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Some believe that carotid endarterectomy (CEA) for carotid near occlusion is a necessary emergency procedure while others call it dangerous. We used the North American Symptomatic Carotid Endarterectomy Trial (NASCET) data to perform an observational study to examine the safety and benefit of CEA for carotid near occlusion. We divided the data of 659 patients into stenosis groups: 70 to 79%, 80 to 89%, 90 to 94%, and near occlusion. The 106 carotid-near-occlusion patients were subdivided into those with a string-like lumen (n = 29) and those without a string-like lumen (n = 77). Of the 48 patients with near occlusion treated with CEA, 3 (6.3%) had perioperative strokes, similar to the 70-94% stenosis group. Only 1 of 58 patients (1.7%) with near occlusion treated medically had a stroke in the first month, suggesting that CEA is not needed on an emergency basis in this circumstance. For medically treated patients, the 1-year risk of stroke increases with escalating degrees of carotid stenosis, where the risk is 35.1% for patients with 90-94% stenosis. For patients with near occlusion, the 1-year stroke risk diminishes to 11.1%, which approximates the risk for patients with 70-89% stenosis. A comparison of treatment differences indicates that surgery reduces the risk of stroke at 1 year by approximately one-half (p < 0.001), regardless of the degree of stenosis or the subcategory of carotid near occlusion (p = 0.89). Our data suggest that CEA is beneficial for near occlusion and not more dangerous than in patients with 70-94% stenosis, provided that the procedure is performed by an experienced surgeon with a low complication rate.

Background and Purpose: Indications for carotid endarterectomy have engendered considerable debate among experts and have resulted in publication of retrospective reviews, natural history studies, audits of community practice, position papers, expert opinion statements, and finally prospective randomized trials. The American Heart Association assembled a group of experts in a multidisciplinary consensus conference to develop this statement., Methods: A conference was held July 16-18, 1993, in Park City, Utah, that included recognized experts in neurology, neurosurgery, vascular surgery, and healthcare planning. A program of critical topics was developed, and each expert presented a talk and provided the chairman with a summary statement. From these summary statements a document was developed and edited onsite to achieve consensus before final revision., Results: The first section of this document reviews the natural history, methods of patient evaluation, options for medical management, results of surgical management, data from position statements, and results to date of prospective randomized trials for symptomatic and asymptomatic patients with carotid artery disease. The second section divides 96 potential indications for carotid endarterectomy, based on surgical risk, into four categories: (1) Proven: This is the strongest indication for carotid endarterectomy; data are supported by results of prospective contemporary randomized trials. (2) Acceptable but not proven: a good indication for operation; supported by promising but not scientifically certain data. (3) Uncertain: Data are insufficient to define the risk/benefit ratio. (4) Proven inappropriate: Current data are adequate to show that the risk of surgery outweighs any benefit., Conclusions: Indications for carotid endarterectomy in symptomatic good-risk patients with a surgeon whose surgical morbidity and mortality rate is less than 6% are as follows. (1) Proven: one or more TIAs in the past 6 months and carotid stenosis > or = 70% or mild stroke within 6 months and a carotid stenosis > or = 70%; (2) acceptable but not proven: TIAs within the past 6 months and a stenosis 50% to 69%, progressive stroke and a stenosis > or = 70%, mild or moderate stroke in the past 6 months and a stenosis 50% to 69%, or carotid endarterectomy ipsilateral to TIAs and a stenosis > or = 70% combined with required coronary artery bypass grafting; (3) uncertain: TIAs with a stenosis < 50%, mild stroke and stenosis < 50%, TIAs with a stenosis < 70% combined with coronary artery bypass grafting, or symptomatic, acute carotid thrombosis; (4) proven inappropriate: moderate stroke with stenosis < 50%, not on aspirin; single TIA, < 50% stenosis, not on aspirin; high-risk patient with multiple TIAs, not on aspirin, stenosis < 50%; high-risk patient, mild or moderate stroke, stenosis < 50%, not on aspirin; global ischemic symptoms with stenosis < 50%; acute dissection, asymptomatic on heparin. Indications for carotid endarterectomy in asymptomatic good-risk patients performed by a surgeon whose surgical morbidity and mortality rate is less than 3% are as follows. (1) Proven: none. As this statement went to press, the National Institute of Neurological Disorders and Stroke issued a clinical advisory stating that the Institute has halted the Asymptomatic Carotid Atherosclerosis Study (ACAS) because of a clear benefit in favor of surgery for patients with carotid stenosis > or = 60% as measured by diameter reduction. When the ACAS report is published, this indication will be recategorized as proven. (2) acceptable but not proven: stenosis > 75% by linear diameter; (3) uncertain: stenosis > 75% in a high-risk patient/surgeon (surgical morbidity and mortality rate > 3%), combined carotid/coronary operations, or ulcerative lesions without hemodynamically significant stenosis; (4) proven inappropriate: operations with a combined stroke morbidity and mortality > 5%.

Background and Purpose: The importance of carotid plaque ulceration as a cause of cerebral ischemic symptoms remains uncertain. Moreover, its prominence in symptomatic patients with severe carotid stenosis is unknown., Methods: The association between angiographically defined plaque ulceration and risk of subsequent stroke was assessed using Cox proportional hazards regression in 659 patients with severe (70% to 99%) carotid stenosis from the North American Symptomatic Carotid Endarterectomy Trial., Results: Treatment assignment (medical versus surgical) and degree of ipsilateral stenosis were identified as having a significant influence on the results. The risk of ipsilateral stroke at 24 months for medically treated patients with ulcerated plaques increased incrementally from 26.3% to 73.2% as the degree of stenosis increased from 75% to 95%. For patients with no ulcer, the risk of stroke remained constant at 21.3% for all degrees of stenosis. The net result yielded relative risks of stroke (ulcer versus no ulcer) ranging from 1.24 (95% confidence interval, 0.61 to 2.52) to 3.43 (95% confidence interval, 1.49 to 7.88). Conversely, for surgically treated patients with antecedent presence of an ulcerated plaque, the risk of stroke increased slightly at the highest degrees of stenosis. Overall, carotid endarterectomy reduced the risk of ipsilateral stroke at 24 months by at least 50%. Similar results were obtained for risk of major ipsilateral stroke and risk of all strokes and death., Conclusions: The presence of angiographically defined ulceration for medically treated symptomatic patients is associated with an increased risk of stroke. The risk of stroke more than doubles at higher degrees of stenosis. Carotid endarterectomy is beneficial in substantially reducing the risk of stroke, regardless of plaque ulceration and degree of severe carotid stenosis.

Background: Without strong evidence of benefit, the use of carotid endarterectomy for prophylaxis against stroke rose dramatically until the mid-1980s, then declined. Our investigation sought to determine whether carotid endarterectomy reduces the risk of stroke among patients with a recent adverse cerebrovascular event and ipsilateral carotid stenosis., Methods: We conducted a randomized trial at 50 clinical centers throughout the United States and Canada, in patients in two predetermined strata based on the severity of carotid stenosis--30 to 69 percent and 70 to 99 percent. We report here the results in the 659 patients in the latter stratum, who had had a hemispheric or retinal transient ischemic attack or a nondisabling stroke within the 120 days before entry and had stenosis of 70 to 99 percent in the symptomatic carotid artery. All patients received optimal medical care, including antiplatelet therapy. Those assigned to surgical treatment underwent carotid endarterectomy performed by neurosurgeons or vascular surgeons. All patients were examined by neurologists 1, 3, 6, 9, and 12 months after entry and then every 4 months. End points were assessed by blinded, independent case review. No patient was lost to follow-up., Results: Life-table estimates of the cumulative risk of any ipsilateral stroke at two years were 26 percent in the 331 medical patients and 9 percent in the 328 surgical patients--an absolute risk reduction (+/- SE) 17 +/- 3.5 percent (P less than 0.001). For a major or fatal ipsilateral stroke, the corresponding estimates were 13.1 percent and 2.5 percent--an absolute risk reduction of 10.6 +/- 2.6 percent (P less than 0.001). Carotid endarterectomy was still found to be beneficial when all strokes and deaths were included in the analysis (P less than 0.001)., Conclusions: Carotid endarterectomy is highly beneficial to patients with recent hemispheric and retinal transient ischemic attacks or nondisabling strokes and ipsilateral high-grade stenosis (70 to 99 percent) of the internal carotid artery.

Fourteen patients with angiographically demonstrated thrombus in the cerebral vessels were treated immediately with anticoagulant or antiplatelet medication. Follow-up angiograms, obtained in eight cases, showed resolution of the thrombus in seven. In no patient did the thrombus progress to occlude the vessel completely, and no new distal emboli were identified on the follow-up angiograms. There were no new permanent neurologic events in these 14 patients while they were undergoing medical therapy. Six patients subsequently underwent delayed endarterectomy to treat underlying stenoses. Our experience indicates that the presence of intraluminal thrombus may not be a surgical emergency.

The advent of EC/IC Bypass surgery has focused attention on selected patients who might benefit from this innovative procedure. There is a poverty of natural history data pertaining to all such lesions. Two centres (Memphis, Tennessee and London, Ontario) pooled their resources to carry out a retrospective review of 58 patients with angiographically-proven intracranial internal carotid artery stenosis. Only 33% of the patients were alive and free from subsequent cerebral vascular events at the end of the mean follow-up of 30 months. Forty-three percent of the patients died during follow-up: 36% due to stroke and 44% because of cardiac disease. Forty-three percent of the patients suffered cerebral vascular events during the follow-up period: there were 17 strokes (29%) including 9 fatal strokes. The incidence of ipsilateral stroke was 19%; 65% of the strokes were appropriate to the stenotic intracranial carotid lesion under study. The annual ipsilateral stroke rate for patients with this lesion was 7.6% per year. This lesion detected on angiography is indicative of severe atheroma, and carries a serious risk of death due to ischemic heart disease or stroke.

A series of 9 patients have experienced hemisphere and retinal ischemia at an interval after occlusion of appropriate internal carotid arteries. All had radiological evidence of a persisting proximal stump to the occluded artery and, in most, pathological evidence of thrombotic material attached to atheromatous lesions within the stump. Thromboembolism from the stump via the anastomotic supply through ipsilateral common and external carotid arteries is thought to be responsible for the ischemic events to the brain or retina despite absence of flow through the internal carotid artery. Seven of the 9 were treated by surgical excision or obliteration of the stump and, when indicated, common and external carotid endarterectomy. Turbulence in the stump contributed to progressive atherosclerotic changes and probably aggravated thrombogenesis in this location with subsequent embolization into the anastomotic arteries.

Forty-seven patients with ICA occlusion and who presented either without any or only a mild neurological deficit were prospectively followed for an average of 34.4 months. During this period of time, 11 patients (23.5%) suffered a cerebral infarction of which two-thirds were ipsilateral to the occluded artery. The stroke rate distal to an occluded ICA artery was 5% per year. Twenty-four patients (51%) continued to experience TIA's in the territory of the occluded artery. The mortality rate was low (8.5%) during follow-up. Whether extracranial-intracranial bypass surgery will decrease the risk of cerebral infarction in this subgroup of patients is unknown. The International EC/IC Collaborative Trial may elucidate this point because this subgroup represents one of the randomization strata of that study.

The authors describe a case of subarachnoid hemorrhage secondary to moyamoya disease in an adult Negro. To the authors' knowledge, this is the first such case reported. Moyamoya, the Japanese word for "puff of smoke," describes the characteristic angiographic appearance of the collateral arterial network associated with internal carotid artery occlusion. The cause is unknown. Treatment consists of supportive care; the prognosis is variable.

The presenting characteristics of 74 patients with atherosclerotic occlusion of both internal carotid arteries are described. All had suffered either ischaemic hemisphere infarcts (80%) and/or transient ischaemic attacks (80%) involving one (78%) or both (22%) carotid territories. In addition, 10 subjects (14%) incurred recurrent vertebrobasilar or presyncopal episodes, many of which appeared secondary to haemodynamic insufficiency. The incidence of risk factors and concomitant vascular disease was high; 93% gave a history of heavy smoking. Thirty-four subjects were treated conservatively and followed prospectively for a mean of 42 months. Eighteen patients (53%) suffered further cerebrovascular events, an ischaemic event rate of 15% per patient per year. These were isolated transient ischaemic attacks (TIAs) in 7 and stroke in 11 patients. The latter suffered a total of 15 strokes during the follow-up period of 42 months; the annual stroke rate was 13% per patient year. Patients who had presented with ischaemic events involving more than one carotid territory were significantly more prone to subsequent cerebral infarction than those in whom symptoms had been confined to one territory (P less than 0.05). None of the 5 patients with haemodynamic TIAs who were managed conservatively developed a stroke during the follow-up period and their symptoms remitted spontaneously. Deaths per year amounted to 8%. Twenty-four patients (71%) survived, of whom half were either symptom-free or minimally disabled. In this group of preselected patients, which excludes those with severe deficits at presentation, bilateral occlusion of the carotid arteries may be a condition compatible with useful existence.

It has been accepted that transient monocular blindness (TMB) is highly suggestive of an ipsilateral carotid artery lesion in patients with arterial risk factors. We confirmed this in 55 patients, who had an internal carotid artery severe stenosis, occlusion or ulceration on angiography in more than 50 per cent of the cases. However, 12-lead-ECG, 2 D--echocardiography and Holter monitoring also showed a potential cardiac source of emboli in 22 per cent of the patients. Most of these patients (83 per cent) also had an appropriate arterial lesion, and the exact cause of the episodes of TMB remained undetermined. Our study shows that every fourth of fifth patient with TMB may have a potential cardiac source of emboli, the detection of which could alter the management. Systematic non-invasive cardiac investigations are warranted, especially in TMB patients with known heart disease.

Thrombi defined as intraluminal filling defects detected by angiography were identified in 30 patients (29 in the carotid system, one in the vertebral artery). Stroke was the presentation ipsilateral to the thrombus in 22 patients (12 had previous transient ischemic attacks), transient ischemic attacks occurred alone in seven cases, and one patient was asymptomatic. Angiography revealed a severe stenosis in association with the thrombus in 23 patients, a moderate stenosis in four patients, and, in the three patients with only minimal stenosis presumably due to atherosclerosis, there was evidence for a coagulopathy. Sixteen of the 30 patients were operated on urgently, 10 within 24 hours of detection of the thrombus. Twelve of these 16 surgical patients were given anticoagulation before surgery. At endarterectomy, thrombus was identified in 11 of the 14 surgical patients in whom the thrombus was accessible; the other two surgical patients had intracranial thrombus only. In this group, four of 11 surgical patients with accessible thrombi suffered perioperative episodes of new or larger infarction. Fourteen of the 30 patients initially received medical management with no complication. Eight of these 14 medical patients had repeat angiography; seven exhibited complete resolution of thrombus, and six of these seven patients subsequently underwent delayed endarterectomy for the stenosis. No thrombus was identified at surgery in any of the six. One of the six delayed surgery patients suffered a perioperative stroke. Although these numbers are small, reflecting the rarity of thrombus demonstrated by angiography, undetected thrombus is often found at endarterectomy. Its presence may increase operative risk.(ABSTRACT TRUNCATED AT 250 WORDS)

Two hundred fifty consecutive patients with carotid transient ischemic attacks (TIAs) and no previous stroke were assessed with cerebral angiography (95%), two-dimensional echocardiography (86%), electrocardiography (100%), and Holter monitoring (99 selected patients). Angiography disclosed a lesion appropriate to the TIAs in 84%. Lesions also occurred in the asymptomatic carotid artery, but stenosis of more than 75% of the lumen diameter and ulcers were significantly more frequent on the symptomatic side. Twenty-three percent of the patients had a potential source of emboli from the heart, usually in the context of symptomatic heart disease. Among the 205 patients who underwent full angiographic and cardiac investigations, 6% had an isolated potential cardiac source of emboli and 19% had a potential cardiac source of emboli associated with appropriate carotid disease. The search for a potential cardiac source of emboli is strongly indicated in patients with carotid TIAs and known heart disease. In the patients with no history of heart disease, the yield of this search is low, but our results suggest that at least 14 of such patients have an undetected potential cardiac source of emboli. Cardiac and arterial lesions commonly coexist in carotid TIAs.

Vascular reconstruction was attempted in 109 patients with carotid artery occlusion or stenosis. The follow-up on those with restored or improved flow was as long as nine years (average: two and one-half years).Arteriographic demonstration of lesions is mandatory. Complications were reduced by pre-arteriographic administration of anticoagulants and retrograde brachial arteriographic techniques.Although patients with stenosis are the best candidates, an attempt to restore flow in occluded vessels is warranted in all patients, except those with advanced disease or those who are drowsy and hemiplegic. Flow was restored in two-thirds of those who underwent early operation (under three days) and in one-quarter of those undergoing late operation. Even late operation restored flow in five of nine patients who presented with transient ischemic attacks.IN COMPLETED STROKES, OPERATION SHOULD BE LIMITED TO PATIENTS WITH: (1) minor strokes, (2) extensive strokes of short duration, and (3) extensive strokes of longer duration but with a worth-while outlook.When flow was restored or improved, symptoms were arrested in 93% of patients with transient ischemia, and at follow-up this result was maintained in 86%. Symptoms were arrested in 83% of those with strokes in evolution, and this was maintained at follow-up.Reconstruction combined with anticoagulant therapy of limited duration appears to be the optimal method of treatment.

Context: Therapeutic trials generally have not distinguished outcomes of stroke according to cause.Objective: To determine whether stroke and subsequent disability was of large-artery, lacunar, or cardioembolic origin in patients with different degrees of symptomatic and asymptomatic carotid stenosis.Design: Observational study of prospective data collected from the North American Symptomatic Carotid Endarterectomy Trial between 1987 and 1997.Setting and Patients: A total of 2885 patients from 106 sites in the United States and abroad (median age, 67 years; 70% male) who had symptomatic internal carotid artery stenosis.Main Outcome Measure: Risk of stroke from each of the 3 causes at 5 years by territory and degree of stenosis.Results: During an average follow-up of 5 years, 749 patients had 1039 strokes, including 112 of cardioembolic, 211 of lacunar, 698 of large-artery, 17 of primary intracerebral hemorrhage, and 1 of subarachnoid hemorrhage origin. The 5-year risk of first stroke after entry into the trial in any territory was 2.6% of cardioembolic cause, 6.9% of lacunar cause, and 19.7% of large-artery cause. The proportion of cardioembolic strokes in the territory of the symptomatic artery was 12.0% and 6.9% in 60% to 69% and 70% to 99% arterial stenosis, respectively; large-artery strokes predominated (78.4%) at 70% to 99% arterial stenosis. With 70% to 99% arterial stenosis, the proportion of strokes of cardioembolic and lacunar origin was 43.5% and 21.6% in asymptomatic and symptomatic arteries, respectively. A total of 67.6% of cardioembolic, 16.7% of lacunar, and 33.0% of large-artery strokes in the territory of the asymptomatic artery were disabling or fatal.Conclusions: Our data suggest that approximately 20% and 45% of strokes in the territory of symptomatic and asymptomatic carotid arteries with 70% to 99% stenosis, respectively, are unrelated to carotid stenosis. The cause of subsequent strokes in similar types of patients should be considered when making treatment decisions involving carotid endarterectomy for patients with asymptomatic carotid stenosis, since lacunar and cardioembolic strokes cannot be prevented by endarterectomy. [ABSTRACT FROM AUTHOR]