Carotid endarterectomy after reversible ischemic neurologic deficit or stroke: Is it of value?

Transcription

1 Carotid endarterectomy after reversible ischemic neurologic deficit or stroke: Is it of value? David Rosenthal, MD, Edgar Borrero, MD, Michael D. Clark, MD, Pano A. Lamis, MD, and Wayne W. Daniel, Phl), Atlanta, Ga. The benefit of carotid endarterectomy (CE) in preventing recurrent stroke and improving survival in the patient who has sustained a reversible ischemic neurologic deficit (RIND) or stroke is still controversial. To determine the long-term benefits and value of CE in these patients, a 10-year review of 253 patients who suffered a RIND or stroke was conducted. All patients had CT brain scans, as well as arch, extracranial, and intracranial arteriography; any patients without demonstrated carotid bifurcation disease were excluded from the study. On the basis of clinical symptoms and CT scan findings, 66 patients were categorized as having sustained a RIND and 187 a stroke. One hundred fifty-one patients who suffered a RIND or stroke had CE, whereas 102 patients with RIND or stroke did not have CE and served as a control group. All endarterectomies were performed with a temporary indwelling shunt. Postoperative complications included two deaths (1%), six strokes (4%), and 10 transient neurologic deficits (7%). In follow-up extending to 10 years the cumulative incidence of recurrent stroke was only 7% (11 patients) in the operated group, whereas 18% of patients in the nonoperated control group (18) sustained a recurrent stroke (p < 0.05), As anticipated, the leading cause of death during follow-up was cardiac related; although CE did not significantly improve long-term survival, there was more than a twofold decrease in the incidence of recurrent stroke as a cause of death in the group having CE. This experience indicates that CE in the patient who has suffered a RIND or stroke is beneficial in preventing recurrent stroke and thereby improving long-term quality of life. (J VASC SURG 1988;8: ) Stroke is the third leading cause of death in the United States, exceeded only by heart disease and cancer. It kills more than 200,000 American men and women annually, and its medical and social impact is dramatically emphasized by the estimated cost of stroke, which in 1987 will be in excess of $3 billion.: A completed stroke is characterized by a fixed, nonprogressive neurologic deficit that lasts longer than 24 hours and is due to cerebral infarction, whereas a reversible ischemic neurologic deficit (RIND) lasts longer than 24 hours but resolves completely within 3 weeks. It is thought that a RIND results from sustained ischemia not severe enough to produce infarction. 2 The benefit of carotid endarterectomy (CE) in preventing recurrent stroke and improving survival in the patient who has sustained a From the Department of Vascular Surgery, Georgia Baptist Medical Center--Medical College of Georgia. Presented at the Twelfth Annual Meeting of the Southern Association for Vascular Surgery, St. Thomas, Virgin Islands, Jan , Reprint requests: David Rosenthal, MD, 315 Blvd. NE, Suite 412, Atlanta, GA stroke or RIND has been controversial. This review was undertaken to evaluate the role of CE in preventing recurrent stroke in patients who have sustained RIND or stroke compared with a similar cohort of patients treated nonoperatively during the same time period. MATERIAL AND METHODS Two hundred fifty-three patients who sustained stroke or RIND and had documented evidence of extracranial carotid disease were evaluated at Georgia Baptist Medical Center, Atlanta, Georgia, between June 1977 and June A stroke was defined as a fixed, nonprogressive neurologic deficit that lasted longer than 24 hours with infarction demonstrated by CT brain scan. An RIND, by definition, lasts longer than 24 hours, resolves completely within 3 weeks, and with no infarction identified by CT brain SCan. Thc neurologic deficit of each patient was assessed and classified by the neurology and/or vascular surgery staffs (Table I). Mild deficits were those that did not interfere with normal activities, and only min- 527

2 528 Rosenthal et al Iournal of VASCULAR SURGERY 100, ~-z 80[,,, 60 0 n- "' 40 n 20 0 CAHD HT DM SMOKING Fig. 1. Patient profile risk factors for operated and nonoperated patients. CAHD, Coronary artery heart disease; HT, hypertension; DM, diabetes mellims; black bars, operated patients; gray bars, nonoperated patients. Table I. Neurologic deficit at the time of operation or initial evaluation Operated Nonoperated Stroke severity % No. % No. None Mild Moderate Severe imal residual abnormalities were present (e.g., clumsiness or positive Babinski sign). Moderate deficits were those that obviously impaired the patient's lifestyle (e.g., assistance needed with ambulation, unable to perform occupation), whereas severe deficits were those that produced major neurologic sequelae interfering with daily activity (e.g., hemiplegia, aphasia). On the basis of clinical symptoms or radiologic evidence of cerebral infarction, patients were placed into a "poststroke" or a "post-rind" group. All patients had CT brain scans, and 26 underwent sodium pertechnetate technetium 99m radionuclide brain scans as well. One hundred nineteen patients had contrast enhancement CT scans obtained by giving 150 ml of isothalamate meglumine injection (Conray 60) immediately before the scan. All patients had contrast evaluation of the extracranial circulation: 239 patients had four-vessel arch arteriography with visualization of the extracranial and intracranial circulation, whereas 14 had digital subtraction arteriography. Any patient who did not have extracranial carotid disease was excluded from the study. One hundred fifty-one patients had CE; 104 of these patients had previously sustained stroke and 47 RIND. The interval between stroke and CE ranged from 9 days to 11 months (mean 5.2 weeks), whereas the interval between RIND and operation ranged from 3 days to 8 months (mean 3.8 weeks). One hundred two patients did not have operation and served as a control group; 83 of these patients had previously suffered stroke and 19 RIND. These patients did not have operations because of the judgment by the referring physician (86 patients), reluctance by the family or patient (10), or were considered prohibitive surgical risks (six). These six patients were deemed prohibitive surgical risks because of severe coronary artery disease. All CEs were performed with the patient under general anesthesia and with a shunt. The patient profile risk factors between the operated and nonoperated poststroke and post-rind groups were similar (Fig. 1). The mean age was 67 years (range 42 to 81 years). A history consistent with coronary artery disease was present in 162 patients, hypertension in 134, diabetes mellitus in 101, and cigarette smoking in 103 patients. One hundred sixty-five of the patients studied were men. All patients having surgery were clinically evaluated in the immediate postoperative (a0-day) period; long-term follow-up ranged from 1 to 10 years (mean _+ 1 standard deviation, 52.7 _ months, median 46 months, range 116 months). The long-term follow-up for the patients not operated on also ranged from 1 to 8 years (mean months; median 48 months; range 118 months). If follow-up evaluation showed no new episodes of hemispheric or vertebrobasilar insufficiency symptoms, the patient was classified as improved or asymptomatic. To gather surgical data and to determine the qual-

3 Volume 8 Number 4 October 1988 Carotid endarterectomy after RIND or stroke 529 Table II. Life table for survival of patients having surgery No. of Cum. Follow-up patients No. of Interval stroke interval* entering strokes in stroke rate (vr) interval interval (%) (%) Totals Gum. stroke-free No. withdrawn rate No. lost to alive (alive at No. of (%) follow-up end of study) deaths _ ~Interval is up to but does not include the second figure. Table III. Life table for survival of patients not having surgery No. of Interval Cure. patients No. of stroke stroke Follow-up entering strokes in rate rate interval (yr) interval interval (%) (%) Gum. stroke-free No. withdrawn rate No. lost to alive (alive at No. of (%) follow-up end of study) deaths Totals O _ ity of life after CE, the patients were evaluated during office visits, contacted by letter, or interviewed by telephone. Forty-two patients were lost to followup, 26 from the operated group and 16 from the nonoperated group. To determine the patient's neurologic status, 56% of the operated patients (84 of 151) (Table II) alive at long-term follow-up were evaluated by office visit and 41% of the nonoperated patients alive (42 of 102) were evaluated at office visit by the neurology or medical staff (Table III). RESULTS The neurologic deficit of all patients was graded at the time of CE and at the time of their original stroke (Table I). There was no significant difference between the operated and nonoperated patients with respect to severity of their presenting neurologic deficits. CT scans performed within 72 hours after the onset of neurologic deficits demonstrated cerebral infarction in 48% of the patients (121 of 253). Nineteen percent of the patients (25 of 132) with persistent neurologic deficits, despite a normal admission CT scan, had evidence of infarction when contrast enhancement was used on a repeat CT scan within 5 days. Another 35 patients with continued neurologic deficits, despite repeat CT scan with contrast enhancement, ultimately had evidence of infarction when a CT scan was performed (17 to 120 days). Seventy-two patients with a suspected RIND (normal admission CT scan and resolution of neurologic deficit within 3 weeks) had contrastenhancement CT scanning. Six of the 72 scans (8%) showed enhancement or evidence of infarction; these patients were then placed into the stroke group. In the remaining 66 scans, no enhancement or infarction was identified; therefore the RIND group comprised these patients. Radionuclide brain scans were also done in 26 patients and corroborated the diagnosis of infarction

4 530 Rosenthal et al. Journal of VASCULAR SURGERY PERCENT I O 7O 6O 50 4O 3O 2o (P = 0.05) 10 I I I I I I I I I I I YEARS Operated Group Nonoperated Group Fig. 2. Cumulative ipsilateral stroke-free rate in operated and nonoperated patients. Bars indicate standard error. Table IV. Arteriographic findings Operated Nonoperated (n = ls]) (n = 102) % No. % No. Ipsilateral excavated plaque Ipsilateral stenosis > 75% Contralateral bifurcation disease Intracranial occlusive disease I7 17 in 10 (43%). The diagnostic accuracy of the radionuclide scans was greatest during the second week after stroke and was not so sensitive as the early (72 hours) enhancement CT scan. Twenty-nine poststroke patients with a limited, stable stroke and an abnormal CT scan had CE within 21 days (range 9 to 21 days). These patients had arteriographically proven hemodynamic stenosis (greater than 75%) of the internal carotid artery or complex macrotdcerated plaque. In this subset of patients, one postoperative stroke occurred (3%) and three patients (10%) sustained a focal, minor transient ischemic attack (TIA) that resolved uneventfully. Seventy-five poststroke patients had significant infarcts on CT scan and demonstrated gradual improvement of their neurologic deficits. These patients subsequently had CE after 28 days (range 28 days to 8 months) and among the patients, four postoperative strokes occurred. Thirty-one post-rind patients, whose neurologic deficit resolved, had a hemodynamically significant stenosis of the internal carotid artery at arteriography and had CE within 21 days (range 3 to 21 days). Among these post-rind patients, one postoperative stroke (3%) and one TIA (3%) occurred. The remaining 16 post-rind patients did not suffer a postoperative stroke. As indicated, all patients were subjected to contrast or digital subtraction arteriography (Table IV). Of the 151 patients who suffered RIND or stroke and had CE, excavated plaque was identified in 49% (74 of 151 patients), and 5i% (77 of 151 patients) had stenosis of the internal carotid artery greater than 75 % diameter reduction. Contralateral carotid artery disease (excavated plaque or stenosis of the internal carotid artery greater than 50% diameter reduction) was identified in 30% of the operated patients (46 of 151 patients), and 34% (51 of 151 patients) had significant intracranial occlusive disease. Among the 102 post-rind or poststroke patients who did not have CE, excavated plaque was identified in 51% (52 patients) and stenosis greater than 75% diameter reduction of the internal carotid artery was found in 49% (50 patients). Stenosis greater than 75% diameter reduction of the contra-

5 Volume 8 Number 4 October 1988 Carotid endarterectomy a~er RIND or stroke 531 PERCENT I I I I I 1 I I YEARS Operated Group [] Nonoperated Group Fig. 3. Cumulative 10-year survival. Bars indicate standard error. lateral carotid artery was found in 44% (44 patients). Contrallateral carotid artery disease among these patients was identified in 29% (29 patients), and 17% had significant intracranial occlusive disease. Three patients suffered transient worsening of their neurologic deficits after arteriography. All CEs were performed with the patients under general anesthesia with continuous arterial blood pressure monitoring and temporary shunts were used in all patients. At the time of operation no patients had altered levels of consciousness and only 13 had severe neurologic deficits. These deficits consisted of contralateral upper or lower extremity paralysis in nine patients and hemiplegia in four. All of these patients had severe extracranial occlusive disease and recurrent neurologic symptoms despite medical treatment with antiplatelet medications or anticoagulants. Postoperative complications included two deaths (1%), six strokes (4%), and 10 transient neurologic deficits (7%). One death occurred in a patient who suffered a postoperative myocardial infarction and subsequent episode of ventricular fibrillation. The other death occurred in a hypertensive patient who sustained an ipsilateral intracranial hemorrhage on the third postoperative day. Three of the six postoperative strokes were thromboembolic in origin and Table V. Causes of death ffi CVA CA Other Operated group (n = 39) Nonoperated group (n = 40) MI, Myocardial infarction; CVA, stroke; CA, cancer. were documented at an emergency sccond operation. These carotid arteries became thrombosed because of technical error: an intimal flap was identified in two and a lateral tear repair site in the third. Two other postoperative strokes were due to an intracranial embolic "shower," which was verified with arteriography at repcat operation. The sixth postoperative stroke (mentioned earlier) occurred 3 days after CE when a markedly hypertensive patient suffered an intracranial hemorrhage and ultimately died. In follow-up extending to 10 years, 72% of the operated patients available for evaluation remained stroke free and only 11 strokes occurred (Table II). However, among the nonoperated patients only 26% were stroke free, 18 patients having sustained an ipsilateral stroke (p < 0.05) (Table III, Fig. 2). Among the operated patients, 4 of the 11 recurrent strokes were believed to be thromboembolic. All four patients had nonhcmorrhagic infarcts on CT scan, and

6 532 Rosenthal et al. Journal of VASCULAR SURGERY two had arteriography that demonstrated recurrent excavated plaque in the operated carotid artery. Six of the recurrent strokes were due to intracerebral hemorrhages documented by CT scan; four of these patients died. One patient died shortly after the onset of a recurrent stroke and did not have diagnostic studies. Of the 18 recurrent strokes in the nonoperative patients, 11 were believed to be thromboembolic in origin. These patients also had nonhemorrhagic infarcts by CT scan, with most occurring within 3 years after their initial presenting stroke. Eight of these recurrent strokes occurred without antecedent TIAs and six were fatal. Five other patients had massive hemorrhagic infarcts by CT scan and four were fatal; two other recurrent strokes and deaths occurred and the cause of the recurrent strokes could not be determined. During 10-year follow-up, 39 patients in the operated group died (26%), whereas 40 patients in the nonoperated group died (40%) (Table V). As anticipated, the leading cause of death in both groups was cardiac related. However, in the nonoperated group there was more than a twofold increase of recurrent stroke as a cause of death than among the operated patients (p < 0.02). Table II summarizes in life-table form the survival data for the two study groups. The mean survival for the operated group was 6.8 years and for the nonoperated group 5.8 years. However, the survival rates between the study groups were not significantly different (p > 0.10) (Fig. 3). DISCUSSION Wlaen confronted with a patient who has suffered a stroke caused by extracranial carotid disease, the clinician faces a management dilemma: should the patient be treated medically or surgically? Because there is no consensus on the safest way to manage these patients, a study was undertaken to evaluate the role of CE in preventing recurrent stroke in patients who have sustained RIND or stroke. The keystone to management of these patients is the CT brain scan. The CT scan may faintly visualize an abnormality as early as 3 hours after the onset of symptoms, and a low-density abnormality may be evident between 24 and 72 hours. 3 In this report, 48% of CT scans (121 of 253 patients) performed within 72 hours after the onset ofa ncurologic deficit visualized areas of cerebral infarction. In patients whose original CT scan is normal but in whom a neurologic deficit persists, a contrast enhancement scan is indicated. Nineteen percent of patients (25 of 132) with a neurologic deficit and normal admission CT scan ul- timately had infarction shown by enhancement scan. CT enhancement is due to a breakdown in the bloodbrain barrier capillary endothclium and extravasation of contrast medium into the extracellular space. The diagnostic yield of a contrast enhancement scan during the first week after infarct is variable and principally due to the differences in infarct origin. Infarcts for which CT scans demonstrate early enhancement are generally embolic in origin, as these infarcts reperfuse early and reveal blood-brain barrier abnormalities not evident in thrombotic infarcts where contrast delivery is insufficient to demonstrate enhancement. 4 Classical teaching dictated that cerebral arteriography should not be performed in patients with an acute neurologic deficit, as an inordinately high incidence ofneurologic complications was observed, s In a previous report, we advocated waiting 10 days before performing arteriography if a radionuclide or enhancement CT scan demonstrated infarction to allow glial repair to occur as a prelude to surgery. 2 However, more recent reports demonstrate that cerebral arteriography can be safely carried out even when acute infarction is identified by CT scan. 6,7 After the CT scan rules out a "mass" lesion (i.e., arteriovenous malformation, subdural hematoma, or neoplasm) in the patient with a mild or moderate fixed deficit, it is our current policy to perform arteriography to evaluate the extracranial and intracranial vasculature. With the advances in digital subtraction techniques, selective vessel catheterization, nonionic contrast agents, and reduced dye loads, angiography can now be safely performed in patients with acute fixed neurologic deficits. All patients in this review had contrast or digital arteriography and only three had transient worsening of their symptoms after angiography. Newer generation ("fast") CT scanners should allow for earlier stroke documentation, as imagedegrading patient motion will present less of a problem. In addition, with the advent and availability of magnetic resonance imaging (MRI), we now have the ability to delineate cerebral infarction more precisely and earlier than with CT scan. 8 However, until a time when objective diagnostic techniques exist to determine when patients can safely undergo CE after RIND or stroke, a combination of CT and MRI, arteriography, and clinical symptoms must all be correlated to formulate safe guidelines of management (Fig. 4). When patients have a neurologic deficit, a CT or MRI scan will usually delineate a mass lesion (arteriovenous malformation, subdural hematoma, or tumor) from infarct immediately. If the CT scan demonstrates no mass lesion, arteriograms should be

7 Volume 8 Number 4 October 1988 Carotid endarterectomy after RIND or stroke 533 CT/MRI ]..~ekss LESION NO INFARCT ARTERIOGRAM DERCIT RESOLVES 3 WEEKS RIND I DEFICIT PERSISTS =l -I. ] -I ENHANCEMENT SCAN SMALL INFARCT FIXED DEFICIT 1 CE/SHUNT PREOCCLUSIVE NO~ITI CROULCER SIMPLE PLAQUE I 4-6 WKS I <4WKS Fig. 4. Algorithm for management of patients with a fixed neurologic deficit. performed. If the CT scan demonstrates no evidence of infarction, and the neurologic deficit resolves within 3 weeks, a diagnosis of RIND is made and the patient can be operated on with a shunt. However, if the deficit persists, a CT enhancement scan is indicated. When the enhancement scan documents a small infarct and arteriography shows a high-grade carotid stenosis or macroulceration (despite a fixed neurologic deficit), CE may again be safely performed with a shunt. However, when a large infarct, with or without enhancement, is documented and the patient has a mild or moderate neurologic deficit, arteriographic findings will delineate the course of action. If a noncritical stenosis or simple plaque is demonstrated, the safest course of action is to wait 4 to 6 weeks to allow insulted brain tissue time to repair. During this interval, the patient is maintained :with antiplatelet medications; if a recurrent neurologic event occurs, the option to operate remains available. However, if arteriography demonstrates a high-grade preocclusive internal carotid artery stenosis or macroulcerated lesion, the surgeon may be forced to operate sooner, recognizing an increased risk for a postoperative neurologic deficit. All endarterectomies were performed with a temporary indwelling shunt. In a previous report we 2 demonstrated that intraoperative electroencephalographic (EEG) surveillance and "stump pressures" were not sensitive enough indicators of cerebral perfusion in the patient who has sustained RIND or stroke, as approximately 10% of our initially reported patients, with normal stump pressure and normal intraoperative electroencephalography, had a recurrent neurologic deficit after CE. It is believed that after RIND or stroke, a zone ofischemic brain tissue persists; this ischemic zone may be more vulnerable to diminished perfusion during CE than normal brain tissuel As this ischemic zone is supplied by collateral vessels, any decrease in perfusion pressure during carotid cross-clamping probably will reinjure already compromised brain tissue. Indeed, the reported incidence of having to use a shunt (on the basis of EEG evidence of cerebral ischemia) in the poststroke or post-rind patient is two or three times more frequent than when endarterectomy is performed in patients with "stable" neurologic symptoms (TIAs, vertebrobasilar insufficiency, or amaurosis fugax) 9 (Callow AD. Personal communication, November 1987). Although the postoperative stroke rate in this series was an elevated 4% (6 of 151 patients), the postoperative strokes were due to technical error (three patients), microemboli (two patients), and intracranial hemorrhage (one patient). None of the postoperative strokes was believed to be due to decreased perfusion during carotid crossclamping because a shunt was used in all patients. In these neurologically "unstable" poststroke and post- RIND patients, where brain tissue has already sustained an insult and may be more sensitive to hypoxia and/or flow deprivation, the safest and wisest course of action would seem to be to maintain uninterrupted cerebral perfusion during CE by the use of prophylactic shunting. CONCLUSIONS The benefit of CE in preventing recurrent stroke and improving survival in the patient who has sustained RIND or stroke has been a matter of controversy. The reported incidence in earlier studies of recurrent neurologic deficit in these patients was re-

8 534 Rosenthal et al. tournal of VASCULAR SURGERY ported to range from 3.8% 1 to 24% ~ in long-term follow-up. In comparison, when patients were treated medically after stroke, the incidence of recurrent neurologic deficit was reported to range from 7% 7 to 53% ~2 during long-term follow-up. Because these reported results were so variable, the polarizing issue of the merit and role of CE in preventing recurrent stroke continued. The reasons for the variation in these results, both in the operative and nonoperative reports, are multifactorial: (1) the studies did not have simultaneous control groups, (2) patient selection in reference to the degree of neurologic deficit at the time of presentation was variable, (3) the arteriographic findings at the time of presentation were not documented, (4) the "laterality" referable to the side of recurrent stroke in relation to the symptomatic artery (ipsilateral or contralateral), and (5) the origin of the recurrent strokes (i.e., thromboembolic or hemorrhagic) was not defined. However, the present study did have simultaneous control groups (Fig. 1), did compare patient selection in reference to presenting neurologic deficits (Table I), and did document arteriographic findings at the time of presentation (Table IV), laterality of recurrent.stroke, and the cause of the recurrent strokes. We specifically did not include late contralateral stroke as "recurrent strokes"; these were independent, initial events. However, 17% of patients (25 of 151) in the operated group and 14% of patients in the nonoperated control group (14 of 102) sustained contralateral strokes during long-term followup. Eighty percent of these late contralateral strokes (31 of 39) occurred in patients who had arteriographically documented contralateral bifurcation disease. This indicates that progression of uncorrected contralateral carotid disease is probably responsible for many late strokes and aggressive surveillance or prophylactic CE of contralateral lesions may be necessary to reduce this incidence of late stroke. This study demonstrated that operative management was superior to medical management in the prevention of recurrent stroke, as 72% of the operated patients vs 26% of the nonoperated patients remained stroke free at follow-up extending to 10 I years. Although CE did not significantly improve long-term survival, because of attrition from coronary artery disease, there was a significant decrease in the incidence of recurrent stroke and more than a twofold decrease in the incidence of recurrent stroke as a cause of death at late fbllow-up. In the patient who has suffered RIND or stroke, this experience indicates that CE is beneficial in preventing recurrent stroke and thereby improving long-term quality of life. REFERENCES 1. U.S. Department of Health and Human Services. A guide to the National Institute of Neurological and Comrnmaicative Disorders and Stroke. Public Health Service, National Institutes of Health, September Rosenthal D, Stanton PE, Lamis PA. Carotid endarterectomy. The unreliability of intraoperative monitoring in patients having had stroke or RIND. Arch Surg 1981;116: i Inoue Y, Takemota K, Yoshikawa N, et al. Sequential computed tomography scans in acute cerebral infarction. Radiology 1980;135: Hayman LB., Sakai F, Meyer JS, et al. Iodine enhanced CT patrems after cerebral arterial embolization in baboons. Am J Neuroradiol i980;1: Eisenhert RL, Banks WO, Hedgwick NW.Neurologic complications of angiography in patients with critical stenosis of the carotid artery. Neurology i98i;12: Haykal HA, Rumbaugh CI. Cerebrovascular accident: angiography/radionuclide brain CT scan. Postgrad Radiol 1984;4:i Buonarmo F, Toole JF. Management of patients with established completed stroke in cerebral infarction. Stroke 1981; i2:7-i6. 8. Zimmerman RD, Fleming CA, Lee BC, et al. Periventricular hyperintensity as seen by magnetic resonance: prevalence and significance. AIR 1986;I46: Whittemore AD, Mannick JA. Surgical treatment of carotid disease in patients with neurologic deficits. J VASC SURG 1987;5: Erickson SE, Luke H, Alto A, et al. Results of 88 consecutive prophylactic carotid endarterectomies in cerebral infarction and transitory ischemic attacks. Acta Neurol Scand 1981; 63: Hertzer NR, Arison R. Cumulative stroke and survival ten years after carotid endarterectomy. J VAsc SUnG 1985;2: i2. Acheson J, Hutchinson EC. The natural history of focal cerebral vascular disease. Q J Med i97i;40:15-23.