Carotid endarterectomy for asymptomatic carotid stenosis: An update Jesse E. T h o m p s o n , M D ,
Dallas, Texas
One of the controversial areas in carotid surgery concerns the advisability of performing arteriography and carotid endarterectomy on patients with asymptomatic carotid stenosis. If all patients were admitted with a transient ischemic attack (TIA), there would be little difficulty; many patients, however, have a frank stroke without an antecedent TIA. The problem is how to predict the stroke risk when a patient is first discovered to have an asymptomatic carotid stenosis so that appropriate management can be carried out, including prophylactic carotid endarterectomy, when indicated. Older data on this subject dealt purely with clinical observations. ~ With the development of noninvasive techniques it is now possible to evaluate patients safely and define more precisely indications for arteriography and operation. Recognition of a carotid stenosis is an important matter. Auscultation of a midcarotid bruit remains the most common method of discovering an asymptomatic stenosis. Although the presence of a bruit in most instances indicates a stenosis at the carotid bifurcation, the absence of a bruit does not mean that no lesion is present. The silent lesions include stenoses of less than 50% diameter stenosis, ulcerated plaques without stenosis, severe stenosis with a lumen diameter of 1 mm or less, and total occlusions of the internal carotid artery. Stenoses therefore must be discovered by other methods, such as noninvasive screening tests, in patients who are suspected to have atherosclerotic lesions at the carotid bifurcation. These include patients before operation who have atherosclerotic lesions elsewhere in the peripheral vasculature especially in the coronary arteries, or patients who are at high risk for atherosclerotic lesions, such as the elderly and those with hypertension or From the Department of Surgery, Baylor University Medical Center, Dallas. Honored guest lecture, presented at the Fourteenth Annual Meeting of the MidwesternVascularSurgicalSociety,Toledo, Ohio, Sept. 14, 1990. Reprint requests: Jesse E. Thompson, MD, Suite 505, 3600 Gaston Ave., Dallas, TX 75246 24/6/27014
diabetes. Other carotid stenoses are discovered purely by serendipity when angiography is performed for other indications. What clinical consequences have been observed in patients with asymptomatic carotid stenoses who are followed for long periods of time? They are (1) no adverse vascular effects may develop, (2) TIAs can occur, (3) frank strokes can appear without episodes of transient ischemia, (4) silent total occlusion of the artery can take place, and (5) total occlusion can produce either transient ischemia or frank stroke. These hazards depend directly on the nature of the lesion and the condition of all vessels both primary and collateral that supply the brain. The early report of Javid et al. 2 on the natural history of growth of carotid atheromas has important implications for the correct management of carotid stenoses. In a study of 86 patients who underwent serial arteriography for periods of i to 9 years, these authors noted no change in size of the atheroma in 35 (41%) of the patients studied but a significant increase in 51 (59%). The increase was greater than 25% per year in 32 patients and less than 25% per year in 19. It is obvious that atherosclerosis progresses unpredictably in each patient. A moderate rate of progression is common for a carotid lesion as it becomes symptomatic within 3 to 4 years. Progress can be very slow, but in other cases the lesion can progress rapidly to produce symptoms within i or 2 years. 3 It is not unreasonable therefore, to consider the asymptomatic carotid stenosis as part of the total picture of cerebrovascular insufficiency rather than view it as an isolated finding. The natural history of ischemic thrombotic stroke caused by extracranial lesions can begin with the formation of a plaque at the common carotid bifurcation; its first physical manifestation could be an asymptomatic bruit. With time this asymptomafic lesion can become symptomatic from ulceration and embolization or from impairment of cerebral blood flow. If the first symptom is a TIA, therapy can be initiated promptly thereafter. At times, however, the first event is 669
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Thompson
hemiplegia, especially if a stenotic carotid undergoes acute total occlusion. Other factors that can complicate such a simplistic scheme include multiple lesions of both extracranial and intracranial vessels, anatomic configurations of cerebral collateral pathways, rate of progression of atherosclerosis in the individual patient, hypertension, diabetes, smoking, and the like. The length of time during which these lesions are known to exist is also an important aspect of the disease.
It is the purpose of this article to point out certain factors which at this time appear to predict an increased incidence of stroke in patients with asymptomatic carotid stenoses, thereby defining more precisely the indications for carotid endarterectomy. My interest in carotid surgery as a means of treating and preventing strokes began in 1957. During an in-depth review of our surgical results in 1966 we were struck by the finding that among 16 patients with asymptomatic carotid bruits not operated on, five of the 16 (31%) sustained frank strokes without antecedent episodes of transient ischemia. 4 Thus began our interest in asymptomatic carotid stenosis. Consequently, two series of patients, an operated group and a nonoperated group, were started and followed prospectively over the years. The results of this study were published in 1978, and a summary of the data is shown in Table I. s Those patients who were operated on had a long-term stroke incidence of 4.6%, whereas those patients who were not operated on had a stroke incidence of 17.4%. Operative mortality rate was zero and strokes related to operation were 1.2%. We concluded from this study that certain patients with asymptomatic carotid bruits were at risk for stroke, that prophylactic carotid endarterectomy could be performed in carefully selected patients with minimal mortality and morbidity rates, and that patients treated by operation appeared to have a more favorable long-term outlook from the standpoint of subsequent ischemic cerebral episodes than their nonoperated counterparts. Since then a considerable body of data beating on this subject have accumulated. In 1978 and 1980 two studies were published presenting data very similar to ours on patients with asymptomatic bruits who were followed but were not operated on (Table II).6"7 In the early studies indications for operation were based solely on clinical and angiographic judgments. At the present time indications can be based on clinical, angiographic, and objective noninvasive
Journal of VASCULAR SURGERY
tests--Doppler scans, duplex scans, ocular pneumoplethysmography (OPG), spectral analysis, and cerebral CT and MR] studies as well as the usual general risk factors of age, diabetes, hypertension, cardiac disease, and smoking. Indications are thus much more precise based on both anatomic and hemodynamic data. A great many authors have now reported shortterm results after carotid endarterectomy for asymptomatic lesions (Table III). The operative mortality rate is quite low, ranging from 0% to 2.1%, averaging 0.7%. The incidence of permanent neurologic deficits related to the operation ranges from 0% to 3.1% with an average of 1.25%. Reports from the current Veterans Administration asymptomatic stenosis study show an operative mortality rate of 1.9% and operation related strokes of 2.4% for a combined mortality-morbidity rate of 4.3%? 7 It is clear that in proper hands the operation can be performed with low and acceptable mortality and morbidity rates. However, reports with unacceptably high mortality-morbidity figures have recently appeared. One such survey revealed an operative mortality rate of 2.3% and a perioperative stroke rate of 5.6% in asymptomatic patients, raising concerns regarding the effectiveness of the operation.~8 Several series have been published in which asymptomatic patients subjected to carotid endarterectomy have been followed for long periods of time. Table IV displays the results of these studies, especially the more recent ones. All of these patients had carotid stenoses of 50% diameter reduction or greater, and were followed for varying lengths of time up to 16 years. The stroke rate per year ranged from 0% to 2%, with an average of 1.2% per year. The incidence of stroke in the normal population of similar age and sex is estimated to be 0.5% per year. 22 The incidence of stroke in unoperated patients exhibiting episodes of transient ischemia has been variously reported from 5% to 12% per year. 23"24 In a recent long-term study of 179 asymptomatic patients subjected to carotid endarterectomy and followed up to 12 years, Callow and Mackey~s reported operative mortality rate of 0.56%, perioperative stroke rate of 1.1%, and long-term stroke incidence of 1.4% per year. Much information is now available on patients with asymptomatic stenoses followed but not operated on, studied by means of various noninvasive examinations. Table V shows a number of these studies together with some early clinical observa-
Volume 13 Number 5 May 1991
Endarterectomy for aaymptomatic carotid stenosis 6 7 1
Table I. Long-term follow-up data on patients operated on or not operated on for asymptomatic carotid bruits (author's series) s
Operated on (132 patients) N o t operated on: (138 patients) Significance
Asyraptomatic
TIAs
Nonfatal stroke
Fatal stroke
Length offollow-up
120 90.9% 77 55.8% p < 0.01
6 4.5% 37 26.8% p < 0.01
3 2.3% 21 15.2% p < 0.01
3 2.3% 3 2.2%
6 to 184 m o (mean, 55 mo) to 199 m o (mean, 55 too)
Table II. Long-term follow-up data on nonoperated patients with carotid bruits No. of patients
Author T h o m p s o n et al. s
138
Cooperman et al. 6
60
Dorazio et al. 7
97
Asymptomatic 77 55.8% 39 65% 68 70.1%
TIAs
Strokes
Length offollow-up
37 26.8% 12 20% 11 11.3%
24 17.4% 9 15% 18 18.6%
To 199 m o (mean, 55 mo) 2-7 yr 5-13 yr (mean, 7 yr)
Table I l L Operative mortality and morbidity rates after carotid endarterectomy for asymptomatic carotid stenosis Authors
No. cases
No. deaths
Operative mortality
Javid et al. s (1971) T h o m p s o n et al. 5 (1978) Hertzer et al. 9 (1978) Moore et al. ~° (1979) Wylie et al. 11 (1980) Whitney et al. ~2 (1980) Moore et al. ~s (1985) Moneta et al. 1~ (1987) Edwards et al. Is (1989) Treiman et al. 16 (1990) T h o m p s o n et al. (1990) (unpublished)
65 167 94 78 312 189 108 56 411 377 326
1 0 2 0 1 2 0 1 1 1 1
1.5% 0 2.1% 0 0.3% 1.1% 0 1.8% 0.2% 0.3% 0.3%
3.1% 1.2% 0 0 1.0% 1.1% 2.1% 1.8% 0.5% 1.8% 1.2%
0.7%
1.25%
Mean
tions. These noninvasive methods include the OPGKartchner, the OPG-Gee, various Doppler methods, the Hokanson scanner, dopscan, digital subtraction angiography (DSA), and the duplex scan. In these studies the stroke rate per year varied from 2.6% to 10.3% with an average of 5.27% per year. This rate of stroke is in marked contrast to that of patients having carotid endarterectomy where the average was 1.2% per year, representing a reduction in the expected stroke incidence of 77.2% in favor of the operated patients. Roederer et al. 3~in 1984 reported on 167 patients studied by duplex scanning who were not operated on but were followed over a 3-year period. They
Permanent strokes
found disease progression in 60% of the patients. They also found that in patients with 80% stenosis or greater the stroke rate was 16%, and the stroke plus TIA incidence was 36%. The incidence of stroke, TIA, and total occlusion of the internal carotid artery was 35% at 6 months and 46% at 12 months. In another study Moneta et al. 32 used spectral analysis in an attempt to predict stroke risk in unoperated patients. They divided patients into two groups, A and B. In group A all patients remained asymptomatic during follow-up, whereas in group B all patients suffered TIAs, strokes, or total occlusion of the internal carotid artery. Twenty-five percent of group A exhibited internal carotid artery end-
672
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Thompson
Table IV. Long-term follow-up stroke incidence per year in patients with asymptomatic carotid stenosis treated by carotid endarterectomy Author Javid et al. 8 ( 1 9 7 1 ) T h o m p s o n et al. 5 ( 1 9 7 8 ) M o o r e et al. 13 ( 1 9 8 5 ) M o n e t a et al? 4 ( 1 9 8 7 ) R o s e n t h a l et a l ) 9 ( 1 9 8 7 ) H e r t z e r 2° ( 1 9 8 8 ) Caracci et al. 2~ ( 1 9 8 9 ) Mean
Criteria for operation; Stroke rate degree of stenosis per year Severe > 50% > 50% > 80% > 50% > 70% > 75%
1.2% 1.0% 1.6% 2.0% 1% 1.4% 0 1.2%
diastolic frequencies equal to or greater than 6.5 kHz, whereas 67% of group B had end-diastolic frequencies equal to or greater than 6.5 kHz. The data from these two reports together with the data in Table V show clearly that asymptomatic patients with severe stenosis of the internal carotid artery determined by various noninvasive examinations are at increased risk for stroke when compared with the normal population and with patients subjected to carotid endarterectomy. The incidence approaches that of patients with TIAs who are followed but are not operated o n . 23 Several series have been reported in which asymptomatic patients both operated and nonoperated from the same institution have been matched and followed contemporaneously. Table VI displays the data from five such series. The overall and the annual stroke incidence are both shown. The overall longterm stroke rate in the nonoperated group varies from 17.4% to 28%, whereas the overall rate in the operated cases varies from 0% to 8%. O f special interest is the last column in the table, which shows the percent reduction in the stroke rate after carotid endarterectomy compared with the stroke rate to be expected had the patient been followed but not operated on. The percent reduction varies from 62% to 100%. The 0% stroke incidence in the Caracci 2~ series probably results from the relatively short postoperative follow-up period. Although these five series were not randomized studies, they do represent patients studied in the same fashion, matched and followed contemporaneously, with the operated and the nonoperated groups being from the same institution in each series. The results are very consistent in the five series, and it would appear that patients treated by carotid endarterectomy have a more
favorable long-term outlook from the standpoint of subsequent cerebral ischemic episodes than their nonoperated counterparts. Another matter, although not strictly relevant, relates to the decision for or against prophylactic endarterectomy of contralateral asymptomatic carotid stenosis, with or without a bruit, in patients who have undergone previous endarterectomy for symptomatic lesions. Data from four series are available and are quite consistent. 33-s6During followups the incidence of TIAs ranged from 13.7% to 16.7%, whereas the incidence of strokes varied only from 2.4% to 4.5%. In the series reported by Durward et al36 those patients whose asymptomatic contralateral stenoses were greater than 90% had a stroke incidence of 22%. A patient who has had prior unilateral endarterectomy for symptoms is not comparable to someone with an unoperated asymptomatic stenosis, because of the increase in cerebral blood flow that results from endarterectomy of the symptomatic lesion. The patient as a whole should be considered as symptomatic or asymptomatic, not the single carotid lesion. The Durward data do point out, however, that patients with very tight contralateral stenoses are at increased risk for stroke. Additional data, which may have some bearing on the indications for operation in patients with asymptomatic stenosis, come from studies of CT scans. Berguer et al. 37 reported an incidence of positive CT scans in 17% of asymptomatic patients. Vollman 38 reported an incidence of 18%, while Street et al. 39 gave an incidence of 22.2% silent infarcts. Just how these data will influence indications for operation remains to be seen. A controversial matter is the management of the patient with a nonstenotic asymptomatic ulcerative lesion of the carotid artery. Dixon et al.40 have divided these ulcers into three categories, A, B, and C, depending on the severity of the ulcerated plaque. During a follow-up to 120 months they reported an annual stroke rate of 4.5% in patients with B ulcers and an annual rate of 7.5% in C ulcers. They have recommended, therefore, that patients with B and C ulcers be offered prophylactic carotid endarterectomy as stroke prevention. A related problem is how to manage the patient found to have an asymptomatic stenosis who is to undergo a major operation of another sort. The risk of stroke associated with major operations is quite low. If the other operation is entirely elective and the carotid lesion a severe one, carotid endarterectomy
Volume 13 Number 5 May 1991
Endarterectomy for asymptomatic carotid stenosis 6 7 3
Table V. Long-term follow-up stroke incidence per year in patients with asymptomatic carotid stenosis not treated by operation Author
Criteriafor selection; method of study
Stroke rate per year
Thompson et al.5 (1978) Cooperman et al.6 (1978) Dorazio et al.7 (1980) Kartchner et al.26 (1979) Busuttil et al.27 (1981) Meissner et al22 (1987) Barnes et al.28 (1985) Moore et al)s (1985) Chambers et al.29 (1986) Moneta et al) 4 (1987) Hertzer 2° (1988) Taylor et al.s0 (1988) Caracci et al?l (1989)
Clinical Clinical Clinical Pos. O P G - Kartchner Pos. O P G - G e e Pos. O P G - G e e Doppler-various > 50%-Hokanson > 75% - Dopscan > 80%-Duplex > 70%-DSA-venous > 50%-Duplex + progressing > 7 5 % - Duplex
3.8% 3.75% 2.7% 6.0% 2.6% 3.4% 4.0% 4.2% 5.5% 9.5% 5.6% 7.2% 10.3%
Mean
5.27%
Table VI. Percent reduction in long-term stroke incidence after endarterectomy, operated and nonoperated cases from the same institution Annual Stroke Incidence Authors
Follow-up
Nonoperated
Operated
Thompson et alp (1978)
To 199 mo Mean, 55 mo 60 mo LT 24 mo LT 60 mo LT To 36 mo Mean, 21 mo
3.8% (17.4%) 4.2% (21%) 9.5% (19%) 5.6% (28%) 10.3% (18%)
1% (4.6%) 1.6% (8%) 2% (4%) 1.4% (7%) 0
Moore et alY (1985) Moneta et al. 14 (1987) Hertzer 2° (1988) Caracci et al.2~ (1989)
Percent reduction 74% 62% 79% 75% 100%
(o)
Total stroke incidence in parentheses. LT, Life table analysis.
may be performed first. Kartchner and McRae, 26 using the OPG as a preoperative test in 234 patients, have shown that those with a markedly positive OPG had a 17% incidence of stroke associated with cardiovascular operations, whereas patients with a negative OPG had a 1% incidence of stroke. Gutierrez et al.41 have reported a similar experience. In patients with asymptomatic carotid bruits with negative OPG-Gee the incidence of stroke in 75 operations was zero. By contrast, in those patients who had hemodynamically significant lesions as indicated by a positive OPG-Gee test, the incidence of stroke in 19 operations was 16%. Preoperative noninvasive screening tests are indicated in patients suspected of having hemodynamically significant carotid stenoses if they are to undergo other major
operations. The incidence of stroke is very low, but accidents do occasionally occur, which may be prevented by prior prophylactic carotid endarterectomy. Management of the patient with combined carotid and coronary artery disease is complicated, and recommendations vary.42'43 In general, staged operations carry lower mortality and morbidity rates than combined procedures. In most instances the candidate for coronary artery bypass graft (CABG) with an asymptomatic carotid lesion does not need the combined procedure but should have myocardial revascularization first followed by carotid endarterectomy at a later date, when indicated. Occasionally if the carotid lesions are bilateral or severe and coronary disease is stable, endarterectomy may precede CABG.
674 Thompson
A detailed discussion of this matter warrants a separate presentation and is not within the scope of this paper. It is difficult to document prolongation of survival of patients who have had prophylactic carotid endarterectomy, although one would expect some improvement in long-term survival because of the lower incidence of long-term stroke. Survival data for our two groups of asymptomatic bruit patients show an 11% superiority for the operated patients at five years (77%vs 66%), reflecting a decreased mortality rate from stroke. However, at 8 years the curves come together, and at 11 years the rates are essentially the same with 39% survival for the nonoperated cases and 33% for the operated group. 44 Survival of the operated group is far below that of the normal population of the same age and is a reflection of the incidence of generalized atherosclerotic disease, especially coronary artery disease, in patients with carotid atherosclerosis. The only way that long-term survival in these patients can be expected to improve is by modification of risk factors, especially coronary artery disease, as has been demonstrated by Hertzer et al.4s in patients with TIAs who have had CABG procedures performed. Thus the 5-year survival for carotid endarterectomy patients without prior coronary artery bypass was only 63%, whereas for those with coronary bypass it was 85%. For our patients with TIAs operated on it was 71%. These data are encouraging and give us hope that the long-term mortality rate from coronary artery disease in certain carotid patients may be modified by appropriate application of myocardial revascularization or other methods of therapy. PROTOCOL FOR MANAGEMENT
How then should one manage the patient suspected of having an asymptomatic carotid stenosis? Management follows three steps. The first step is noninvasive screening. Various types of studies are available at the present time, but the one most commonly used is the duplex scan. If the noninvasive screening test is positive, the second step is arteriography. Here the indications may be fairly liberal, especially since the advent of arterial DSA. The third step is operation, carotid endarterectomy, and here the indications must be highly selective. Multiple risk factors, especially cardiac, should be minimal or absent. An experienced and skilled operative team should be available. Operative management must be faultless, and appropriate cerebral protection must be
Journal of VASCULAR SURGERY
used. The method we recommend is routine shunting during endarterectomy, with the patient under general anesthesia. After noninvasive screening and arteriography, specific indications for carotid endarterectomy may be listed as follows: (1) severe unilateral stenosis greater than 70%, (2) bilateral stenoses greater than 50%, (3) unilateral stenosis and contralateral occlusion, (4) progressing stenosis to greater than 50%, (5) positive noninvasive tests such as duplex scan, spectral analysis, OPG, and perhaps CT and MRI studies, (6) before other major surgery if the noninvasive tests and arteriography are strongly positive, and (7) a markedly ulcerated plaque. From the available data it appears that asymptomatic carotid stenoses increase the risk for cerebral ischemic events in certain subgroups of patients who can be identified by means of modern noninvasive and angiographic methods. Those with high-grade hemodynamically significant stenoses (greater than 70%) determined by whatever means, especially if bilateral, with progressing stenosis, and with large ulcers are at greatest risk for stroke. When critical selection of patients for operation is made according to proper indications, when angiography is performed by skillful persons, and when appropriate surgical therapy is carried out by well-trained, experienced operators, the operative mortality and morbidity rates are low and acceptable, the immediate results are excellent, and patients treated by endarterectomy appear to have a more favorable outlook from the standpoint of subsequent cerebral ischemic episodes than their nonoperated counterparts. Two prospective randomized trials, which are currently in progress, ideally will shed additional light on the proper management of asymptomatic carotid stenoses. REFERENCES 1. Thompson JE, Garrett WV, Talkington CM. The use of operation for asymptomatic carotid bruits. In: Delaney JP, Varco RL, eds. Controversies in surgery II. Philadelphia: W B Saunders Co, 1983;121-31. 2. Javid H, Ostermiller WE, Hengesh JW, et al. Natural history of carotid bifurcation atheroma. Surgery 1970;67:80-6. 3. DeBakeyME. Patterns ofatherosclerosis and rates of progression. Atherosclerosis Rev 1978;3:1-56. 4. Thompson JE, Kartchner MM, Austin DJ, et al. Carotid endarterectomy for cerebrovascular insufficiency (stroke): follow-up of 359 cases. Ann Surg 1966;163:751-63. 5. Thompson JE, Patrnan RD, Talkington CM. Asymptomatic carotid bruits-long-term outcome of patients having endar-
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Endarterectomyfor asymptomatic carotid stenosis 675 24. Rosenberg N. Handbook of carotid artery surgery: facts and figures. Boca Raton, Florida: CRC Press, Inc, 1989; 284. 25. Callow AD, Mackey WC. Long-term foUow-up of surgicaUy managed carotid bifurcation atherosclerosis. Ann Surg 1989; 210:308-16. 26. Kartchner MM, McRae LP. Non-invasive laboratory evaluation. The clinical use of oculoplethysmography and carotid phonoangiography. In: Baker WH, ed. Diagnosis and treatment of carotid artery disease. Mount Kisco, NY: Futura Publishing Company, 1979;55-81. 27. Busuttil RW, Baker D, Davidson RK, Machleder HI. Carotid artery stenosis-hemodynamic significance and clinical course. JAMA 1981;245:1438-45. 28. Barnes RW, Nix ML, Sansonetti D, Turley DG, Goldman MR. Late outcome of untreated asymptomatic carotid disease following cardiovascular operations. J VAsc SURG 1985;2: 843 -9. 29. Chambers BR, Norris JW. Outcome in patients with asymptomatic neck bruits. N Engl J Med 1986;315:860-5. 30. Taylor LM Jr, Loboa L, Porter JM. The clinical course of carotid bifurcation stenosis as determined by duplex scanning. J VASCSURG 1988;8:255-61. 31. Roederer GO, Langlois YE, Jager KA, et al. The natural history of carotid arterial disease in asymptomatic patients with cervical bruits. Stroke 1984;15:605-13. 32. Moneta GL, Taylor DC, Zierler RE, et al. Asymptomatic high-grade internal carotid artery stenosis: is stratification according to risk factors or duplex spectral analysis possible? J VAsc SURG 1989;10:475-83. 33. Humphries AW, Young JR, Santilli PH, et al. Unoperated asymptomatic significant internal carotid artery stenosis: a review of 182 instances. Surgery 1976;80:695-8. 34. Johnson N, Burnham SJ, Flanigan DP, et al. Carotid endarterectomy: a follow-up study of the contralateral nonoperated carotid artery. Ann Surg 1978;188:748-52. 35. Podore PC, DeWeese JA, May AG, Rob CG. The asymptomatic contralateral carotid artery stenosis: a five-year follow-up study following carotid endarterectomy. Surgery 1980;88:748-52. 36. Durward OJ, Ferguson GG, Barr HWK. The natural history of asymptomatic carotid bifurcation plaques. Stroke 1982; 13:459-64. 37. Berguer R, Sieggreen MY, Lazo A, Hodakowski GT. The silent brain infarct in carotid surgery. J VASC SURG 1986;3: 442-7. 38. Vollman RW. In discussion: Berguer R, Sieggreen MY, Lazo A, Hodakowski GT. The silent brain infarct in carotid surgery. J VASCSURG 1986;3:442-7. 39. Street DL, O'Brien MS, Ricotta JJ, et al. Observations on cerebral computed tomography in patients having carotid endarterectomy. J VAsc SURG 1988;7:798-801. 40. Dixon S, Pais SO, Raviola C, et al. Natural history of nonstenotic asymptomatic ulcerative lesions of the carotid artery. Arch Surg 1982;117:1493-8. 41. Gutierrez IZ, Barone DL, Makula PA. The risk of perioperative stroke in patients with asymptomatic carotid bruits undergoing peripheral vascular surgery. Am Surg 1987;53: 487-9. 42. Brener BJ, Brief DK, Alpert J, et al. The risk of stroke in patients with asymptomatic carotid stenosis undergoing
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676 Thompson cardiac surgery: a follow-up study. J VASCSURG1987;5:26979. 43. Hertzer NR, Loop FD, Beven EG, O'Hara PJ, Krajewski LP. Surgical staging for simultaneous coronary and carotid disease: a study including prospective randomization. J VAsc SURG 1989;9:455-63. 44. Thompson JE. Carotid endarterectomy, 1982-the state of the art. Br J Surg 1983;70:371-6.
45. Hertzer NR, Loop FD, Taylor PC, Beven EG. Combined myocardial revascularization and carotid endarterectomy. Operative and late results in 331 patients. J Thoracic Cardiovasc Surg 1983;85:577-89.
Submitted Oct. 9, 1990; accepted Nov. 26, 1990.
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Dallas, Texas
One of the controversial areas in carotid surgery concerns the advisability of performing arteriography and carotid endarterectomy on patients with asymptomatic carotid stenosis. If all patients were admitted with a transient ischemic attack (TIA), there would be little difficulty; many patients, however, have a frank stroke without an antecedent TIA. The problem is how to predict the stroke risk when a patient is first discovered to have an asymptomatic carotid stenosis so that appropriate management can be carried out, including prophylactic carotid endarterectomy, when indicated. Older data on this subject dealt purely with clinical observations. ~ With the development of noninvasive techniques it is now possible to evaluate patients safely and define more precisely indications for arteriography and operation. Recognition of a carotid stenosis is an important matter. Auscultation of a midcarotid bruit remains the most common method of discovering an asymptomatic stenosis. Although the presence of a bruit in most instances indicates a stenosis at the carotid bifurcation, the absence of a bruit does not mean that no lesion is present. The silent lesions include stenoses of less than 50% diameter stenosis, ulcerated plaques without stenosis, severe stenosis with a lumen diameter of 1 mm or less, and total occlusions of the internal carotid artery. Stenoses therefore must be discovered by other methods, such as noninvasive screening tests, in patients who are suspected to have atherosclerotic lesions at the carotid bifurcation. These include patients before operation who have atherosclerotic lesions elsewhere in the peripheral vasculature especially in the coronary arteries, or patients who are at high risk for atherosclerotic lesions, such as the elderly and those with hypertension or From the Department of Surgery, Baylor University Medical Center, Dallas. Honored guest lecture, presented at the Fourteenth Annual Meeting of the MidwesternVascularSurgicalSociety,Toledo, Ohio, Sept. 14, 1990. Reprint requests: Jesse E. Thompson, MD, Suite 505, 3600 Gaston Ave., Dallas, TX 75246 24/6/27014
diabetes. Other carotid stenoses are discovered purely by serendipity when angiography is performed for other indications. What clinical consequences have been observed in patients with asymptomatic carotid stenoses who are followed for long periods of time? They are (1) no adverse vascular effects may develop, (2) TIAs can occur, (3) frank strokes can appear without episodes of transient ischemia, (4) silent total occlusion of the artery can take place, and (5) total occlusion can produce either transient ischemia or frank stroke. These hazards depend directly on the nature of the lesion and the condition of all vessels both primary and collateral that supply the brain. The early report of Javid et al. 2 on the natural history of growth of carotid atheromas has important implications for the correct management of carotid stenoses. In a study of 86 patients who underwent serial arteriography for periods of i to 9 years, these authors noted no change in size of the atheroma in 35 (41%) of the patients studied but a significant increase in 51 (59%). The increase was greater than 25% per year in 32 patients and less than 25% per year in 19. It is obvious that atherosclerosis progresses unpredictably in each patient. A moderate rate of progression is common for a carotid lesion as it becomes symptomatic within 3 to 4 years. Progress can be very slow, but in other cases the lesion can progress rapidly to produce symptoms within i or 2 years. 3 It is not unreasonable therefore, to consider the asymptomatic carotid stenosis as part of the total picture of cerebrovascular insufficiency rather than view it as an isolated finding. The natural history of ischemic thrombotic stroke caused by extracranial lesions can begin with the formation of a plaque at the common carotid bifurcation; its first physical manifestation could be an asymptomatic bruit. With time this asymptomafic lesion can become symptomatic from ulceration and embolization or from impairment of cerebral blood flow. If the first symptom is a TIA, therapy can be initiated promptly thereafter. At times, however, the first event is 669
670
Thompson
hemiplegia, especially if a stenotic carotid undergoes acute total occlusion. Other factors that can complicate such a simplistic scheme include multiple lesions of both extracranial and intracranial vessels, anatomic configurations of cerebral collateral pathways, rate of progression of atherosclerosis in the individual patient, hypertension, diabetes, smoking, and the like. The length of time during which these lesions are known to exist is also an important aspect of the disease.
It is the purpose of this article to point out certain factors which at this time appear to predict an increased incidence of stroke in patients with asymptomatic carotid stenoses, thereby defining more precisely the indications for carotid endarterectomy. My interest in carotid surgery as a means of treating and preventing strokes began in 1957. During an in-depth review of our surgical results in 1966 we were struck by the finding that among 16 patients with asymptomatic carotid bruits not operated on, five of the 16 (31%) sustained frank strokes without antecedent episodes of transient ischemia. 4 Thus began our interest in asymptomatic carotid stenosis. Consequently, two series of patients, an operated group and a nonoperated group, were started and followed prospectively over the years. The results of this study were published in 1978, and a summary of the data is shown in Table I. s Those patients who were operated on had a long-term stroke incidence of 4.6%, whereas those patients who were not operated on had a stroke incidence of 17.4%. Operative mortality rate was zero and strokes related to operation were 1.2%. We concluded from this study that certain patients with asymptomatic carotid bruits were at risk for stroke, that prophylactic carotid endarterectomy could be performed in carefully selected patients with minimal mortality and morbidity rates, and that patients treated by operation appeared to have a more favorable long-term outlook from the standpoint of subsequent ischemic cerebral episodes than their nonoperated counterparts. Since then a considerable body of data beating on this subject have accumulated. In 1978 and 1980 two studies were published presenting data very similar to ours on patients with asymptomatic bruits who were followed but were not operated on (Table II).6"7 In the early studies indications for operation were based solely on clinical and angiographic judgments. At the present time indications can be based on clinical, angiographic, and objective noninvasive
Journal of VASCULAR SURGERY
tests--Doppler scans, duplex scans, ocular pneumoplethysmography (OPG), spectral analysis, and cerebral CT and MR] studies as well as the usual general risk factors of age, diabetes, hypertension, cardiac disease, and smoking. Indications are thus much more precise based on both anatomic and hemodynamic data. A great many authors have now reported shortterm results after carotid endarterectomy for asymptomatic lesions (Table III). The operative mortality rate is quite low, ranging from 0% to 2.1%, averaging 0.7%. The incidence of permanent neurologic deficits related to the operation ranges from 0% to 3.1% with an average of 1.25%. Reports from the current Veterans Administration asymptomatic stenosis study show an operative mortality rate of 1.9% and operation related strokes of 2.4% for a combined mortality-morbidity rate of 4.3%? 7 It is clear that in proper hands the operation can be performed with low and acceptable mortality and morbidity rates. However, reports with unacceptably high mortality-morbidity figures have recently appeared. One such survey revealed an operative mortality rate of 2.3% and a perioperative stroke rate of 5.6% in asymptomatic patients, raising concerns regarding the effectiveness of the operation.~8 Several series have been published in which asymptomatic patients subjected to carotid endarterectomy have been followed for long periods of time. Table IV displays the results of these studies, especially the more recent ones. All of these patients had carotid stenoses of 50% diameter reduction or greater, and were followed for varying lengths of time up to 16 years. The stroke rate per year ranged from 0% to 2%, with an average of 1.2% per year. The incidence of stroke in the normal population of similar age and sex is estimated to be 0.5% per year. 22 The incidence of stroke in unoperated patients exhibiting episodes of transient ischemia has been variously reported from 5% to 12% per year. 23"24 In a recent long-term study of 179 asymptomatic patients subjected to carotid endarterectomy and followed up to 12 years, Callow and Mackey~s reported operative mortality rate of 0.56%, perioperative stroke rate of 1.1%, and long-term stroke incidence of 1.4% per year. Much information is now available on patients with asymptomatic stenoses followed but not operated on, studied by means of various noninvasive examinations. Table V shows a number of these studies together with some early clinical observa-
Volume 13 Number 5 May 1991
Endarterectomy for aaymptomatic carotid stenosis 6 7 1
Table I. Long-term follow-up data on patients operated on or not operated on for asymptomatic carotid bruits (author's series) s
Operated on (132 patients) N o t operated on: (138 patients) Significance
Asyraptomatic
TIAs
Nonfatal stroke
Fatal stroke
Length offollow-up
120 90.9% 77 55.8% p < 0.01
6 4.5% 37 26.8% p < 0.01
3 2.3% 21 15.2% p < 0.01
3 2.3% 3 2.2%
6 to 184 m o (mean, 55 mo) to 199 m o (mean, 55 too)
Table II. Long-term follow-up data on nonoperated patients with carotid bruits No. of patients
Author T h o m p s o n et al. s
138
Cooperman et al. 6
60
Dorazio et al. 7
97
Asymptomatic 77 55.8% 39 65% 68 70.1%
TIAs
Strokes
Length offollow-up
37 26.8% 12 20% 11 11.3%
24 17.4% 9 15% 18 18.6%
To 199 m o (mean, 55 mo) 2-7 yr 5-13 yr (mean, 7 yr)
Table I l L Operative mortality and morbidity rates after carotid endarterectomy for asymptomatic carotid stenosis Authors
No. cases
No. deaths
Operative mortality
Javid et al. s (1971) T h o m p s o n et al. 5 (1978) Hertzer et al. 9 (1978) Moore et al. ~° (1979) Wylie et al. 11 (1980) Whitney et al. ~2 (1980) Moore et al. ~s (1985) Moneta et al. 1~ (1987) Edwards et al. Is (1989) Treiman et al. 16 (1990) T h o m p s o n et al. (1990) (unpublished)
65 167 94 78 312 189 108 56 411 377 326
1 0 2 0 1 2 0 1 1 1 1
1.5% 0 2.1% 0 0.3% 1.1% 0 1.8% 0.2% 0.3% 0.3%
3.1% 1.2% 0 0 1.0% 1.1% 2.1% 1.8% 0.5% 1.8% 1.2%
0.7%
1.25%
Mean
tions. These noninvasive methods include the OPGKartchner, the OPG-Gee, various Doppler methods, the Hokanson scanner, dopscan, digital subtraction angiography (DSA), and the duplex scan. In these studies the stroke rate per year varied from 2.6% to 10.3% with an average of 5.27% per year. This rate of stroke is in marked contrast to that of patients having carotid endarterectomy where the average was 1.2% per year, representing a reduction in the expected stroke incidence of 77.2% in favor of the operated patients. Roederer et al. 3~in 1984 reported on 167 patients studied by duplex scanning who were not operated on but were followed over a 3-year period. They
Permanent strokes
found disease progression in 60% of the patients. They also found that in patients with 80% stenosis or greater the stroke rate was 16%, and the stroke plus TIA incidence was 36%. The incidence of stroke, TIA, and total occlusion of the internal carotid artery was 35% at 6 months and 46% at 12 months. In another study Moneta et al. 32 used spectral analysis in an attempt to predict stroke risk in unoperated patients. They divided patients into two groups, A and B. In group A all patients remained asymptomatic during follow-up, whereas in group B all patients suffered TIAs, strokes, or total occlusion of the internal carotid artery. Twenty-five percent of group A exhibited internal carotid artery end-
672
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Thompson
Table IV. Long-term follow-up stroke incidence per year in patients with asymptomatic carotid stenosis treated by carotid endarterectomy Author Javid et al. 8 ( 1 9 7 1 ) T h o m p s o n et al. 5 ( 1 9 7 8 ) M o o r e et al. 13 ( 1 9 8 5 ) M o n e t a et al? 4 ( 1 9 8 7 ) R o s e n t h a l et a l ) 9 ( 1 9 8 7 ) H e r t z e r 2° ( 1 9 8 8 ) Caracci et al. 2~ ( 1 9 8 9 ) Mean
Criteria for operation; Stroke rate degree of stenosis per year Severe > 50% > 50% > 80% > 50% > 70% > 75%
1.2% 1.0% 1.6% 2.0% 1% 1.4% 0 1.2%
diastolic frequencies equal to or greater than 6.5 kHz, whereas 67% of group B had end-diastolic frequencies equal to or greater than 6.5 kHz. The data from these two reports together with the data in Table V show clearly that asymptomatic patients with severe stenosis of the internal carotid artery determined by various noninvasive examinations are at increased risk for stroke when compared with the normal population and with patients subjected to carotid endarterectomy. The incidence approaches that of patients with TIAs who are followed but are not operated o n . 23 Several series have been reported in which asymptomatic patients both operated and nonoperated from the same institution have been matched and followed contemporaneously. Table VI displays the data from five such series. The overall and the annual stroke incidence are both shown. The overall longterm stroke rate in the nonoperated group varies from 17.4% to 28%, whereas the overall rate in the operated cases varies from 0% to 8%. O f special interest is the last column in the table, which shows the percent reduction in the stroke rate after carotid endarterectomy compared with the stroke rate to be expected had the patient been followed but not operated on. The percent reduction varies from 62% to 100%. The 0% stroke incidence in the Caracci 2~ series probably results from the relatively short postoperative follow-up period. Although these five series were not randomized studies, they do represent patients studied in the same fashion, matched and followed contemporaneously, with the operated and the nonoperated groups being from the same institution in each series. The results are very consistent in the five series, and it would appear that patients treated by carotid endarterectomy have a more
favorable long-term outlook from the standpoint of subsequent cerebral ischemic episodes than their nonoperated counterparts. Another matter, although not strictly relevant, relates to the decision for or against prophylactic endarterectomy of contralateral asymptomatic carotid stenosis, with or without a bruit, in patients who have undergone previous endarterectomy for symptomatic lesions. Data from four series are available and are quite consistent. 33-s6During followups the incidence of TIAs ranged from 13.7% to 16.7%, whereas the incidence of strokes varied only from 2.4% to 4.5%. In the series reported by Durward et al36 those patients whose asymptomatic contralateral stenoses were greater than 90% had a stroke incidence of 22%. A patient who has had prior unilateral endarterectomy for symptoms is not comparable to someone with an unoperated asymptomatic stenosis, because of the increase in cerebral blood flow that results from endarterectomy of the symptomatic lesion. The patient as a whole should be considered as symptomatic or asymptomatic, not the single carotid lesion. The Durward data do point out, however, that patients with very tight contralateral stenoses are at increased risk for stroke. Additional data, which may have some bearing on the indications for operation in patients with asymptomatic stenosis, come from studies of CT scans. Berguer et al. 37 reported an incidence of positive CT scans in 17% of asymptomatic patients. Vollman 38 reported an incidence of 18%, while Street et al. 39 gave an incidence of 22.2% silent infarcts. Just how these data will influence indications for operation remains to be seen. A controversial matter is the management of the patient with a nonstenotic asymptomatic ulcerative lesion of the carotid artery. Dixon et al.40 have divided these ulcers into three categories, A, B, and C, depending on the severity of the ulcerated plaque. During a follow-up to 120 months they reported an annual stroke rate of 4.5% in patients with B ulcers and an annual rate of 7.5% in C ulcers. They have recommended, therefore, that patients with B and C ulcers be offered prophylactic carotid endarterectomy as stroke prevention. A related problem is how to manage the patient found to have an asymptomatic stenosis who is to undergo a major operation of another sort. The risk of stroke associated with major operations is quite low. If the other operation is entirely elective and the carotid lesion a severe one, carotid endarterectomy
Volume 13 Number 5 May 1991
Endarterectomy for asymptomatic carotid stenosis 6 7 3
Table V. Long-term follow-up stroke incidence per year in patients with asymptomatic carotid stenosis not treated by operation Author
Criteriafor selection; method of study
Stroke rate per year
Thompson et al.5 (1978) Cooperman et al.6 (1978) Dorazio et al.7 (1980) Kartchner et al.26 (1979) Busuttil et al.27 (1981) Meissner et al22 (1987) Barnes et al.28 (1985) Moore et al)s (1985) Chambers et al.29 (1986) Moneta et al) 4 (1987) Hertzer 2° (1988) Taylor et al.s0 (1988) Caracci et al?l (1989)
Clinical Clinical Clinical Pos. O P G - Kartchner Pos. O P G - G e e Pos. O P G - G e e Doppler-various > 50%-Hokanson > 75% - Dopscan > 80%-Duplex > 70%-DSA-venous > 50%-Duplex + progressing > 7 5 % - Duplex
3.8% 3.75% 2.7% 6.0% 2.6% 3.4% 4.0% 4.2% 5.5% 9.5% 5.6% 7.2% 10.3%
Mean
5.27%
Table VI. Percent reduction in long-term stroke incidence after endarterectomy, operated and nonoperated cases from the same institution Annual Stroke Incidence Authors
Follow-up
Nonoperated
Operated
Thompson et alp (1978)
To 199 mo Mean, 55 mo 60 mo LT 24 mo LT 60 mo LT To 36 mo Mean, 21 mo
3.8% (17.4%) 4.2% (21%) 9.5% (19%) 5.6% (28%) 10.3% (18%)
1% (4.6%) 1.6% (8%) 2% (4%) 1.4% (7%) 0
Moore et alY (1985) Moneta et al. 14 (1987) Hertzer 2° (1988) Caracci et al.2~ (1989)
Percent reduction 74% 62% 79% 75% 100%
(o)
Total stroke incidence in parentheses. LT, Life table analysis.
may be performed first. Kartchner and McRae, 26 using the OPG as a preoperative test in 234 patients, have shown that those with a markedly positive OPG had a 17% incidence of stroke associated with cardiovascular operations, whereas patients with a negative OPG had a 1% incidence of stroke. Gutierrez et al.41 have reported a similar experience. In patients with asymptomatic carotid bruits with negative OPG-Gee the incidence of stroke in 75 operations was zero. By contrast, in those patients who had hemodynamically significant lesions as indicated by a positive OPG-Gee test, the incidence of stroke in 19 operations was 16%. Preoperative noninvasive screening tests are indicated in patients suspected of having hemodynamically significant carotid stenoses if they are to undergo other major
operations. The incidence of stroke is very low, but accidents do occasionally occur, which may be prevented by prior prophylactic carotid endarterectomy. Management of the patient with combined carotid and coronary artery disease is complicated, and recommendations vary.42'43 In general, staged operations carry lower mortality and morbidity rates than combined procedures. In most instances the candidate for coronary artery bypass graft (CABG) with an asymptomatic carotid lesion does not need the combined procedure but should have myocardial revascularization first followed by carotid endarterectomy at a later date, when indicated. Occasionally if the carotid lesions are bilateral or severe and coronary disease is stable, endarterectomy may precede CABG.
674 Thompson
A detailed discussion of this matter warrants a separate presentation and is not within the scope of this paper. It is difficult to document prolongation of survival of patients who have had prophylactic carotid endarterectomy, although one would expect some improvement in long-term survival because of the lower incidence of long-term stroke. Survival data for our two groups of asymptomatic bruit patients show an 11% superiority for the operated patients at five years (77%vs 66%), reflecting a decreased mortality rate from stroke. However, at 8 years the curves come together, and at 11 years the rates are essentially the same with 39% survival for the nonoperated cases and 33% for the operated group. 44 Survival of the operated group is far below that of the normal population of the same age and is a reflection of the incidence of generalized atherosclerotic disease, especially coronary artery disease, in patients with carotid atherosclerosis. The only way that long-term survival in these patients can be expected to improve is by modification of risk factors, especially coronary artery disease, as has been demonstrated by Hertzer et al.4s in patients with TIAs who have had CABG procedures performed. Thus the 5-year survival for carotid endarterectomy patients without prior coronary artery bypass was only 63%, whereas for those with coronary bypass it was 85%. For our patients with TIAs operated on it was 71%. These data are encouraging and give us hope that the long-term mortality rate from coronary artery disease in certain carotid patients may be modified by appropriate application of myocardial revascularization or other methods of therapy. PROTOCOL FOR MANAGEMENT
How then should one manage the patient suspected of having an asymptomatic carotid stenosis? Management follows three steps. The first step is noninvasive screening. Various types of studies are available at the present time, but the one most commonly used is the duplex scan. If the noninvasive screening test is positive, the second step is arteriography. Here the indications may be fairly liberal, especially since the advent of arterial DSA. The third step is operation, carotid endarterectomy, and here the indications must be highly selective. Multiple risk factors, especially cardiac, should be minimal or absent. An experienced and skilled operative team should be available. Operative management must be faultless, and appropriate cerebral protection must be
Journal of VASCULAR SURGERY
used. The method we recommend is routine shunting during endarterectomy, with the patient under general anesthesia. After noninvasive screening and arteriography, specific indications for carotid endarterectomy may be listed as follows: (1) severe unilateral stenosis greater than 70%, (2) bilateral stenoses greater than 50%, (3) unilateral stenosis and contralateral occlusion, (4) progressing stenosis to greater than 50%, (5) positive noninvasive tests such as duplex scan, spectral analysis, OPG, and perhaps CT and MRI studies, (6) before other major surgery if the noninvasive tests and arteriography are strongly positive, and (7) a markedly ulcerated plaque. From the available data it appears that asymptomatic carotid stenoses increase the risk for cerebral ischemic events in certain subgroups of patients who can be identified by means of modern noninvasive and angiographic methods. Those with high-grade hemodynamically significant stenoses (greater than 70%) determined by whatever means, especially if bilateral, with progressing stenosis, and with large ulcers are at greatest risk for stroke. When critical selection of patients for operation is made according to proper indications, when angiography is performed by skillful persons, and when appropriate surgical therapy is carried out by well-trained, experienced operators, the operative mortality and morbidity rates are low and acceptable, the immediate results are excellent, and patients treated by endarterectomy appear to have a more favorable outlook from the standpoint of subsequent cerebral ischemic episodes than their nonoperated counterparts. Two prospective randomized trials, which are currently in progress, ideally will shed additional light on the proper management of asymptomatic carotid stenoses. REFERENCES 1. Thompson JE, Garrett WV, Talkington CM. The use of operation for asymptomatic carotid bruits. In: Delaney JP, Varco RL, eds. Controversies in surgery II. Philadelphia: W B Saunders Co, 1983;121-31. 2. Javid H, Ostermiller WE, Hengesh JW, et al. Natural history of carotid bifurcation atheroma. Surgery 1970;67:80-6. 3. DeBakeyME. Patterns ofatherosclerosis and rates of progression. Atherosclerosis Rev 1978;3:1-56. 4. Thompson JE, Kartchner MM, Austin DJ, et al. Carotid endarterectomy for cerebrovascular insufficiency (stroke): follow-up of 359 cases. Ann Surg 1966;163:751-63. 5. Thompson JE, Patrnan RD, Talkington CM. Asymptomatic carotid bruits-long-term outcome of patients having endar-
Volume 13 Number 5 May 1991
6. 7.
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Endarterectomyfor asymptomatic carotid stenosis 675 24. Rosenberg N. Handbook of carotid artery surgery: facts and figures. Boca Raton, Florida: CRC Press, Inc, 1989; 284. 25. Callow AD, Mackey WC. Long-term foUow-up of surgicaUy managed carotid bifurcation atherosclerosis. Ann Surg 1989; 210:308-16. 26. Kartchner MM, McRae LP. Non-invasive laboratory evaluation. The clinical use of oculoplethysmography and carotid phonoangiography. In: Baker WH, ed. Diagnosis and treatment of carotid artery disease. Mount Kisco, NY: Futura Publishing Company, 1979;55-81. 27. Busuttil RW, Baker D, Davidson RK, Machleder HI. Carotid artery stenosis-hemodynamic significance and clinical course. JAMA 1981;245:1438-45. 28. Barnes RW, Nix ML, Sansonetti D, Turley DG, Goldman MR. Late outcome of untreated asymptomatic carotid disease following cardiovascular operations. J VAsc SURG 1985;2: 843 -9. 29. Chambers BR, Norris JW. Outcome in patients with asymptomatic neck bruits. N Engl J Med 1986;315:860-5. 30. Taylor LM Jr, Loboa L, Porter JM. The clinical course of carotid bifurcation stenosis as determined by duplex scanning. J VASCSURG 1988;8:255-61. 31. Roederer GO, Langlois YE, Jager KA, et al. The natural history of carotid arterial disease in asymptomatic patients with cervical bruits. Stroke 1984;15:605-13. 32. Moneta GL, Taylor DC, Zierler RE, et al. Asymptomatic high-grade internal carotid artery stenosis: is stratification according to risk factors or duplex spectral analysis possible? J VAsc SURG 1989;10:475-83. 33. Humphries AW, Young JR, Santilli PH, et al. Unoperated asymptomatic significant internal carotid artery stenosis: a review of 182 instances. Surgery 1976;80:695-8. 34. Johnson N, Burnham SJ, Flanigan DP, et al. Carotid endarterectomy: a follow-up study of the contralateral nonoperated carotid artery. Ann Surg 1978;188:748-52. 35. Podore PC, DeWeese JA, May AG, Rob CG. The asymptomatic contralateral carotid artery stenosis: a five-year follow-up study following carotid endarterectomy. Surgery 1980;88:748-52. 36. Durward OJ, Ferguson GG, Barr HWK. The natural history of asymptomatic carotid bifurcation plaques. Stroke 1982; 13:459-64. 37. Berguer R, Sieggreen MY, Lazo A, Hodakowski GT. The silent brain infarct in carotid surgery. J VASC SURG 1986;3: 442-7. 38. Vollman RW. In discussion: Berguer R, Sieggreen MY, Lazo A, Hodakowski GT. The silent brain infarct in carotid surgery. J VASCSURG 1986;3:442-7. 39. Street DL, O'Brien MS, Ricotta JJ, et al. Observations on cerebral computed tomography in patients having carotid endarterectomy. J VAsc SURG 1988;7:798-801. 40. Dixon S, Pais SO, Raviola C, et al. Natural history of nonstenotic asymptomatic ulcerative lesions of the carotid artery. Arch Surg 1982;117:1493-8. 41. Gutierrez IZ, Barone DL, Makula PA. The risk of perioperative stroke in patients with asymptomatic carotid bruits undergoing peripheral vascular surgery. Am Surg 1987;53: 487-9. 42. Brener BJ, Brief DK, Alpert J, et al. The risk of stroke in patients with asymptomatic carotid stenosis undergoing
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676 Thompson cardiac surgery: a follow-up study. J VASCSURG1987;5:26979. 43. Hertzer NR, Loop FD, Beven EG, O'Hara PJ, Krajewski LP. Surgical staging for simultaneous coronary and carotid disease: a study including prospective randomization. J VAsc SURG 1989;9:455-63. 44. Thompson JE. Carotid endarterectomy, 1982-the state of the art. Br J Surg 1983;70:371-6.
45. Hertzer NR, Loop FD, Taylor PC, Beven EG. Combined myocardial revascularization and carotid endarterectomy. Operative and late results in 331 patients. J Thoracic Cardiovasc Surg 1983;85:577-89.
Submitted Oct. 9, 1990; accepted Nov. 26, 1990.
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