal carotid artery in normal segment several centimeters distal to stenosis.

An alternative (although one that is less frequently used during catheter-based arteriography) is to determine the degree of the carotid artery stenosis by using the European Carotid Surgery Trial (ECST) criteria. In the ECST approach, the smallest residual lumen at the level of stenosis is compared with the local estimated diameter of the carotid bulb.

A 70% carotid stenosis calculated according to the NASCET criteria corresponds to an 85% carotid stenosis calculated according to the ECST criteria. By the NASCET criteria, moderate stenosis is defined as 50-69% stenosis and severe stenosis as 70-99%. By the ECST criteria, the corresponding values are 75-84% for moderate stenosis and 85-99% for severe.

Duplex ultrasonography (US) is currently the imaging modality of choice for the diagnosis of carotid artery stenosis (see the image below); it is safe, quick, and reliable in experienced hands. [11, 12, 13, 14] However, the accuracy of duplex US is highly operator-dependent. In addition, factors that affect flow velocities, such as severe contralateral ICA stenosis or occlusion, can cause compensatory elevations of velocity and result in overestimation of the degree of stenosis. [15, 16, 17, 18, 19]

A. Arterial flow (red) is displayed in internal ca A. Arterial flow (red) is displayed in internal carotid artery (ICA) and common carotid artery (CCA). Sampling for flow velocities and spectral waveform analysis is carried out in center stream of ICA, and waveform is shown below. Peak systolic and end-diastolic velocities are measured on representative wave. B. Same general area is being interrogated in diseased ICA. Lumen appears to narrow, and red color becomes variegated and lighter. Arterial flow is sampled in area of maximal disturbance and narrowing, and resultant waveform is displayed below.

Computed tomography (CT) and magnetic resonance angiography (MRA) can be used to identify plaque morphology and in cases in which US is technically difficult (eg, heavily calcified or high lesions), and this can be helpful in planning CEA or stenting (see the image below). [20, 21, 22, 23, 24, 25, 26]

Representative image of extracranial circulation o Representative image of extracranial circulation obtained with CT angiography and 3-dimensional reconstruction. Arrow points to stenosis in left internal carotid artery.

Technical Considerations

The underlying etiology of carotid artery stenosis (see the image below) is the formation of atheromatous plaque at the bifurcation of the common carotid artery (CCA) and in the origins of the ICA or, less frequently, the external carotid artery (ECA). [27, 28, 29] The temporary or permanent clinical manifestations of carotid artery stenosis (TIA or stroke) result from cerebral hypoperfusion through the embolized artery in most cases, as well as stenosis due to plaque progression in situ. [30, 31]

Underlying etiology of carotid artery stenosis is Underlying etiology of carotid artery stenosis is formation of atheromatous plaque at bifurcation of common carotid artery and in origins of internal carotid artery.

The reduction in the radius of carotid blood vessels has a significant negative effect on cerebral perfusion, in that blood flow through these vessels, as determined by Poiseuille’s law, is directly related to the fourth power of their radius.

Atheromatous plaque not only reduces cerebral blood flow but also represents an irregular surface within the lumen of the carotid artery that is prone to thrombus formation (see the image below). [32, 33, 34, 35, 36] Ulceration and rupture of the plaque create a highly thrombogenic surface that promotes platelet aggregation and creates thromboembolic debris, which subsequently leads to distal arterial embolization. [37, 38, 39, 40, 41, 42]

A. Simplified flow patterns at carotid bifurcation A. Simplified flow patterns at carotid bifurcation demonstrate complex reversal of flow along posterior wall of carotid sinus. This region is most vulnerable to plaque development. B. Established plaque at carotid bifurcation. C. Soft, central necrotic core with overlying thin fibrous cap. This area is prone to plaque rupture. D. Disruption of fibrous cap allows necrotic cellular debris and lipid material from central core to enter lumen of internal carotid artery, thus becoming atherogenic emboli. Patient may experience symptoms (transient ischemia, stroke, or amaurosis fugax) or remain asymptomatic, depending on site of lodgment and extent of tissue compromise. E. Empty necrotic core becomes deep ulcer in plaque. Walls of ulcer are highly thrombogenic and reactive with platelets. This leads to thromboembolism in internal carotid artery circulation.

Extracranial cerebrovascular atherosclerosis, which accounts for most carotid artery disease, is responsible for 15-52% of all ischemic strokes. [43, 44] Hypertension is another important cause of stroke. Other rare entities of carotid artery disease include fibromuscular dysplasia, arterial kinking secondary to elongation, extrinsic compression, carotid body tumors, traumatic occlusion, intimal dissection, and radiation.



The efficacy of surgical treatment of atherosclerotic carotid stenosis in the prevention of stroke has been well documented. [45, 46, 47, 48, 49, 50, 51, 1] Level 1 data from several large multicenter clinical trials, as well as data from National Surgical Quality Improvement Program (NSQIP) database and large multicenter studies, have validated the efficiency and safety of CEA as the treatment of choice for reducing the risk of ipsilateral stroke in both asymptomatic and symptomatic patients with moderate-to-severe carotid artery stenosis. [52, 53, 54, 55, 56, 57, 58, 59]

In NASCET, the 5-year incidence of ipsilateral stroke was 15.7% in patients with moderate stenosis treated surgically, compared with 22.2% in patients with moderate stenosis who received optimal medical therapy. [52] NASCET also demonstrated a cumulative risk of ipsilateral stroke of 26% and 9% at 2-year follow-up in patients treated medically and those treated with CEA, respectively. This reduction in the incidence of stroke in the CEA group was demonstrated in patients with symptomatic, high-grade stenosis (ie, 70-99%).

Similarly, ECST data demonstrated that the 3-year risk of ipsilateral stroke was 2.8% in patients randomized to undergo CEA and 16.8% in those randomized to receive medical therapy alone. [53] The 3-year risk of disabling or fatal stroke or death was 6.0% and 11.0% for surgically and medically treated patients, respectively. Both patient cohorts were symptomatic and had high-grade carotid stenosis.

In the Asymptomatic Carotid Atherosclerosis Study (ACAS), a randomized clinical trial from North America comparing best medical therapy with surgery in 1622 asymptomatic patients with carotid artery stenosis, CEA significantly reduced the overall 5-year risk of ipsilateral stroke and any perioperative stroke or death from 11.0% to 5.1% in patients with asymptomatic carotid stenosis greater than 60%. [60] This corresponded to a relative risk reduction of 53% and an absolute risk reduction of approximately 1% per year.

Similarly, in the Asymptomatic Carotid Surgery Trial (ACST), a study carried out in Europe, the investigators demonstrated that CEA yielded a significant reduction in the 5-year risk of stroke or death, from 11.8% to 6.4%. [61]

Numerous randomized and nonrandomized prospective studies have validated eCEA as a safe and effective method for the surgical treatment of carotid stenosis and have shown it to be characterized by low restenosis rates. [62, 63, 64, 65, 66, 67]

Data from the Eversion Carotid Endarterectomy Versus Standard Trial (EVEREST), which included 1353 patients, demonstrated that eCEA and patch angioplasty had significantly lower restenosis rates when compared with primary closure CEA. [68]

A Cochrane review of the literature that included close to 2500 patients from 5 controlled clinical trials found that eCEA was associated with a lower risk of restenosis than patch angioplasty CEA. [69] Data from the same study showed no significant differences between the two groups with respect to the rate of perioperative stroke (1.7% for eCEA and 2.4% for patch angioplasty) and perioperative mortality (2.0% and 1.9%).

In 2014, Ballotta et al published results of a study that evaluated 2007 consecutive primary CEAs in 1773 patients over 12 years. [70] ACAS and NASCET recommendations were used as inclusion criteria for asymptomatic and symptomatic patients, respectively. Of the 2007 patients, 1446 (72.1%) were symptomatic at the time of surgery. All procedures were performed by the same surgeon in patients under general anesthesia. Intraoperative electroencephalography was used for the assessment of cerebral perfusion and need for the selective shunting.

During the course of the study, [70] there were nine (0.47%) asymptomatic late carotid restenosis (six moderate [50%-69%] and three severe [≥70%]) and one (0.05%) carotid occlusion. Data from Kaplan-Meyer analysis demonstrated the rates of freedom from restenosis and/or occlusion of 99.9±0.1%, 99.3±0.2%, 99.3±0.2%, and 99.3±0.2% at 1, 5, 10, and 12 years, respectively. Data also showed a perioperative stroke rate of 0.4% and no intraoperative mortality. This study demonstrated that eCEA can be performed in both asymptomatic and symptomatic patients with extremely low perioperative morbidity and mortality, as well as low restenosis rates.

A study by Schneider et al, using data from the Society for Vascular Surgery Vascular Quality Initiative (SVS VQI) database for 2003-2013, found that  eCEA and conventional CEA were comparable in terms of freedom from neurologic morbidity, death, and reintervention; that eCEA was associated with significantly shorter procedure times; and that eCEA reduced certain expenses more commonly associated with conventional CEA. [71]  In a study of 1385 consecutive cases, Ben Ahmed et al found eCEA to be both safe and cost-effective. [72]

The choice of surgical technique for the treatment of carotid artery stenosis should depend on the clinical judgment, experience, and preference of the operating surgeon, in the context of a discussion of the options with the patient.