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(Stroke. 1997;28:2084-2093.)
© 1997 American Heart Association, Inc.

Articles

Symptomatic Carotid Artery Occlusion

A Reappraisal of Hemodynamic Factors

Catharina J. M. Klijn, MD; L. Jaap Kappelle, MD; Cornelis A. F. Tulleken, MD; Jan van Gijn, MD, FRCPE

From the University Departments of Neurology (C.J.M.K., L.J.K., J. van G.) and Neurosurgery (C.A.F.T.), University Hospital Utrecht (Netherlands).

Correspondence to C.J.M. Klijn, MD, University Department of Neurology, University Hospital Utrecht, PO Box 85500, 3508 GA Utrecht, Netherlands. E-mail cklijn{at}neuro.azu.nl.

	Abstract

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Background Over the last several years evidence has accumulated that in addition to embolism, a compromised cerebral blood flow may play an important role in causing transient ischemic attacks and ischemic stroke in patients with occlusion of the internal carotid artery. This evidence is found in both clinical features and ancillary investigations, particularly measurements of cerebral blood flow.

Summary of Review On the basis of 20 follow-up studies in patients with transient ischemic attacks or minor ischemic stroke associated with an occluded carotid artery, the annual risk of stroke was 5.5% (95% confidence interval [CI], 5.0% to 6.0%), and that of ipsilateral stroke (distinguished in 11 of the 20 studies) was 2.1% (95% CI, 1.6% to 2.8%). Patients with a compromised cerebral blood flow as measured by positron emission tomography, single-photon emission CT, transcranial Doppler, or stable xenon CT (six studies) have an even higher annual risk of stroke (all strokes: 12.5%; 95% CI, 8.9% to 17.6%; ipsilateral stroke: 9.5%; 95% CI, 6.4% to 14.0%).

Conclusions Because a compromised cerebral blood flow may be an important causal factor in patients with symptomatic carotid artery occlusion, medical and surgical options for treatment are reviewed in this light.

Key Words: carotid artery occlusion • cerebral ischemia • hemodynamics • outcome

	Introduction

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Patients with TIAs or minor ischemic stroke who are found to have an ipsilateral occlusion of the ICA are at risk for further stroke and other vascular events. The causes of ischemic stroke associated with a previously occluded ICA are still a matter of debate. It has been hypothesized that the deficits are caused by emboli, either from the distal or proximal stump or from atherosclerotic plaques in the common carotid artery or ECA, which find their way to the ipsilateral hemisphere or retina via collateral pathways involving the ECA.^{1 2 3} In addition, transhemispheric passage of microemboli may cause ischemic events ipsilateral to the occluded ICA.⁴ Arguments in favor of this hypothesis are the cessation of symptoms after excision or clipping of the proximal stump,³ after endarterectomy in contralateral ICA stenosis,⁴ or after treatment with antithrombotic agents.³ In addition, some pathological evidence is consistent with embolism from the distal tail of the occluded ICA.¹

Over the last several years, evidence has been accumulating that in addition to embolism a compromised CBF may play a role in causing TIAs and stroke in patients with occlusion of the ICA. In such cases ischemia would occur by failure of the collateral blood flow via the circle of Willis, the ophthalmic artery, or the leptomeningeal collaterals. On this general assumption,

EC-IC bypass surgery was introduced to increase the blood flow to the symptomatic hemisphere. However, in 1985 the EC-IC Bypass Study Group showed in a large randomized trial that STA to MCA bypass surgery does not prevent stroke in patients with symptomatic occlusion of the ICA.⁵ As a result, no treatment of proven value is available for these patients other than treatment of risk factors and secondary prevention with antithrombotic agents. Proponents of the hemodynamic theory have emphasized that the power of the study may not have been sufficient to detect a therapeutic effect in the small subgroup of patients who had ongoing symptoms of cerebral or retinal ischemia after proven occlusion of the ICA despite medical treatment (see below), and also that documented hemodynamic compromise was not part of the inclusion criteria.^{6 7 8 9} In this view there might still be a role for EC-IC bypass surgery for secondary prevention of stroke in a highly selected group of patients with symptomatic ICA occlusion.

In this article we will review the evidence for hemodynamic compromise as a causal factor for cerebral ischemia in patients with ICA occlusion.

	Clinical Features of Hemodynamically Induced Cerebral or Retinal Ischemia in Patients With ICA Occlusion

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Presenting Symptoms
Ischemic stroke caused by ICA occlusion can present with clinical features that are indistinguishable from those associated with other causes of stroke. In some patients, however, careful history taking may uncover a hemodynamic origin of cerebral or retinal ischemia, suggesting ICA occlusion. Occurrence of TIA or stroke subsequent to extensive blood loss, cardiac failure, or, more commonly, to rising from a sitting or lying position may indicate a hemodynamic cause.^{10 11 12 13} In addition, stroke subsequent to postprandial hypotension has been described.¹⁴ Another symptom attributed to hemodynamic compromise is "limb shaking," first described by Fisher in 1962.¹⁵ Patients complain of repetitive involuntary movements of one or both limbs on one side, resembling partial seizures. Electroencephalograms during attacks do not show any epileptiform activity,^{16 17 18} diminished CBF has been documented,¹⁹ and symptoms may disappear after endarterectomy or STA-MCA bypass surgery.^{16 17 18} Less well known are symptoms of (transient) retinal ischemia that occur on looking into bright light (retinal claudication), caused by an increase in metabolic demand in the retina that cannot be met by an already marginal perfusion.^{20 21} In addition, diversion of blood to a dilated ECA capillary bed, viz, after transition from a cold to a warm environment, can induce retinal perfusion pressure to fall below the critical level.²¹ In these cases retinal perfusion pressure, measured by ophthalmodynamometry, is often low.²¹ Precipitation of symptoms by exercise has been observed as well²¹ ; probably diversion of blood to different parts of the body is responsible for retinal or cerebral ischemia.

Clinical features indicative of a hemodynamic origin of symptoms have been correlated with impaired cerebrovascular reserve in PET studies^{22 23} but seem to occur in only a small proportion of patients with ICA occlusion.^{22 23 24} In other words, the positive predictive value of features such as limb shaking in diagnosing poor hemodynamic tolerance of ICA occlusion is rather high, but the negative predictive value is rather poor.

Chronic Ocular Ischemia
While sudden (transient) monocular blindness is a well-known symptom of acute retinal ischemia most often caused by embolism from the ICA, occlusion or severe stenosis of the ICA may lead to SCOI, first described by Kearns and Hollenhorst in 1963.²⁵ Patients complain of progressive loss of visual acuity, often but not necessarily accompanied by pain around the eye. Early retinal signs of SCOI are midperipheral microaneurysms and small dot-and-blot intraretinal hemorrhages or nerve fiber layer splinter hemorrhages, narrowing of arteries, and dilatation and tortuosity of veins, a pattern often referred to as venous stasis retinopathy. Cotton-wool spots and edema of the optic disc may develop, as well as (in a later stage) neovascularization of the optic disc, retina, and iris (rubeosis iridis), in turn leading to uveitis and neovascular glaucoma.^{26 27 28} Rubeosis iridis is considered a bad prognostic sign.²⁷ Manifestations of SCOI have been reported in 4% to 18% of patients with severe stenosis or occlusion of the ICA.^{25 29 30} Life-table analysis of follow-up (mean, 3.2 years) of 52 patients with SCOI showed an annual risk of stroke of 4%, including two strokes after endarterectomy³¹ ; this risk is similar to that in transient monocular blindness.^{32 33}

The gradual progression of symptoms over time in SCOI as well as the low retinal artery pressure often found with ophthalmodynamometry³⁴ supports the concept of a hemodynamic explanation of chronic ocular ischemia. Early recognition of SCOI is important not only because chances of recovery of vision are less favorable with more advanced disease but also because it allows secondary prevention of stroke and cardiovascular disease.

Cognitive Deficit Related to Chronic Cerebral Ischemia
Stroke is well recognized as a risk factor for the development of dementia.^{35 36} Fisher³⁷ was the first to postulate that chronic cerebral ischemia caused by occlusion of the ICA could cause dementia. Since then a number of case reports have been published^{38 39 40 41 42} but no large series. Improvement of cognitive function after EC-IC bypass surgery^{39 41 42} supports the notion that a decreased blood supply of the brain may be related to deterioration of cognitive functioning. Tatemichi et al⁴¹ recently reported reversibility of cognitive impairment by EC-IC bypass surgery in a patient with compromised CBF and metabolism (according to PET); concomitant improvement of CBF and metabolism occurred. However, others could not show any effect of EC-IC bypass surgery^{43 44 45 46} on cognition. Hachinski⁴⁷ recently drew attention to the wide spectrum of cognitive deficits from vascular causes in terms of severity as well as pathogenesis. Whether ICA occlusion causing a chronic low-flow state of the brain is an independent risk factor for developing dementia remains controversial.

	Diagnosing Hemodynamic Compromise in Patients With Symptomatic ICA Occlusion

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Specific Pattern of Infarcts
Infarction in the border zone area between the vascular territories of major cerebral arteries has been assumed to indicate a hemodynamic origin of ischemic stroke. Although microembolism is a (rare) cause of border zone infarcts,⁴⁸ hypotension and severe carotid occlusive disease are the main causes.^{49 50} A CT study recently showed ICA occlusion to be significantly more frequent in a group of patients with border zone infarcts than in patients with other infarcts.⁵¹ In addition, CO₂ reactivity measured by TCD or SPECT (see below) is more severely reduced in patients with border zone infarcts than in patients with territorial infarcts.^{52 53 54 55} In these studies the positive predictive value of finding an infarct of the border zone type is rather high (with a border zone infarct, chances are high that ICA occlusion and impaired hemodynamic measurements exist), but sensitivity is low (not all patients with ICA occlusion and impaired hemodynamic have border zone infarcts). The presence of border zone infarcts implies a higher annual rate of stroke and death than do territorial infarcts.⁵⁶ A problem in diagnosing border zone infarcts from their appearance on CT or MRI is that for a given patient it is hard if not impossible to determine the exact location of the vascular territories of the major cerebral arteries.^{57 58}

Hemodynamic Measurements
Assessment of cerebral hemodynamics by PET has provided insight into the effect of carotid artery disease on CBF.⁵⁹ CBF, determined by the ratio of CPP to CVR in a particular region, is kept constant under a wide variety of conditions through a mechanism of autoregulation. Since CPP is relatively constant, CBF depends mainly on a change in CVR resulting from vasoconstriction or vasodilation of arterioles, with a concomitant change in CBV. When CPP falls and vasodilation, associated with an increase in CBV, cannot compensate sufficiently to maintain CBF, the OEF will increase.⁵⁹ PET studies in patients with symptomatic ICA occlusion have shown decreased CBF-CBV ratios, most marked in patients with bilateral occlusion.^{22 60} A raised OEF occurred only below a critical level of CBF-CBV ratio and was found in four of 11 patients with but none of 18 patients without presumably hemodynamic symptoms.²² In addition, CBF-CBV ratios were lower in the group with hemodynamic symptoms than in those without.²²

Another way to obtain hemodynamic measurements is by comparison of CBF at rest and after challenge with increasing CO₂ levels, a vasodilatory stimulus obtained by inhalation of carbogen or by breath holding. Vasodilation can also be obtained by administration of acetazolamide, presumably through a decrease in pH of the brain.⁶¹ So-called CO₂ reactivity or cerebrovascular reactivity reflects the residual capacity of the resistance of the arterioles after a vasodilatory stimulus. In patients with severe stenosis or occlusion of the ICA, CBF is often not increased after a vasodilatory challenge, presumably because autoregulation has already caused maximal vasodilation in response to a reduced CPP. After a vasodilatory stimulus, a decrease in CBF may be observed instead of an increased or unchanged flow.^{62 63} This "steal effect" is presumed to be caused by redistribution of blood to the areas where vasodilation still can occur at the expense of the regions where vasodilation was already at its maximum.

Because PET facilities are expensive and not generally available, cerebral hemodynamics are also measured by other techniques such as ¹³³Xe inhalation⁶⁴ and injection⁶⁵ techniques, stable Xe studies,^{66 67} TCD,^{68 69 70} hexamethylpropyleneamine oxime or iofetamine hydrochloride ¹²³I (¹²³I-labeled IMP) SPECT,⁷¹ dynamic CT,⁷² and near-infrared spectroscopy.⁷³ Special MR techniques, eg, MR spectroscopy,^{74 75 76} angiography,⁷⁷ and diffusion and perfusion⁷⁸ imaging may provide additional evidence for the role of compromised CBF in stroke, but studies in patients with symptomatic ICA occlusion have not been published thus far. The OEF can only be measured by PET. Approximately 12% of patients with an ICA occlusion have an exhausted CO₂ reactivity and 29% a diminished CO₂ reactivity measured by TCD.⁷⁰ An exhausted CO₂ reactivity is found more frequently in patients with recent symptoms (<3 months),⁷⁰ indicating that a compromised CBF can improve spontaneously over time.

In patients with ICA occlusion or severe stenosis, impaired CO₂ reactivity is associated with border zone infarcts^{52 53 54 55 79} and with poor collateral blood flow patterns on cerebral angiography.^{80 81 82} Collateral blood flow through the ophthalmic arteries or leptomeningeal collaterals is often considered less sufficient than collateral circulation via the circle of Willis (the anterior or the posterior communicating artery). Prospective studies on the prognostic value of collateral blood flow patterns are scarce. Subgroup analysis in the EC-IC Bypass Study of patients with large, small, or no collateral circulation via the ECA failed to show any benefit of EC-IC bypass surgery in any of these subgroups.⁸³ Measurements of CO₂ reactivity were not part of the selection criteria in the EC-IC Bypass Study⁵ but are currently proposed for selection of patients who may benefit from this procedure.^{64 79 84}

	Outcome in Patients With Symptomatic Occlusion of the ICA

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Table 1 summarizes the results of 20 observational studies published between 1960 and 1995 describing the risk of recurrent stroke and death in patients with TIA or stroke in the presence of occlusion of the ICA but without any measurement of the CBF.^{2 5 85 86 87 88 89 90 91 92 93 94 95 96 97 98 99 100 101 102} Occlusion of the ICA was demonstrated with angiography in 17 studies, with either angiography or autopsy in 1,⁸⁵ and with ultrasound techniques with or without angiography in 2.^{101 102} The annual stroke rate in these studies varied enormously, between 0% and 20.1%; the combined annual stroke risk of the 20 studies was 5.5% (95% CI, 5.0% to 6.0%; Poisson regression analysis). Nine of the 20 follow-up studies did not specify whether strokes occurred ipsilateral or contralateral to the occlusion (Table 1). On the basis of the 11 other studies, the risk of ipsilateral stroke was 2.1% (95% CI, 1.6% to 2.8%; Poisson regression analysis). Average ages and proportions of male patients were similar for most studies. Variation in medical regimens may partly account for the differences in stroke and death rates reported. Selection bias with a view to surgery may have influenced stroke and death rates in one study⁸⁹ that describes patients in the medical arm of a surgical trial. Patients with bilateral carotid occlusion seem to suffer a high stroke rate, with or without bypass surgery.²⁴ Except for the report of the EC-IC Bypass Study Group,⁵ none of the studies provide information on whether symptoms occurred after proven occlusion of the ICA. This is important because symptoms may occur only at the very moment the ICA becomes occluded. If no further symptoms occur, there is no indication for surgical treatment. The EC-IC Bypass Study Group reported on a subgroup that experienced ongoing symptoms after angiographic demonstration of the occlusion, but they could not demonstrate a beneficial effect of conventional EC-IC bypass surgery in this subgroup.⁵ The annual stroke rate in the group of medically treated patients with ongoing symptoms (n=147) was 7.5% compared with 5.6% in the group of medically treated patients without ongoing symptoms after demonstration of the ICA occlusion (n=276). This difference did not reach statistical significance (relative risk, 1.3; 95% CI, 1.0 to 1.8).

View this table: [in this window] [in a new window]   Table 1. Outcome in Patients With Symptomatic ICA Occlusion

Role of Hemodynamic Measurements
To date, 7 studies have compared prognosis in medically treated patients with and without compromised CBF. The results of 6 studies are summarized in Table 2. One study was excluded because stroke rates were reported for the number of hemispheres distal to an ICA occlusion instead of patients with ICA occlusion.⁷⁰ In 3 studies not only were patients with symptomatic ICA occlusion included but also patients with symptomatic MCA stenosis or occlusion and patients with symptomatic ICA stenosis.^{71 103 104} Only 2 of the 6 provided information on the frequency of symptoms of cerebral ischemia and whether they occurred after proven occlusion.^{103 104}

View this table: [in this window] [in a new window]   Table 2. Outcome in Medically Treated Patients With ICA Occlusion or Intracerebral ICA or MCA Stenosis, With and Without Compromised CBF

In 2 of the 6 studies, no clear association between a compromised CBF and an increased risk of stroke during follow-up could be demonstrated.^{71 103} Powers et al¹⁰³ investigated with PET 30 medically treated symptomatic patients with greater than 75% stenosis of the intracranial ICA or MCA or occlusion of the ICA.¹⁰³ One of 9 patients with normal hemodynamics and none of 21 patients with compromised hemodynamics suffered an ipsilateral stroke after 1-year follow-up (P=.3; Fisher's exact test). Later the same author reported the 2-year follow-up of these patients as well as of 29 patients who underwent EC-IC bypass surgery. Fifty-six of these 59 patients had their symptoms less than 3 months before the PET investigation. The risk of stroke at 2 years was 28% in 14 patients with an increased OEF at baseline versus 14% in 42 patients with normal OEF measurements.⁵⁹ In this study the difference again did not reach statistical significance (P=.2; Fisher's exact test). In the second study no strokes were observed at all during a follow-up period of 1.5 years in 51 patients with symptomatic occlusion or intracranial stenosis of the ICA or MCA, 20 of whom had impaired cerebrovascular reactivity measured by [¹²³I]IMP SPECT with acetazolamide.⁷¹

In each of the other four studies, patients with compromised CBF were shown to have a worse prognosis than similar patients with normal CBF measurements. (Table 2).^{66 67 69 104} Kleiser and Widder⁶⁹ investigated CO₂ reactivity with TCD in 85 patients (39 symptomatic, 46 asymptomatic). Patients with absent CO₂ reactivity significantly more often suffered ipsilateral stroke than patients with decreased or normal cerebrovascular reactivity (P<.0006). Yonas et al⁶⁷ reported stroke during follow-up in 5 of 16 patients with compromised CBF versus no strokes in 25 patients without compromised CBF (P=.0005). Webster et al⁶⁶ performed stable Xe CT before and after acetazolamide treatment in 64 patients with symptomatic ICA occlusion.⁶⁶ Ten of 38 patients with loss of cerebrovascular reactivity suffered a stroke during an average follow-up period of 19.6 months versus none of 26 patients with intact cerebrovascular reactivity (P=.003). Seven strokes occurred ipsilateral and three contralateral to the side that was previously symptomatic. In 3 of the 7 patients with ipsilateral recurrent stroke the initial symptoms were bilateral, and 1 of these patients had bilateral carotid occlusion.⁶⁶ Yamauchi et al¹⁰⁴ followed 40 patients with symptomatic ICA or MCA occlusive disease by means of PET scanning; none was surgically treated. Seven ischemic strokes occurred within the first year of follow up: two (ipsilateral) strokes occurred in the group of 33 patients with normal OEF (6.1%), whereas 5 of 7 patients with an increased OEF suffered a stroke (71%; 4 ipsilateral and 1 contralateral). This suggests that patients with an increased OEF are at particular high risk of ischemic stroke.

The combined annual stroke risk in the subgroups that had impaired hemodynamic measurements of any severity (in Table 2, groups a, A, b, and B) was 12.5% for all strokes (95% CI, 8.9% to 17.6%; Poisson regression analysis) and 9.5% (95% CI, 6.4% to 14.0%; Poisson regression analysis) for ipsilateral stroke, suggesting a definitely worse prognosis in patients with impaired cerebral perfusion than in those without. Patients with severely impaired hemodynamic measurements (in Table 2, groups a and A) probably have an even worse prognosis; based on three studies that distinguish these,^{69 103 104} the annual risk of all strokes was 41.4% (95% CI, 23.5% to 72.9%) and the annual risk of ipsilateral stroke was 31.0% (95% CI, 16.2% to 59.7%). This information is important when symptoms continue in the individual patient after carotid occlusion and the risk of a surgical procedure must be weighed against the risk of stroke.

	Treatment of Patients With Symptomatic Carotid Artery Occlusion

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Modification of Risk Factors
Hypertension, hyperlipidemia, diabetes, smoking, and alcohol abuse are well-known risk factors for vascular disease and should be treated rigorously. In patients with symptomatic carotid occlusion, however, treatment of hypertension should not be too aggressive because in some patients a relatively slight decrease in blood pressure can induce cerebral ischemia. Although tapering of antihypertensive treatment in hypertensive patients with ICA occlusion and recurrent TIAs has never been systematically studied, it should be considered when symptoms are likely to be of hemodynamic origin on the basis of both clinical features and hemodynamic measurements.

Antithrombotic Agents
Patients with TIAs or nondisabling ischemic stroke from any cause have a combined annual risk of subsequent death from all vascular causes, nonfatal stroke, or nonfatal myocardial infarction of 3.6% to 15.7% per year.¹⁰⁵ This risk can be reduced by approximately 13% (95% CI, 4% to 21%) with aspirin.¹⁰⁵ Antithrombotic agents are usually also prescribed in the subgroup of patients with symptomatic carotid artery occlusion. Oral anticoagulants are sometimes prescribed in the first 6 to 8 weeks after demonstration of an ICA occlusion instead of antiplatelet agents, although their efficacy has never been shown to be superior. No information is available on the effect of antithrombotic agents on stroke risk in the even smaller proportion of patients in whom hemodynamic factors are identified.

EC-IC Bypass Surgery
The large international, randomized clinical trial investigating the efficacy of STA to MCA bypass in preventing stroke in patients with symptomatic ICA or MCA occlusion or high-grade intracranial stenosis could not demonstrate a benefit of this procedure over treatment with medication alone.⁵ This procedure consists of an anastomosis between the STA and a cortical branch of the MCA. The total number of strokes observed during the average period of follow-up of 55.8 months (fatal and nonfatal, ipsilateral and contralateral) was 205, both in the group of 714 patients randomized for medical therapy and in the group of 663 patients randomized for STA-MCA bypass surgery. The rate of major perioperative stroke was 4.5%. On the basis of these results, benefit of the STA-MCA bypass operation of 3% or more could be rejected (P=.05). The study was not designed to identify patients with compromised CBF,^{6 7 9} and meanwhile the collective evidence suggests that such patients with impaired CBF have a relatively poor prognosis (see above). There is ample evidence that the STA-MCA bypass is able to improve compromised CBF in patients with symptomatic unilateral carotid occlusion.^{71 84 106 107 108 109 110 111} However, improvement in cerebrovascular reactivity has also been shown to occur spontaneously.⁷⁰ Failure to distinguish patients in whom ischemic episodes were caused by low flow may explain the apparent paradox that the outlook was better in patients in whom the bypass failed to open up well or became occluded.⁵

Recently a new technique for the EC-IC bypass operation has been developed.^{112 113} By means of a venous transplant, a bypass is made between the proximal STA (just in front of the ear) and the most distal, intracranial part of the ICA or the proximal MCA. The distal anastomosis is made with the Excimer laser, which technique allows connection of the distal anastomosis without the need to temporarily clamp the ICA. The major advantage of this procedure is that it results in an EC-IC bypass with a more proximal access to the vascular tree and a larger diameter. In this way a larger increase in blood flow can be expected and is actually found (C.A.F. Tulleken, unpublished data, 1997) than could be obtained with the original EC-IC bypass procedure. We are currently investigating the safety of this "high-flow" EC-IC bypass operation in selected patients with symptomatic ICA occlusion. The only way to demonstrate the efficacy of any type of bypass in preventing stroke in patients with symptomatic carotid artery occlusion is by a new randomized clinical trial. Based on the current collective evidence, such a trial should consist of patients with recurrent symptoms after demonstration of the ICA occlusion and compromised hemodynamic measurements. PET with measurement of the OEF would be the measurement of choice, but techniques such as TCD or SPECT with measurement of CO₂ reactivity could be cheaper and more available alternatives. The feasibility of such a trial has been considered,^{9 114} but to date such a trial has not commenced, probably because it would involve another protracted multicenter trial. If an ipsilateral stroke rate of 9.5% (Table 2) is assumed, a new trial would require approximately 1500 patient-years in each group to demonstrate a 30% risk reduction in recurrent ipsilateral stroke by EC-IC bypass surgery. If only patients with severely compromised hemodynamic measurements would be included (annual risk of ipsilateral stroke of 31%), 350 patient-years would be needed in each group.

The role of EC-IC bypass surgery in patients with SCOI and ICA occlusion is uncertain. Many authors advocate EC-IC bypass surgery.^{29 115 116 117 118} However, in a series of 52 patients, Sivalingam et al²⁷ could not demonstrate a positive effect of surgery (EC-IC bypass or endarterectomy) on stabilization or improvement of vision in patients with SCOI and occlusion or high-grade stenosis of the ICA.²⁷ Panretinal photocoagulation can often^{119 120 121} but not always¹²² diminish neovascularization in both the posterior and anterior segments. Kiser et al¹¹⁹ described the remarkable and encouraging improvement of a patient with poor visual acuity, iris neovascularization, and neovascular glaucoma to a vision of 6/12 after combined medical therapy of glaucoma, cryoablation of the ciliary body, and EC-IC bypass surgery.

Endarterectomy of a Hemodynamically Significant Stenosis of the Contralateral ICA
Endarterectomy of a contralateral, hemodynamically significant ICA stenosis has been advocated in the treatment of patients with symptomatic carotid occlusion.^{123 124} This procedure may be particularly effective if perfusion of the hemisphere ipsilateral to the occlusion is provided by the stenotic contralateral ICA. A randomized trial proving a beneficial effect of the procedure for this indication has never been conducted. Carotid endarterectomy in patients with symptomatic carotid stenosis is associated with a relatively high risk if the contralateral carotid artery is occluded in some series¹²⁵ but not in all.^{126 127} Few studies report on the effect of the procedure on long-term risk of stroke,^{124 125 126 128 129} but often no clear distinction is made between symptomatic occlusion with contralateral stenosis and symptomatic stenosis with contralateral occlusion. Improvement of cerebral hemodynamics after carotid endarterectomy, measured by TCD and the breath-holding test, has been shown not only in the hemisphere ipsilateral to the stenosis but also in the hemisphere on the side of the occluded ICA.¹³⁰

Endarterectomy of the Ipsilateral ECA
Collateralization via branches of the ECA can markedly contribute to the intracerebral circulation in patients with ICA occlusion, in particular in those patients that have an incomplete circle of Willis. In these patients stenosis of the ECA may cause recurrent retinal or hemispheric ischemic symptoms by either embolization or hypoperfusion.^{1 3}

An overview is available of series and cases of revascularization of the ECA in the presence of carotid occlusion, published between 1967 and 1987.¹³¹ Some patients (mean age, 62 years; range, 40 to 84 years) were symptomatic; others had nonspecific symptoms such as dizziness or imbalance or were asymptomatic (4%) but were believed to be at high risk of subsequent stroke (criteria not given). Perioperative case fatality was 3% (7 of 218 procedures), in two cases attributable to stroke. Long-term follow-up was available in 196 patients and ranged from 1 month to 5 years. Eight patients (4.1%) died (all from cardiac disease), and 7 patients (3.6%) suffered a stroke, in all cases contralateral to the side of ECA revascularization. This overview and two subsequent studies^{132 133} allow the tentative conclusion that ECA revascularization is a reasonably safe and potentially effective procedure in patients with symptomatic carotid occlusion and ipsilateral stenosis of the ECA.

	Conclusions

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Patients with transient or slightly disabling symptoms of retinal or cerebral ischemia ipsilateral to carotid occlusion have a risk of ischemic stroke of approximately 5.5% per year; the risk of ipsilateral ischemic stroke is 2.1% per year, and the annual death rate is approximately 6.3% per year. It is important to distinguish between patients with and without ongoing symptoms after occlusion of the ipsilateral ICA because patients with recurrent symptoms probably are at higher risk than patients with a single event that probably occurred at the very moment of occlusion. Evidence accumulates that in a sizeable proportion of patients with ICA occlusion the recurrent symptoms are caused by a compromised CBF. Accordingly, patients with symptomatic carotid occlusion with a decreased cerebrovascular reactivity have a higher risk of stroke than similar patients with normal cerebrovascular reactivity, at 12.5% or more per year for all strokes and up to 9.5% for ipsilateral stroke. When hemodynamic measurements are severely impaired, the risk of stroke is probably even higher (41.4% for total and 31.0% for ipsilateral annual stroke rate). EC-IC bypass surgery as well as carotid endarterectomy for severe contralateral ICA stenosis can improve impaired CVR in these patients. Only a new randomized clinical trial can answer the question of whether EC-IC bypass surgery in addition to treatment with antithrombotic medication and modification of risk factors can prevent stroke in patients with ICA occlusion with recurrent symptoms and evidence of compromised CBF. The high-flow EC-IC bypass operation in particular seems to be a promising technique because it involves construction of a bypass with a large caliber and proximal access to the vascular tree.

	Selected Abbreviations and Acronyms

 

CBF = cerebral blood flow CBV = cerebral blood volume CI = confidence interval CPP = cerebral perfusion pressure CVR = cerebrovascular resistance ECA = external carotid artery EC-IC = extracranial-intracranial ICA = internal carotid artery MCA = middle cerebral artery OEF = oxygen extraction fraction PET = positron emission tomography SCOI = syndrome of chronic ocular ischemia SPECT = single-photon emission computed tomography STA = superficial temporal artery TCD = transcranial Doppler ultrasonography TIA = transient ischemic attack

	Acknowledgments

 
This study was supported by the Netherlands Heart Foundation (grant 94.085) (Dr Klijn). The authors thank Professor B.C. Eikelboom, MD, for reviewing the manuscript.

	Footnotes

 
The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.

Received February 14, 1997; revision received April 25, 1997; accepted May 29, 1997.

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