Late outcome of untreated asymptomatic carotid disease following cardiovascular operations

Transcription

1 Late outcome of untreated asymptomatic carotid disease following cardiovascular operations Robert W. Barnes, M.D., M. Lee Nix, R.N., B.S.N., Diane Sansonetti, M.D., D. Glenn Turley, B.S., and Mitchell R. Goldman, M.D., * Little Rock, Ark. and Richmond, Val n a previous prospective study of 449 patients undergoing coronary or peripheral arterial reconstruction, 85 patients had preoperative evidence ofasymptomatic bruit and/or >50% carotid obstruction by routine Doppler screening. No patient had prophylactic carotid endarterectomy. This article reviews the late postoperative outcome (2 to 61 months, mean 35 months) of 67 patients with asymptomatic carotid disease who survived operation without perioperative deficit. Eleven patients died (16%) including four of myocardial infarction and two of stroke. Neurologic deficits occurred in the late postoperative period in 22 patients (32.8%) after an average interval of 31 months, including transient ischemic attacks in 15 patients (22.4%); only four of these 15 were appropriate to the side of carotid disease documented preoperatively. Seven patients (10.4%) suffered stroke, only three (4.5%) of which were in the territory of carotid disease detected preoperatively. The cumulative rate of carotid disease progression was 34%, including three patients who suffered carotid occlusion. Two of the latter had the only fatal strokes. This study suggests that patients with asymptomatic carotid disease, although not at significant risk of perioperative stroke, require careful follow-up for late postoperative neurologic deficits, the majority of which (68%) are transient ischemic attacks. (J VAsc SURG 1985; 2:843-9.) The controversy about the most appropriate management of patients with asymptomatic carotid disease will be resolved only when its natural history is better understood and the relative efficacy of medical and surgical therapy is clarified. 1,2 Previous reports about the risks of asymptomatic carotid bruit or disease have evaluated three categories of patients: (1) patients with asymptomatic bruit discovered incidentally at physical examination, (2) patients with angiographic evidence of asymptomatic carotid disease contralateral to symptomatic lesions, and (3) patients with asymptomatic carotid bruit or disease discovered incidentally prior to anticipated major operation, usually a cardiovascular procedure. Of these From the Departments of Surgery, Medical College of Virginia (Dr. Sansonetti, Ms. Nix, and Mr. Turley) and the University of Arkansas for Medical Sciences (Dr. Barnes), Presented in part at the Ninth Annual Meeting of the Southern Association for Vascular Surgery, West Palm Beach Gardens, Jan. 30-Feb. 2, Supported by the National Heart, Lung, and Blood nstitute grant No. 5 RO1 HL Reprint requests: Robert W. Barnes, M.D., Mail Slot 520, UAMS, 4301 West Markham, Little Rock, AR ~Professor of Surgery and Chief of Vascular and Transplant Surgery, University of Tennessee Memorial Hospital, Knoxville. three classes of patients, the one in which prophylactic carotid endarterectomy has been most commonly recommended is the group of patients undergoing a major cardiovascular operation. However, recent prospective studies suggest that patients with asymptomatic carotid disease do not have a risk of perioperative stroke significantly greater than patients without such disease. Such data suggest that prophylactic carotid endarterectomy before major cardiovascular operation may be beneficial only in the prevention of late postoperative stroke. This hypothesis requires a knowledge of the natural history of unoperated asymptomatic carotid disease in the late postoperative period in such patients. Few reports have been made about the late outcome of patients with nonoperated asymptomatic carotid lesions discovered before major operation. Cooperman, Martin, and Evans 3 followed up 256 patients 2 to 7 years after peripheral arterial reconstruction. These authors found a significantly greater risk of cerebrovascular insufficiency in 60 patients with preoperative evidence of asymptomatic bruit than in patients without bruit (35% vs. 16%). However, their study was retrospective and did not document the status of the carotid arteries by noninva- : " 843

2 844 Barnes et al. Journal of VASCULAR SURGERY _ 80_ "--~ ~ "1 1 J L-- CAD! 1 cao,= Pw~= / Months Alter Operation Fig. 1. Cumulative actuarial survival of patients with coronary artery disease (CAD) and peripheral vascular disease (PVD). sive techniques or angiography. n a previous report of a prospective study of 449 patients undergoing coronary or peripheral vascular reconstruction, we found 85 patients with preoperative evidence of asymptomatic carotid bruit and/or >50% carotid obstruction by routine Doppler Screening. 4 No patient had prophylactic carotid endartercctomy. No correlation was evident between asymptomatic carotid disease and perioperative neurologic deficits but asymptomatic carotid disease was strongly associated with perioperative death, usually from myocardial infarction. n a preliminary report of the late outcome of these patients with unoperated asymptomatic carotid disease, we found a 19% incidence of neurologic deficits in a follow-up period extending to 2 years? The majority of these deficits were transient ischemic attacks and they often occurred in a vascular territory unrelated to preoperative evidence of carotid disease. The present report extends the follow-up on patients with asymptomatic carotid disease who survived operation without perioperative neurologic deficit. MATERAL AND METHODS Patients. From March 1979 through December i980, 449 patients with coronary artery disease (CAD) or peripheral vascular disease (PVD) were evaluated preoperatively at the Medical College of Virginia and the McGuire Veterans Administration PVg Medical Center in Richmond. All patients wel~ screened by a single experienced vascular technologist. Patients with a previous history of transient ischemic attack or stroke or persons who had undergone prior carotid endarterectomy were excluded from this study. Patients were evaluated for the presence or absence of cervical bruit. All patients were screened by indirect and direct carotid Doppler studies, as described later. Eighty-five patients had an asymptomatic carotid bruit and/or Doppler evidence of significant carotid obstruction (>50% diameter reduction). No patient underwent prophylactic carotid endarterectomy. The perioperative and early postoperative outcome of these patients has been previously reported. 4 Periopcrativc neurologic deficits developed in eight patients, four of whom had preoperative evidence of asymptomatic carotid bruit and/ or carotid obstruction by Doppler examination. O~ the 10 perioperative deaths nine were patients with evidence of carotid disease. All but two of the deaths were due to myocardial infarction. Seventy-two patients with asymptomatic carotid disease survived operation without neurologic deficits. Five patients were lost to follow-up. The present report reveals the late outcome of the remaining 67 patients with unoperated asymptomatic carotid disease. The study included 59 men and eight women whose ages ranged from 37 to 79 years (mean 58 years). The indication for operation was symptomatic coronary artery disease in 40 patients and peripheral [;.:.'vascular disease in 27 persons. Risk factors included cigarette smoking in 51 patients, hypertension that required medication in 38 patients, and diabetes mellitus in 22 persons. A history of cardiac symptoms was elicited from 59 subjects. Postoperative follow,_ up extended from 2 to 61 months (mean 35 month@ Follow-up studies. After corresponding with their private physicians, all patients were interviewed by one of the authors. A directed history of symptoms suggesting transient ischemic attack or stroke was solicited from each patient. n patients who died, the cause of death was ascertained from the autopsy report or death certificate. All patients were encouraged to return to the Noninvasive Peripheral Vascular Laboratory for follow-up noninvasive carotid studies. Fifty-one patients agreed to return for one or more studies, which included a directed neurovascular physical examination and indirect and direct noninvasive carotid evaluation. ndirect carotid studies included periorbital Doppler ultrasound and ocular pneumoplethysmography (OPG). Direct carotid studies included carotid phonoangiography, audible carotid Doppler flow signal

3 Volume 2 Number 6 November 1985 Outcome of untreated carotid disease after cardiovascular surgery 845,analysis, and carotid velocity evaluation by a realtime sound spectrum analyzer with quantification of spectral parameters described previously.s Carotid artery flow signals were categorized as normal, less than 50% stenotic, greater than 50% stenotic, or occluded. The accuracy of direct carotid Doppler assessment with spectral analysis in our laboratory has been previously reported with a sensitivity of 97% for carotid lesions of 40% diameter reduction or greater and a specificity of 86% in identifying normal carotid arteries. Data analysis. The major response variables analyzed in this study included death, stroke, and transient ischemic attack. The outcomes were analyzed separately for patients with PVD and CAD, because several previous studies have reported patients with only one of these operative indications. Deaths Were analyzed for cardiovascular causes, including myocardial infarction and stroke. Strokes were evaluated for their anatomic correlation with the side of carotid bruit or disease detected preoperatively or the presence of disease progression postoperatively. Transient ischemic attacks were likewise assessed for their,correlation with preoperative or postoperative evidence of carotid disease in the hemispheric or vertebrobasilar system. A minor response variable was the evidence for carotid disease progression based on serial nonin- Vasive diagnostic techniques. Disease progression was defined by carotid Doppler spectral analysis suggesting a change from either no or insignificant (<50%) carotid disease to >50% stenosis or occlusion of the vessel. Because of the variable time period of recruitment of patients into the study and the differing lengths of follow-up for each patient, all data regarding the postoperative incidence of death, stroke, transient ischemic attack, and carotid disease progression were analyzed by the actuarial life-table method. The significance of differences in cumulative rates of these response variables in patients with PVD and CAD at each interval of follow-up was estimated from the critical ratios calculated by Greenwood's approximation of standard errors. 6 n addition chi-square analysis with correction for continuity was performed to compare differences in overall outcomes of patients with PVD and CAD. A probability value of less than 0.05 was considered significant. RESULTS Deaths. During the follow-up period 11 patients (16.4%) died at a mean interval of 21.7 months after operation (range 2 to 44 months). Fig. 1 depicts the e 2, = c.~dr,= 40 PVOn= r L---] ---"1.... "1 i! p = L CAD PVD p = Months After Operation Fig. 2. Cumulative actuarial survival free of neurologic deficits of patients with coronary artery disease (CAD) and peripheral vascular disease (PVD). T/A = transient ischemic attack. cumulative survival rate for patients with CAD and PVD. During the follow-up period seven patients (25.9%) with PVD died compared with four patients (10.0%) with CAD. This difference is not statistically significant (p > 0,10). Furthermore, at no point during the period of cumulative survival depicted in Fig. 1 is there a significant difference between patients with PVD and CAD. Of the 11 late postoperative deaths, six were due to cardiovascular causes including four deaths from myocardial infarction and two from stroke. Five of the six cardiovascular deaths were patients with PVD, including both of the fatal strokes. Late neurologic deficits. Twenty-two patients (32.8%) had neurologic deficits in the follow-up period at a mean of 31 months (range 8 to 53 months). Transient ischemic attacks occurred in 15 patients (22.4%) and stroke occurred in seven (10.4%). Fig. 2 depicts the cumulative survival rate frec of neurologic deficits (transient ischemic attack or stroke) for patients with CAD and PVD. Deficits occurred in 15 patients (55.6%) with PVD and seven patients (i7.5%) with CAD. This difference is highly significant (p < 0.00l). However, from the cumulative life-table analysis, the difference in incidence ofneurologic deficits between patients with PVD and CAD is significant only for the intervals after 48 months of follow-up.

4 . CAB 846 Barnes et al. Journal of VASCULAR SURGERY "io0-80 7O 60 5O ~ 'l CAD.= PVD.= p = 0.012,, p = [ [ Months After Operation PVO Fig. 3. Cumulative actuarial survival free of stroke of patients with coronary artery disease (CAD) and peripheral vascular disease (PVD). Of the 15 patients with transient ischemic attacks, the deficits were in the hemispheric territory in nine patients and in the vertebrobasilar system in six patients, Only four of the 15 transient ischemic attacks occurred ipsilateral to carotid disease detected preoperatively. No significant difference was evident in the incidence of hemispheric or vertebrobasilar transient ischemic attacks in patients with PVD or CAD, although the incidence was somewhat higher in patients with PVD (five of nine patients with hemispheric transient ischemic attacks and four of six patients with vertebrobasilar insufficiency). All seven late strokes were hemispheric in territory. Only three of the seven strokes were ipsilateral to carotid disease detected preoperatively. Fig. 3 depicts the cumulative survival rate free of stroke for patients with CAD and PVD. Stroke occurred in six patients (22.2%) with PVD and one patient (2.5%) with CAD. This difference is statistically significant (p < 0.05). Once again, the cumulative survival curves reveal that the difference in stroke rates between patients with CAD and PVD achieves significance only for the interval after 48 months of followup. Both of the two fatal strokes occurred in patients with PVD at 9 and 13 months following operation. Neither had a history of antecedent transient ischemic attacks. Both were associated with evidence of progression to bilateral internal carotid artery occlusion. Late disease progression. Of the 67 patients i~, this study, 51 people agreed to return to the Noninvasive Peripheral Vascular Laboratory for serial follow-up studies. Fig. 4 shows the cumulative survival free of carotid disease progression over the duration of this follow-up study. Forty-one patients (80.4%) showed no major change in the degree of carotid disease over the period of follow-up. New carotid stenoses developed in seven patients (13.7%) and three persons (5.9%) suffered new occlusions of the internal carotid artery. The incidence of disease progression was similar in patients with PVD (14.8%) and patients With CAD (15.0%). Two of the three patients With internal carotid occlusion suffered strokes, both of which were fatal. These two patients had documented prior occlusion of the contralatcral internal carotid artery..... DSCUSSON Despite the continuing controversy about the role of prophylactic carotid cndarterectomy in asymptomatic carotid disease, most clinicians assume that such patients arc at greatest risk at the time of major operation. Fields 7 was the first to suggest that patients with asymptomatic bruit were at significantly increased risk of stroke in the pcrioperativc period after major operation. Asa result of that report, most physicians in the interim have recommended prophylactic carotid endarterectomy for severe carotid disease prior to major operation, particularly coronary or peripheral arterial reconstruction. However, a review of the reported studies of patients undergoing major operation in the presence of unopcrated asymptomatic carotid disease suggests that a more conservative approach is advisable. The clinicia~,~ must be aware of the risk of asymptomatic disease in the preoperative patient in one of two contexts: the risk of perioperative stroke and the risk of stroke in the late follow-up period after major operation. Most of the reported series have addressed the stroke risk of patients with asymptomatic carotid disease in the perioperative period associated with major operation. Furthermore, most of the studies in the literature have reviewed patients undergoing major peripheral arterial or coronary artery reconstruction. The three retrospective studies of Carney et al.,8 Evans and Cooperman, 9 and Treiman et al.lo found no correlation between asymptomatic carotid bruit and perioperative stroke risk in patients undergoing major peripheral artery reconstruction. Ropper, Wechsler, and Wilson lj likewise found no correlation between asymptomatic carotid bruit and perioperative stroke in a large series of patients undergoing general,

5 Volume 2 Number 6 November 1985 Outcome of untreated carotid disease after cardiovascular surgery 847 coronary, or peripheral artery surgery. The three reports of Turnipseed, Berkoff, and Belzer, 12 Breslau et al.,13 and Barnes et al.4 represent the only prospective studies with direct carotid noninvasive techniques used to identify patients with asymptomatic carotid disease that was not corrected prior to major coronary or peripheral arterial reconstruction. n none of these three series was the risk ofperiopcrative stroke in patients with documented asymptomatic carotid obstruction greater than in patients without detectable carotid disease. t is interesting that the risk of perioperative stroke in patients with unoperated asymptomatic carotid disease (3.4%) was no greater than the risk of stroke in patients undergoing concomitant carotid and coronary artery reconstruction (3.5%) in the prospective study ofbrener et al.14 The report by Kartchner and McRac ~s is the only study suggesting that unoperated asymptomatic disease detected by noninvasive techniques (OPG) poses a significant risk of perioperative stroke prior to major cardiovascular operation. However, the study by Kartchner and McRae is retrospective and does not represent a homogeneous sample of patients treated in a consistent manner before major operation. There have been few reports of the late outcome of patients undergoing major operation in whom asymptomatic carotid disease discovered incidentally was followed nonoperatively. Cooperman, Martin, and Evans 3 in a follow-up study of patients undergoing major peripheral operation reported a significantly higher incidence of stroke in patients with unoperated asymptomatic carotid disease (15 %) than in patients without detectable bruit (3.6%). However, the study suffers the limitations of being retrospective with no objective data about the status of the carotid arteries other than bruit assessment, which shows a poor correlation with the severity of carotid disease. Our prospective study 4a6 provides the only available data about the perioperative and late postoperative natural history of asymptomatic carotid disease documented by noninvasive direct carotid screening techniques prior to major coronary and peripheral arterial reconstruction. n our last report, 4 we noted a prevalence of asymptomatic cervical bruit in 44 patients (9.8 %) and carotid obstruction by Doppler ultrasound in 63 (14.0%) of 449 patients undergoing coronary or peripheral arterial revascularization. The prevalence of carotid artery disease was significantly higher in patients with PVD (28.8%) than in patients with CAD (15.1%) (p < 0.05). We noted poor correlation between the presence of cervical bruit and carotid obstruction. Only ~= 70 ~_ 60 o ~ 40 -~ 30 ~ 2O ;,~oo CAO Pvo~ = carotid occlusion ++ = fatal stroke [ Months After Operation Fig. 4. Cumulative actuarial survival free of carotid disease progression assessed by Doppler spectral analysis of patients with coronary artery disease (CAD) and peripheral vascular disease (PVD). 36.9% of the arteries associated with bruit had significant obstruction detectable by Doppler ultrasound. Conversely, only 27.3% of arteries that showed significant obstruction by Doppler examination were associated with a cervical bruit. There was no significantly greater risk of perioperative stroke in patients with asymptomatic cervical bruit or carotid obstruction by Doppler ultrasound compared with patients with no evidence of carotid disease. Only one of the eight perioperative neurologic deficits occurred on the side of detectable carotid obstruction by Doppler ultrasound. n our original report, 16 we noted that asymptomatic carotid disease correlated with a significantly increased risk of perioperative death. The perioperative mortality rate of patients with carotid artery disease was 10.6% compared with 0.3% in patients without detectable carotid disease. 4 Eight of the 10 perioperative deaths were the result of myocardial infarction. During the first 2 years of follow-up of these patients, 4 there was a significant incidence of postoperative ncurologic deficits, the majority of which were transient ischemic attacks. n that report the incidence of postoperative neurologic deficits in patients with asymptomatic disease (16.7%) was significantly higher than in patients without preoperative evidence of carotid disease (0.8%). All except PVD

6 848 Barnes et al. Journal of VASCULAR SURGERY two of the postoperative deficits were transient ischemic attacks. Seven of the 12 deficits involved a cerebral hemisphere that was not associated with significant carotid obstruction. Our last report 4 documented that patients with asymptomatic carotid disease had a significantly greater risk of postoperative death (9.2%) than patients without detectable preoperative carotid disease (0.8%, p < 0.001). The majority of the postoperative deaths were due to myocardial infarction. This correlation of preoperative carotid disease with postoperative deaths from myocardial infarction has been emphasized by others, a,7,17 The present study provides a longer postoperative follow-up of the available patients from our original study who survived operation without neurologic deficit and who had uncorrected asymptomatic carotid disease. Several facts emerged from this study of the natural history ofasymptomatic carotid disease following major cardiovascular operation. Patients with carotid disease were at significant risk of eventual death from cardiovascular cause, usually myocardial infarction or stroke. Uncorrected asymptomatic carotid disease, although not a significant risk factor for perioperative stroke, resulted in a significant incidence of late postoperative neurologic deficit (33%). Such deficits were significantly more common in patients with PVD than individuals with CAD. However, life-table analysis supported such significant differences only after 48 months of followup. Less than one third of the neurologic deficits occurred ipsilatcral to carotid disease detected preoperatively. n this study, two thirds of the late postoperative deficits were transient ischemic attacks. Late postoperative strokes were significantly more common in patients with PVD than in patients with CAD. Once again, this difference was noted only after 48 months of follow-up. Life-table analysis revealed a cumulative stroke rate of less than 10% over the first 3 years of follow-up for patients with both PVD and CAD. Both of the two fatal postoperative strokes occurred in patients whose carotid disease progressed to the point of bilateral internal carotid artery occlusion. Noninvasive evidence of late carotid disease progression occurred in 20% of patients, which was equally prevalent in patients with PVD and CAD. However, noninvasive evidence of carotid disease progression was documented in only 27% of the patients who developed postoperative neurologic deficits. CONCLUSONS We believe that our prospective study does not support the common practice of routine prophylactic carotid endarterectomy to treat incidentally discovered asymptomatic carotid disease in patients who are candidates for major cardiovascular operation. Had we entertained such a philosophy, we would estimate that only 4 of 12 perioperative and late postoperative strokes might have been prevented by such a practice. The anticipated operative and late postoperative stroke rate for the 63 patients with preoperative evidence of significant carotid obstruction by Doppler ultrasound might have equalled this number of patients benefited by the procedure. Our philosophy is shared by Chambers and Norris 18 who believe that the risks of prophylactic endarterectomy outweigh benefits unless a subgroup of patients with a spontaneous stroke risk of at least 5% each year can be identified. For the first 3 years of follow-up in our study the stroke rate was less than 3% each year by the life-table analysis. However, our conservatism regarding operative intervention for asymptomatic carotid disease in no way implies a complacent attitude about the longterm risk of neurologic deficits in these patients. We think that detected asymptomatic carotid disease is a harbinger for future neurologic deficits as well as death from cardiovascular causes, particularly myocardial infarction. We would encourage physicians to closely follow patients with asymptomatic carotid disease with the goal of identifying those persons who subsequently suffer transient ischemic attacks, which are usually the first signs of neurologic symptoms. We believe that a concerted effort in educating patients about the nature and significance of transient ischemic attacks is the best method to identify those patients who are at greatest risk of future stroke. We do not share literally the tongue-in-cheek philosophyof Kuller and Sutton 2 that patients "should be advised and required to sign informed consent prior to auscultation of the neck." However, we do think that physicians have a mandate to inform the patients of the need to report promptly the evanescent symptoms heralding stroke that often go unrecognized by the patient and physician alike. For those patients who have postoperative transient ischemic attacks, expeditious angiographic evaluation and appropriate operative intervention may be the most efficacious method of preventing stroke. However, for the majority of patients who will remain without symptoms, we believe that nonoperative intervention is the most rational method of managing their asymptomatic carotid disease. REFERENCES 1. Fields WS. The asymptomatic carotid bruit--operate or not? Stroke 1978; 9:

7 Volume 2 Number 6 November 1985 Outcome of untreated carotid disease after cardiovascular surgery Kuller LH, Sutton KC. Carotid artery bruit: s it safe and effective to auscultate the neck? Stroke 1984; 5: Cooperman M, Martin EW, Evans WE. Significance of asymptomatic carotid bruits. Arch Surg 1978; 113: Barnes RW, Liebman PR, Marszalek PB, Kirk CL, Goldman MH. The natural history of asymptomatie carotid disease in patients undergoing cardiovascular surgery. Surgery 1981; 90: Rittgers SE, Thomhill BM, Barnes RW. Quantitative analysis of carotid artery Doppler spectral waveforms: Diagnostic value of parameters. Ultrasound Med Biol 1983; 9: Greenwood M. The errors of sampling of the survivorship tables. Appendix 1. n: Reports on public health and statistical subjects, No. 33, London: His Majesty's Stationery Office, Fields WS. Neurologic disorders related to alterations in blood pressure. Cardiovasc Res Cent Bull 1964; 2: Carney W, Stewart WB, DePinto DJ, Mucha SJ, Roberts B. Carotid bruit as a risk factor in aortoiliac reconstruction. Surgery 1977; 81: Evans WE, Cooperman M. The significance ofasymptomatic unilateral carotid bruits in preoperative patients. Surgery 1978; 83: i0. Treiman RL, Foran RF, Cohen JL, Levin PM, Cossman DV. Carotid bmit--a follow-up report on its significance in patients undergoing an abdominal aortic operation. Arch Surg 1979; 114: Ropper AH, Wechsier LR, Wilson LS. Carotid bruit and the risk of stroke in elective surgery. New Engl J Med 1982; 307: Turnipseed WD, Berkoff HA, Belzer FO. Postoperative stroke in cardiac and peripheral vascular disease. Ann Surg 1980; 192: Breslau PJ, Fell G, vey TD, Bailey WW, Miller DW, Strandness Jr DE. Carotid arterial disease in patients undergoing coronary artery bypass operations, l Thorac Cardiovasc Surg 1981; 82: Brener BJ, Brief DK, Alpert J, Goldenkranz RJ, Parsonnet V, Feldman S, Gielchinsky, Abel RM, Hochberg M, Hussain M. A four-year experience with preoperative noninvasive carotid evaluation of two thousand twenty-six patients undergoing cardiac surgery. J VAsc SURG 1984; 1: Kartchner MM, McRae LP. Carotid occlusive disease as a risk factor in major cardiovascular surgery. Arch Surg 1982; 117: Barnes RW, Marszalek PB. Asymptomatic carotid disease in the cardiovascular surgical patient: ls prophylactic endarterectomy necessary? Stroke i981; 12: Burke PA, Callow AD, O'Donnell Jr TF, Kelly JJ, Welch H. Prophylactic carotid endarterectomy for asymptomatic bruit. Arch Surg 1982; 117: Chambers BR, Norris JW. The case against surgery for asymptomatic carotid stenosis. Stroke 1984; 15:964-7.