stenosis on the side of operation as well as to document whether there is any progression of disease on the contra lateral, nonoperative side. If that test is unremarkable, then the next study will be at the 1-year anniversary. We will then see the patient on a yearly basis and obtain a bilateral carotid duplex scan as a part of that visit.

32.1  Commentary

Many decisions concerning recommendation to perform carotid endarterectomy are based upon the symptomatic status of the patient and the degree of stenosis, as measured by a percentage, in the carotid artery. The NASCET and ECST trials have clearly demonstrated the value of carotid endarterectomy over medical management in symptomatic patients with hemodynamically significant carotid stenoses. It is also well documented that the risk of stroke is greatest within the immediate time frame following the onset of hemispheric TIAs, and gradually diminishes during the course of a year. For this reason, patients and their physicians should be advised to consider the onset of TIAs as an urgent if not emergent indication for workup and intervention. All of the randomized trials have reported their data and have established a baseline threshold stenosis as an appropriate indication for carotid endarterectomy. While this would appear to be a very tangible and straightforward method of quantifying a carotid stenosis, confusion has developed because there are at least two different techniques for measuring percent of carotid stenosis: the North American method and the European method. The North American method was first described in a publication by Hass et al. as part of the Extracranial Arterial Occlusive Disease Study of the 1960s.2 This method was used in the Veterans Administration Asymptomatic Carotid Stenosis trial and the Asymptomatic Carotid Atherosclerosis Study (ACAS), and was subsequently adopted by North American Carotid Endarterectomy Trial (NASCET) as their method of measurement. The North American method utilizes the following formula: percentage stenosis = 1 – R/D, where R is the minimal residual lumen diameter in millimeters, and D is the diameter of the normal internal carotid artery, distal tothebulb,wherethewallsofthearterybecomeparallel.Incontrast,theEuropeanmethod, which has been used in European trials, including the European Carotid Surgery Trial (ECST) trial, uses the following formula: percentage stenosis = 1 – R/B, where R again is the minimal residual lumen diameter in millimeters, and B is the projected diameter of the carotid bulb. Since the bulb is not visualized on a carotid arteriogram of a patient with carotid stenosis, a theoretical line is drawn outlining the bulb, emphasising the atheromatous burden within the bulb. Because of these two different methods, percentage stenoses as expressed in the European literature are not equal to percentage stenosis as measured by the North American method. For example, a 60% stenosis European is equal to an 18% stenosis North American; 70% stenosis European equals 40% stenosis North American; 80% stenosis European equals 61% stenosis North American; and 90% stenosis European equals 80% stenosis North American. Thus, when reading a specific article relating to carotid stenosis, it is important to determine which method of measurement is used in order to appropriately follow the recommendations made by the authors. The conservative management of an asymptomatic patient with moderate carotid stenosis includes the use of

a statin and either an ACE inhibitor or a Beta blocker. The SPARCL study has clearly demonstrated the role of medical management in the primary prevention of stroke.

The management of patients with asymptomatic high-grade carotid stenosis has been controversial. However, following publication of ACAS and subsequent validation in the ACST study, the approach to management of patients who are asymptomatic has received more universal acceptance. The findings of the ACAS trial demonstrated that there was a 53% relative risk reduction of stroke in patients who underwent carotid endarterectomy for lesions producing at least a 60% diameter-reducing stenosis, by angiography, when compared with medical management alone.3 It was also pointed out that a 60% diameter-reduc- ing stenosis by angiography is not the same as a 60% stenosis as measured by duplex scan, since the duplex scan criteria for stenosis are concerned with carotid bulb measurement rather than a stenosis as compared with the diameter of the distal internal carotid artery. It is generally accepted that a 60% diameter-reducing stenosis of the internal carotid artery, by angiography, usually corresponds to a duplex scan finding of an 80–99% stenosis.3 The ACST study performed in the UK found almost identical results.4 One of the emerging issues concerning the management of asymptomatic patients with hemodynamically significant stenoses has been the improvement in medical management of these patients with the use of statin drugs. While statins were available during the later part of the ACAS trial and during the ACST trial, their use was not mandated as a part of medical management for either the control or the intervention group. Statins in combination with beta blockers or ACE inhibitors have clearly been shown to have a beneficial effect in reducing stroke morbidity and mortality in patients with carotid bifurcation disease who are treated medically alone or who undergo operation. While a post hoc analysis in the ACST trial failed to show any difference in result between those who were and were not on statins with respect to the benefit of carotid endarterectomy, there is clearly the need to repeat the asymptomatic trials in which modern medical management is used in both the control and intervention groups. However and until there are new trial data available, the level 1 evidence still supports the preferential use of carotid endarterectomy in well selected patients with asymptomatic, hemodynamically significant carotid stenosis for the primary prevention of stroke. While this approach will result in many patients receiving CEA who may never have had a stroke, there is still no reliable way to differentiate in advance those patients who will and those who will not have a stroke in the future. Clearly this information needs to be discussed with the patient and the treatment plan selected on the basis of preference and comfort level of the individual patient.

Patients with carotid artery disease who develop symptoms of hemispheric or monocular transient ischaemic events, or who have had a stroke with good recovery, are clearly good candidates for carotid endarterectomy providing that they have a diameter-reducing stenosis of 50% or greater by angiography. This is now accepted uniformly and has been well established by prospective randomized trials in both North America and the UK.1,5,6

The work-up of patients with carotid bifurcation disease for operation used to require the performance of a contrast angiogram to confirm the lesion, establish the degree of stenosis, and evaluate the intracranial circulation for other pathology, such as a stenosis of the carotid siphon or an aneurysm of the intracranial branches. As the quality and accuracy of carotid duplex scanning has improved in accredited laboratories throughout the world, the practice of using carotid duplex scan data as the sole imaging requirement before

endarterectomy has proliferated. Most centers also require a confirmatory study such as an MRA or CTA before proceeding with operation. In our own unit, the accuracy of carotid duplex scanning in our laboratory is continually compared with the operative findings at the time of carotid endarterectomy. Initially, the carotid duplex scan data were compared with angiography. As our level of comfort with carotid duplex scanning has increased, contrast angiography has essentially been eliminated in our protocol. The only time we resort to additional contrast imaging is when the carotid duplex scan data and the clinical picture fail to correlate.

If the patient has equal upper-extremity blood pressures, as well as good and equal quality pulses in the carotid artery bilaterally, then the likelihood of the patient harboring a lesion at the level of the aortic arch is quite small. The only other pathology that might bemissedintheabsenceofacontrastcarotidangiogramistherareoccurrenceofanintracranial lesion. It has been our practice to carry out completion angiography following carotid endarterectomy on the operating table. When the completion study is performed, we always make an effort to examine the intracranial circulation as well. To date, after many hundreds of carotid endarterectomy without angiography, there have only been two instances in which significant intracranial arterial pathology has been found. One was a small intracranial aneurysm measuring less than 10 mm; the other was a siphon stenosis, which,haditbeenknownpreoperatively,wouldnothavechangedtheindicationforcarotid endarterectomy. Based upon this experience, we routinely carry out carotid endarterectomy on the basis of duplex scan alone. However, this duplex scan must be performed in our own laboratory, as we are unwilling to accept data from other laboratories as the sole basis for proceeding with operation. While there are many excellent laboratories that provide reliable data, we routinely cross-check data from outside laboratories with a test in our own laboratory. Since duplex scanning is relatively inexpensive, and since it has become a substitute for expensive studies associated with morbidity and mortality, such as contrast angiography, it is our opinion that this additional cost is money well spent.7 Contrast angiography, while a longstanding gold standard, is expensive, promotes patient anxiety, and is associated with neurological morbidity and mortality. In the ACAS, where angiography was required before carotid endarterectomy, the risk of the angiogram with respect to stroke morbidity and mortality was equal to the risk of the operation itself.1 MRA, while noninvasive, tends to be less accurate than a well-performed carotid duplex scan. MRA of the carotid bifurcation will frequently overestimate the percentage of stenosis­ and will lead to unnecessary operation in many instances. CT angiography, while more accurate, requires a large intravenous contrast bolus to perform the study. [Q4: D]

Another controversy in the management of patients with carotid bifurcation disease concerns the question of whether a carotid arteriotomy should be closed primarily or with a patch angioplasty. For many years, we routinely closed arteriotomies primarily when the vessel appeared to be of good calibre. A retrospective review of our data suggested that this had been a good practice in that our incidence of restenosis had been quite low. Many retrospective comparisons as well as prospective trials have shown inconclusive data concerning the merit of patch angioplasty versus primary closure. However, recently, a prospective trial in patients scheduled for staged bilateral carotid endarterectomy in whom one side was primarily closed and the second side closed with patch angioplasty conclusively demonstrated that those sides closed with patch angioplasty were associated

with a statistically lower incidence of restenosis and complication. Based upon these convincing data, it is now our practice to routinely close all arteriotomies with a patch angioplasty.8 [Q5: B]

Other surgeons have modified their surgical practice to perform the operation using eversionendarterectomy,thusavoidingalongitudinalarteriotomy.Forthosesurgeonswho are experienced with this technique, and in properly selected patients, this also appears to be a satisfactory alternative. The postoperative monitoring of the patients is important in ensuring the best outcome for these patients. In the past, it had been our practice to monitor patients routinely in the intensive care unit. However, with a retrospective review of our experience, the likelihood of having an untoward event requiring intensive-care nursing in a patient who was neurologically intact and with a normal blood pressure was extremely low. Therefore the cost/benefit advantage of intensive care unit utilization was clearly not there. We now routinely send patients to a regular hospital room. To date, there have been no untoward incidents that have led us to regret this policy. [Q6: D]

References

 1. Moore WS, Barnett HJ, Beebe HG, et al. Guidelines for carotid endarterectomy: a multidisciplinary consensus statement from the ad hoc committee, American Heart Association. Stroke. 1995;26:188-201.

 2. Hass WK, Fields WS, et al. Joint study of extracranial arterial occlusion. II. Arteriography, techniques, sites, and complications. JAMA. 1968;203(11):961-968.

 3. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study (ACAS). Endarterectomy for asymptomatic carotid artery stenosis. JAMA. 1995;273:1421-1428.

 4. AsymptomaticCarotidSurgeryTrialCollaborators.TheMRCAsymptomaticCarotidSurgery Trial(ACST): carotid endarterectomy prevents disabling and fatal carotid territory strokes. Lancet. 2004;363:1491-1502.

 5. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. N Engl J Med. 1998;339:1415-1425.

 6. European Carotid Surgery Trialists Collaborative Group. Randomized trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European Carotid Surgery Trial. Lancet. 1998;351:1379-1387.

 7. Chervu A, Moore WS. Carotid endarterectomy without arteriography. Personal series and review of the literature. Ann Vasc Surg. 1994;8:296-302.

 8. AbuRahma AF, Robinson PA, Saiedy S, Richmond BK, Khan J. Prospective randomized trial of bilateral carotid endarterectomies: primary closure versus patching. Stroke. 1999;30:1185-1189.

 9. Goldstein LB, Amarenco P, Lamonte M, et al. Relative effects of statin therapy on stroke and cardiovascular events in men and women: secondary analysis of the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) study. Stroke. 2008;39(9): 2444-2448.

10.Johnston SC. Transient ischemic attack: a dangerous harbinger and an opportunity to intervene. Semin Neurol. 2005;25:362-370.

11.Rothwell PM, Giles MF, Flossmann E, et al. simple score(ABCD) to identify individuals at high early risk of stroke after transient ischaemic attack. Lancet. 2005;366:29-36.