In 1954, Eastcott, Pickering, and Rob introduced carotid endarterectomy (CEA).1 Although the procedure effectively prevented ischemic stroke resulting from atheroembolic extracranial vascular disease, the technique drew much criticism. After a period of nearly 20 years, two widely accepted studies (NASCET and ACAS) finally proved CEA effective in both symptomatic and asymptomatic patients with appropriate degrees of stenosis and other risk factors.2-5 It is important to note that the “proof” of CEA had little to do with acute results but rather the outcome over a period of years following the procedure.6 Although the surgical techniques that are the foundation of CEA have changed little, the patient selection, intraprocedural cerebral monitoring, as well as postprocedural follow-up and care have been greatly refined.

The current excitement regarding the efficacy of angioplasty and carotid artery stenting (CAS) is mainly due to a large group of physicians that have no prior experience in treating extracranial cerebrovascular disease or in the evaluation or follow-up of these patients. As the debate about the rates of acute success with interventional techniques rages on, many physicians seem to have forgotten the three lessons so clearly demonstrated throughout the development of CEA:
• the importance of careful patient evaluation and selection;
• the need for specialized clinical and surgical training and practice; and
• the value of careful follow-up and outcomes analysis.

Unlike therapy for coronary and most other peripheral vascular occlusive disease, the critical aspect of extracranial cerebrovascular disease is not chronic ischemia and lack of blood flow (for which stents were designed) but rather embolic events. Although we continue to use the degree of stenosis as a primary objective finding in the evaluation of appropriate candidates for therapy, symptoms are the most predictive finding. Physicians remain unable to determine the nature of plaque stability and still do not understand the critical events that transform a “dormant” lesion into an “active” one displaying acute changes and embolic phenomena. The results of therapy directed at removing the plaque (CEA) rather than trying to stabilize or “cage” it with a stent (CAS), are independent of this fundamental lack of knowledge about plaque behavior and composition.

All therapy for extracranial cerebrovascular disease is prophylactic. A physician must treat more than 20 patients with asymptomatic disease to affect the outcome of one. Control is the name of the game. Given our inability to determine the fragility and embolic potential of a particular plaque, any technique that aims to achieve very low (<1%) procedural embolic rates must reduce potential manipulation of plaque. An increase as low as 1% in stroke or death can negate the efficacy of therapy directed at the carotid bifurcation. Because of this possible increase, most high-volume surgical centers have improved their results by avoiding the use of interventional diagnostic techniques.7-9 The ACAS study demonstrated the rationale for noninvasive diagnosis and preoperative workup with a stroke rate of 1.2% after diagnostic cerebral angiography.4 Our lack of understanding regarding the characterization and behavior of the plaque itself is fundamental to the principles of not manipulating the plaque in any way until the distal circulatory bed has been protected, and in removing the entire plaque.

CEA provides a number of advantages over CAS. Open surgical exposure of the carotid bifurcation represents a small physiologic insult to the patient that can be performed under either local or general anesthesia (Figure 1). Numerous surgical centers use local anesthesia in more than 95% of cases. In addition, the procedure allows for the maximum amount of control by employing distal control of the internal carotid, flow reversal in the internal carotid prior to restoring antegrade flow, visual inspection and debridement of the plaque site, and control of the proximal and distal endpoints of the endarterectomy site. The results of CEA are uniform despite the nature of the lesion (ie, soft versus calcific), its morphology (ie, tapering, globular, or ulcerated), or the tortuosity of the artery.

In summary, CEA possesses four fundamental strengths:
• control is easily and reliably achieved without additional manipulation;
• complete plaque removal eliminates the problems associated with the poorly understood variables of plaque composition and vagaries of anatomic configuration;
• lumen size enlargement ensures that the lumen of an endarterectomized vessel is actually larger than the native vessel lumen. Patch angioplasty provides redundancy in preventing restenosis; and
• minimal physiologic insult occurs in a focused and predictable location with subcutaneous exposure. Use of local anesthesia reduces the occurrence of cardiac or pulmonary sequelae.

Peripheral vascular surgeons are performing CEA more frequently than in the past. In surgical centers where a significant number of these procedures are carried out, most patients have a completely noninvasive evaluation with duplex ultrasound prior to surgery. The surgery begins with initial control of the internal carotid artery distal to the embolizing lesion (this is commonly referred to as distal protection in the interventional literature). The surgeon removes the offending lesion entirely and widens the arteriotomy by sewing a prosthetic or autogenous patch into the longitudinal defect. This step results in a disease-free carotid lumen that typically measures well over 100% of the native lumen, providing redundancy in the face of intimal hyperplasia (Figures 2 and 3).

The patient typically arrives at the hospital on the day of surgery, undergoes a 1- to 2-hour procedure under local or general anesthetic, stays in the recovery room briefly, and spends one night in a non-ICU inpatient bed. After discharge, patients can resume all normal activities within 1 to 2 weeks. Fewer than 2% of patients will need intervention for the endarterectomized site. This definitive procedure requires only routine hospitalization and costs of physician care (no expensive medical devices are needed).10 In the rare case that a patient requires another procedure, both surgical and interventional options remain available.11

CAS techniques continue to develop rapidly. Proponents of these procedures are quick to recognize their latest acute successes and typically compare them to the least favorable figures available for CEA. The numerous published series describing more than 100 consecutive cases of elective CEA with stroke rates of 3% or less are often ignored.12-14 There are also many surgical series with acute stroke rates of less than 1% and 5-year follow-ups documenting ipsilateral stroke rates of less than 1% per year.6 Although CAS proponents are quick to mention the potential for cranial nerve palsy, they fail to note that this small group of patients usually experiences only a very mild and transient palsy from operative nerve retraction and protection.

The “new” complications associated with CAS are also rarely reported. Complications unique to a remote ap-proach to the carotid bifurcation include femoral access site complications, lower extremity ischemic and embolic events, renal and visceral embolic events, cerebrovascular emboli via the nonoperated carotid and vertebral vessels, and arrhythmias induced by stenting the baroreceptor at the carotid bifurcation. Stenting of the baroreceptor at the carotid bifurcation alone results in a significant incidence of bradycardia and other arrhythmias requiring IV medications and ICU admission. CAS leads to a higher rate of ICU admission and multiday admission than is typical for CEA.

Proponents of CAS also rarely address the fact that the primary method of intervention (ie, dilatation and plaque disruption) produces the very emboli responsible for cerebral events in patients with carotid bifurcation disease. Transcranial Doppler studies have documented an eightfold increase in emboli during angioplasty and stenting procedures versus CEA.15 Although a great deal of research is dedicated to protection devices, their efficacy is far from proven. The addition of each new device to a procedure predicated on simplicity and control brings new risks and failure modes and increases cost.

Although arguments for the expectation of a low restenosis rate are good (ie, high flow, large lumen, short diameter), significant unknown variables may affect the rate of restenosis in the carotid. These variables include the interaction of stent design and construction (ie, rigidity, cell size, metal composition) with an often tortuous vessel in a mobile and compressible location. We also know that poor stent apposition, a known risk factor for restenosis, is often located at a bifurcation where lumen diameter makes a sudden and dramatic change (at the transition from the common carotid to the internal carotid). There is a well-documented history of restenosis at the end of stents (the ?edge effect?); given the current application of CAS, the edge effect can occur well distal in the internal carotid near the base of the skull.

When restenosis occurs after CAS, treatment options are significantly limited compared with those following CEA. Surgical correction of CAS often requires a far more radical and extensive exposure of the carotid vasculature, particularly the more difficult cephalad portion near the base of the skull.16 Repeat interventional therapy for CAS is limited to adding another stent or attempting redilatation.

CAS has achieved more success than anyone would have imagined 10 years ago. However, the technique is far from mature and its development, refinement, and integration into common clinical practice are likely to parallel the timeline of other procedures, requiring several decades of practice. CEA is one of the most highly scrutinized, studied, and ultimately successful surgical procedures available. In comparison, CAS is best suited for patients with higher risk factors for surgical exposure of the carotid (eg, prior radiation, prior carotid surgery, adjacent stomas, skull base lesions). Clinical trials in groups without these risk factors will ultimately determine the role of CAS in those patients. Other distinct patient groups will likely be delineated as reasonable candidates for primary CAS but we are also likely to find those who are at distinctly higher risk for CAS (eg, tortuous carotids, bulky irregular lesions, longer lesions, certain calcific lesions).

The case for endovascular approaches to coronary occlusive disease or aortic aneurysms is far more compelling on an acute basis as the open surgical alternative is a much more invasive and morbid option. This is not the case for carotid intervention. Open CEA is less invasive with respect to the diseased vascular tissue than is the transfemoral approach of CAS. The length of ICU stay and time to discharge are still shorter for CEA than for CAS. The cost of CEA is low and stable; CAS expenses continue to grow with the addition of distal protection devices and the advent of drug-coated stent technology.

Treatment centers that wish to engage in the clinical investigation of CAS need to demonstrate their ability to adequately randomize patients to participate. Surgeons have randomized patients to other very large trials of CEA versus medical therapy for many years and have shown their willingness and ability to participate in well-designed trials. If participation is problematic, it is often the result of trial design. Those new to the cerebrovascular reconstruction field may also have a lack of understanding regarding the proper patient selection and follow-up necessary to determine the efficacy of a new treatment.

Although the technical aspects of CAS are currently in the spotlight, we must focus equal attention on the integration of the necessary preoperative and postoperative clinical care required to achieve optimal results in cerebrovascular reconstruction. The role of diagnostic procedures prior to the therapeutic procedure cannot be underestimated; these procedures have an impact on complications and patient selection. Clinicians skilled in both endovascular and open vascular reconstruction must educate their patients prior to making a decision regarding this prophylactic procedure. After the procedure, the patient must be carefully followed by a skilled clinical team. Follow-up should include routine ultrasound examinations of the carotid vasculature, careful history, and physical examinations noting any changes that might warrant CT or MRI of the brain.

Until we understand the magnitude of the new complications associated with CAS and compare them with the true degree of “conventional” complications in comparable patient groups over an accepted period of rigorous follow-up, we cannot adopt CAS as a first-line therapy. CAS, however, is poised for development. Vigorous support from medical device manufacturers, patients who have anatomic risk factors for open surgical repair, and increased participation in endovascular therapy by clinicians primarily trained in the care of patients with cerebrovascular disease will all fuel the appropriate and rational approach to this new method of therapy. Most experienced clinicians will continue to consider CEA the standard of care; at the same time, endovascular therapy will be available for the few patients that experience clinically significant recurrent disease.

David H. Deaton, MD, is Chief of Endovascular Surgery at Georgetown University Hospital in Washington, DC. Dr. Deaton may be reached at (202) 687-1265;

1. Eastcott HHG, Pickering GW, Rob C. Reconstruction of internal carotid artery in a patient with intermittent attacks of hemiplegia. Lancet. 1954;2:994-996.
2. Clinical alert: Benefit of carotid endarterectomy for patients with high-grade stenosis of the internal carotid artery. National Institute of Neurological Disorders and Stroke; Stroke and Trauma Division. North American Symptomatic Carotid Endarterectomy Trial (NASCET) investigators. Stroke. 1991;22:816-817.
3. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med. 1991;325:445-453.
4. Endarterectomy for asymptomatic carotid artery stenosis. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. JAMA. 1995;273:1421-1428.
5. Hobson RW, Weiss DG, Fields W, et al. Efficacy of carotid endarterectomy for asymptomatic carotid stenosis. The Veterans Affairs Cooperative Study Group. N Engl J Med. 1993;328:221-227.
6. Hallett JW, Pietropaoli JA, Ilstrup DM, et al. Comparison of North American Symptomatic Carotid Endarterectomy Trial and population-based outcomes for carotid endarterectomy. J Vasc Surg. 1998; 27:845-851.
7. Gelabert, HA, Moore WS. Carotid endarterectomy without angiography. Surg Clin North Am. 1990;70:213-223.
8. Kuntz KM, Skillman JJ, Whittemore AD, Kent KC. Carotid endarterectomy in asymptomatic patients—is contrast angiography necessary? A morbidity analysis. J Vasc Surg. 1995;22:706-716.
9. Shifrin EG, Bornstein NM, Kantarovsky A, et al. Carotid endarterectomy without angiography. Br J Surg. 1996;83:1107-1109.
10. Cronenwett JL, Birkmeyer JD, Nackman GB, et al. Cost-effectiveness of carotid endarterectomy in asymptomatic patients. J Vasc Surg. 1997;25:298-311.
11. Hill BB, Olcott C, Dalman RL, et al. Reoperation for carotid stenosis is as safe as primary carotid endarterectomy. J Vasc Surg. 1999;30:26-35.
12. Hoyne RF. Review of 272 consecutive carotid endarterectomies in a smaller community. Surg Gynecol Obstet. 1990;170:522-526.
13. Yates GN, Bergamini TM, George SM, et al. Carotid endarterectomy results from a state vascular society. Kentucky Vascular Surgery Society Study Group. Am J Surg. 1997;173:342-344.
14. Mayo SW, Eldrup-Jorgensen J, Lucas FL, et al. Carotid endarterectomy after NASCET and ACAS: A statewide study. North American Symptomatic Carotid Endarterectomy Trial. Asymptomatic Carotid Artery Stenosis Study. J Vasc Surg. 1998;27:1017-23.
15. Jordan WD, Voellinger DC, Doblar DD, et al. Microemboli detected by transcranial Doppler monitoring in patients during carotid angioplasty versus carotid endarterectomy. Cardiovasc Surg. 1999;7:33-38.
16. Vale FL, Fisher WS, Jordan WD, et al. Carotid endarterectomy performed after progressive carotid stenosis following angioplasty and stent placement. J Neurosurg. 1997;87:940-943.

Figure 1. Incision, exposure, and completed patch angioplasty of the common and internal carotid artery. Figure 2. These images show the same carotid lesion by angiography (A), as a “blood only” 3D CT reconstruction (B), as a “blood and plaque” 3D CT reconstruction (C), and as an intraoperative view of the diseased carotid bifurcation (D). Figure 3. This 3D reconstruction shows the large lumen size realized after endarterectomy. A large amount of plaque with potential for disruption and embolization either spontaneously or with endovascular manipulation is also illustrated.