Oral anticoagulants versus antiplatelet therapy for preventing further vascular events after transient ischemic attack or minor stroke of presumed arterial origin.
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Administration, Oral↗
Biomedical subjects
L J Kappelle
Publications and source records attributed to L J Kappelle.
[Treatment of patients with a TIA or a stroke].
Patients in the acute phase of a stroke ought to be sent to a centre with a well-organised 'stroke unit' where thrombolysis is possible. The integrated approach at a stroke unit is associated with a better outcome than treatment in a general neurology ward. Intravenous thrombolysis can be carried out responsibly if the treatment is started within 3 hours of the onset of clinical symptoms and if certain conditions are satisfied. However, preventive measures provide the greatest benefit to patients who have experienced a transient ischaemic attack (TIA) or a minor stroke. The treatment of vascular risk factors should therefore receive the greatest priority. In addition to the classical risk factors, hyperhomocysteinaemia, infection with Chlamydia pneumoniae and obesity have all recently been indicated as potential risk factors. For patients with a potential source of embolism in the heart, oral anticoagulants are the treatment of choice, whereas platelet aggregation inhibitors should be the first choice for patients with atherosclerotic lesions in the extracranial vessels. Carotid endarterectomy is now a regular form of secondary prevention, whereas the role of endovascular treatment is currently under investigation.
Anticoagulants↗
The effect of tirilazad mesylate on infarct volume of patients with acute ischemic stroke.
The authors investigated whether the lack of effect of tirilazad on clinical outcome in patients with acute ischemic stroke is explained by failure of tirilazad to reduce infarct volume. Overall, tirilazad had no significant effect on infarct volume. In the subgroups of male patients and of those with a cortical infarct, tirilazad significantly reduced infarct volume. These effects were reduced to nonsignificant trends after adjustment for imbalances in baseline characteristics. In conclusion, early treatment of patients with tirilazad has no effect on infarct volume.
Aged↗
Symptomatic carotid artery stenosis.
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Carotid Arteries↗
Endothelial cell activation is associated with cerebral white matter lesions in patients with cerebrovascular disease.
Cerebral MRI scanning frequently shows white matter lesions in elderly people. They are related to cognitive impairment and may result in dementia. Although vascular risk factors are associated with the presence of white matter lesions, the exact pathogenesis remains unclear. Animal studies have indicated involvement of endothelial cells in the pathogenesis of white matter lesions and possibly dementia. We investigated the relation between endothelial cell activation and white matter lesions in individuals with cerebrovascular disease. In 29 patients with an acute stroke (n = 11) or TIAs associated with a symptomatic internal carotid artery stenosis (n = 18), markers of endothelial cell activation such as intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), sE-selectin, and sP-selectin were measured by means of ELISA. All individuals underwent 1.5-T MRI scanning. White matter lesions were rated for the periventricular and the subcortical region separately. Individuals with severe periventricular white matter lesions had higher levels of sP-selectin (245.5 ng/mL vs. 172.7 ng/mL, p = 0.01) and sVCAM-1 (547.8 ng/mL vs. 454.0 ng/mL, p = 0.04) than those without. This association was only found in individuals with a symptomatic carotid artery stenosis. No such association was found for subcortical white matter lesions. We did not detect any relation between sICAM-1 and sE-selectin and white matter lesions. Endothelial cell activation may play a role in the pathogenesis of white matter lesions, especially in periventricular white matter. Possibly, this activation represents the influence of vascular factors on the cerebral endothelium as a prelude to increasingly severe small vessel disease.
Brain↗
Collateral circulation via the ophthalmic artery or leptomeningeal vessels is associated with impaired cerebral vasoreactivity in patients with symptomatic carotid artery occlusion.
BACKGROUND AND PURPOSE: In patients with carotid artery occlusion (CAO), collateral flow may reduce the risk of ischemic stroke. Collateral flow via the ophthalmic artery (OphthA) and flow via leptomeningeal vessels have been considered secondary collaterals, which are recruited only if the primary collateral circulation via the circle of Willis is insufficient. The aim of this study was to investigate whether patients with symptomatic CAO who have secondary in addition to primary collaterals have a worse flow state of the brain than those without secondary collaterals, as measured by vascular reactivity testing. METHODS: We studied 70 patients with symptomatic CAO who were independent for their daily activities. In all patients, collateral circulation through the circle of Willis was present. Vascular reactivity, measured by means of transcranial Doppler sonography with carbogen inhalation, was compared between patients with and without secondary collaterals. RESULTS: CO2 reactivity was lower in 64 patients with (mean +/- standard deviation 8 +/- 14%) than in 6 patients without secondary collaterals (33 +/- 18%) resulting in a mean difference of 24% (95% confidence interval 12-37%; p < 0.01). CONCLUSIONS: Patients with symptomatic CAO with collateral circulation through the OphthA or through leptomeningeal vessels in addition to collaterals via the circle of Willis have a worse hemodynamic status of the brain than those with Willisian collaterals only. Therefore the presence of these collaterals may indicate insufficiency of collateral blood flow via the circle of Willis.
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Inflammatory cell adhesion molecules in ischemic cerebrovascular disease.
BACKGROUND: In this review we discuss the role of inflammatory cell adhesion molecules (CAMs) in ischemic stroke and in delayed cerebral ischemia after subarachnoid hemorrhage. Vascular endothelial cells and leukocytes express several inflammatory adhesion receptors, the most important of which are the selectins, immunoglobulin gene superfamily CAMs, and beta2 integrins. They mediate the transmigration process of leukocytes to the abluminal side of the endothelium. SUMMARY OF REVIEW: There is ample evidence from animal models of middle cerebral artery occlusion that expression of CAMs is associated with cerebral infarct size. Absence of CAMs in knockout animals resulted in reduced infarct size. When middle cerebral artery occlusion in experimental stroke was followed by reperfusion, administration of anti-CAM antibodies decreased infarct size. Thus far, anti-CAM treatment has not been successful in patients with ischemic stroke. Inflammatory CAM may also play a role in the pathogenesis of delayed cerebral ischemia after subarachnoid hemorrhage. In animal models, increased expression of CAMs has been observed in vasospastic arteries. Increased concentrations of CAMs have also been found in cerebrospinal fluid of patients with subarachnoid hemorrhage. CONCLUSIONS: Further research on the role of inflammatory CAMs in the pathogenesis of ischemic cerebrovascular disorders should lead to new diagnostic and therapeutic strategies.
Animals↗
Occurrence of hemispheric and retinal ischemia in atrial fibrillation compared with carotid stenosis.
BACKGROUND AND PURPOSE: The goal of this study was to examine the hypotheses that retinal ischemia is caused more often by carotid atherosclerosis than by atrial fibrillation and that the odds of retinal events compared with hemispheric events increase with worsening carotid stenosis. METHODS: We used data from the Stroke Prevention in Atrial Fibrillation (SPAF) I through III trials and North American Symptomatic Carotid Endarterectomy Trial (NASCET), calculating hemispheric:retinal (H:R) odds for the territory of ischemic events during follow-up in patients with atrial fibrillation and medically treated 50% to 99% carotid stenosis or occlusion in the respective trials. RESULTS: The H:R odds were 25:1 in the SPAF aspirin-assigned patients and 2:1 for NASCET vessels. In NASCET patients, the H:R odds of recurrent ischemic events were 1:4 for vessels randomized initially for retinal symptoms compared with 6:1 for those randomized for hemispheric events (significant difference; P<0.001). Moreover, the H:R odds of first events in the territory of the contralateral asymptomatic artery were 1:1 if the randomized vessel had retinal symptoms compared with 4:1 if the randomized vessel had hemispheric symptoms (significant difference; P<0.01). Increasing carotid stenosis in the 50% to 99% range had no effect on H:R odds (P=0.8). CONCLUSIONS: These findings confirm that retinal symptoms are more typical of carotid stenosis. Hemodynamic effects do not appear to be more important in the pathogenesis of retinal events than hemispheric ones in carotid stenosis. The retinal versus hemispheric location of initial symptoms is strongly predictive of the location of subsequent events in patients with carotid stenosis, even when new symptoms are contralateral to the original ones.
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Hemodynamic and metabolic changes in transient ischemic attack patients: a magnetic resonance angiography and (1)H-magnetic resonance spectroscopy study performed within 3 days of onset of a transient ischemic attack.
BACKGROUND AND PURPOSE: We investigated whether patients with transient ischemic attack (TIA) have systemic low flow to the brain or an abnormal intracranial flow distribution caused by an abnormal anatomy of the circle of Willis. Furthermore, we investigated whether metabolic changes were present in the brain. METHODS: Forty-four patients with clinically diagnosed TIA were prospectively included in our study. Clinical and neurological data were compiled. MR imaging; quantitative flow measurements of the internal carotid, middle cerebral, and basilar arteries; MR angiography of the circle of Willis; and (1)H-MR spectroscopy were performed in all patients within 3 days of onset of symptoms. RESULTS: Compared with control subjects, TIA patients did not have altered flow volume in any of the arteries and had normal flow distribution through the circle of Willis. In TIA patients, the N-acetylaspartate (NAA)/choline ratio in noninfarcted regions was significantly decreased in the symptomatic hemisphere (1.73+/-0.16) compared with the asymptomatic hemisphere (1.84+/-0.19, P<0.05) and control subjects (1.90+/-0.17, P<0.001). In the symptomatic hemisphere, the lactate/NAA ratio was significantly increased (0.04+/-0.08) compared with control subjects (0.00+/-0.01, P<0.05). Patients with a history of prior TIA had a significantly decreased NAA/choline ratio in both the symptomatic (P<0.05) and asymptomatic (P<0.05) hemispheres compared with TIA patients without a prior TIA. CONCLUSIONS: TIA patients have neurological deficits that are transient; however, metabolic damage to the brain is present up to 3 days after the onset of the symptoms. These metabolic changes are not restricted to the symptomatic hemisphere or to areas close to ischemic lesions.
Adult↗
Oral anticoagulants versus antiplatelet therapy for preventing further vascular events after transient ischaemic attack or minor stroke of presumed arterial origin.
BACKGROUND: Patients who are entered in clinical trials after a transient ischaemic attack (TIA) or non disabling ischaemic stroke have an annual risk of important vascular events (death from all vascular causes, non-fatal stroke, or non-fatal myocardial infarction) of between 4 and 11 percent. Aspirin, in a daily dose of 30mg or more, offers only modest protection after cerebral ischaemia: it reduces the incidence of major vascular events by 20 percent at most. Secondary prevention trials after myocardial infarction indicate that treatment with oral anticoagulants is associated with a risk reduction approximately twice that of treatment with antiplatelet therapy. OBJECTIVES: 1) To compare the efficacy of oral anticoagulants and antiplatelet therapy in the secondary prevention of vascular events after cerebral ischaemia of presumed arterial origin. 2) To compare the safety of oral anticoagulants and antiplatelet therapy in the secondary prevention of vascular events after cerebral ischaemia of presumed arterial origin. SEARCH STRATEGY: This review draws on the search strategy developed for the Stroke Group as a whole. Relevant trials were identified in the Specialised Register of Controlled Trials (last searched: June 2000). Authors of published trials were contacted for further information and unpublished data. SELECTION CRITERIA: Randomised trials with concealed treatment allocation on long term (> 6 months) secondary prevention after recent (< 6 months) TIA or minor ischaemic stroke of presumed arterial origin were selected. The oral anticoagulant therapy was to be of specified intensity (by means of the International Normalised Ratio (INR)) with warfarin, phenprocoumon or acenocoumarol versus a single antiplatelet drug (or combination of antiplatelet agents). DATA COLLECTION AND ANALYSIS: Two reviewers selected trials meeting the inclusion criteria and extracted details of randomisation methods, blinding of treatments and assessments, whether intention-to-treat analysis is possible from the published data, whether treatment groups are comparable with regard to major prognostic risk factors for outcomes, the number of patients who are excluded or lost to follow-up, definition of outcomes, and entry and exclusion criteria. The methodological quality of each trial was assessed by the two reviewers using these extracted data. In addition, target INR for anticoagulant treatment and dose and type of antiplatelet drug, duration of follow-up and the numbers of defined outcome events was recorded. The data were analysed according to the intention-to-treat principle. Subgroup analyses with treatment INR 2.1 - 3.6 versus INR 3.0 - 4.5 was performed. Relative and absolute risk reductions were calculated by means of the statistical software provided by the Cochrane Collaboration. MAIN RESULTS: Four trials, with a total of 1870 patients were selected. In the prevention of ischaemic stroke after cerebral ischaemia of presumed arterial origin, the available data do not allow a robust conclusion on whether anticoagulants (in any intensity) are more efficacious than antiplatelet therapy (low intensity anticoagulation RR 0.96, 95% CI 0.38 to 2.42, high intensity anticoagulation RR 1.02, 95% CI 0.49 to 2.13). Treatment with anticoagulation INR 2.1 - 3.6 does not give an importantly higher bleeding risk than treatment with antiplatelet agents (RR 1.19, 95% CI 0.59 to 2.41). It is clear that oral anticoagulants INR 3.0 - 4.5 are not safe, because they yield a higher risk of major bleeding complications (RR 9.0, 95% CI 3.9 to 21). REVIEWER'S CONCLUSIONS: For the secondary prevention of further vascular events after transient ischaemic attack or minor stroke of presumed arterial origin, there is insufficient evidence to justify the routine use of low intensity oral anticoagulants (INR 2.0 - 3.6). More intense anticoagulation (INR 3.0 - 4.5) is not safe and should not be used in this setting.
Administration, Oral↗
Varieties of human spatial memory: a meta-analysis on the effects of hippocampal lesions.
The current meta-analysis included 27 studies on spatial-memory dysfunction in patients with hippocampal damage. Each study was classified on the basis of the task that was used, i.e., maze learning, working memory, object-location memory, or positional memory. The overall results demonstrated impairments on all spatial-memory tasks. Clear differences in effect size were found between positional memory on the one hand and maze learning, object-location memory, and working memory on the other hand. Lateralization was found only on maze learning and object-location memory. These findings clearly indicate that specific aspects of spatial memory can be affected in various degrees in patients with hippocampal lesions. Moreover, these results strongly support the notion that the hippocampus is important in the processing of metric positional information, probably in the form of an allocentric cognitive map.
Animals↗
Clinical features associated with internal carotid artery occlusion do not correlate with MRA cerebropetal flow measurements.
OBJECTIVES: The aetiology of clinical symptoms in patients with severe internal carotid artery (ICA) lesions may be thromboembolic or haemodynamic. The purpose was to assess whether changes in cerebropetal blood flow caused by an ICA occlusion have an effect on clinical symptoms and cerebral metabolism. METHODS: Forty three patients with an ICA occlusion who had hemispheric ischaemia (transient ischaemic attack or stroke), retinal ischaemia, or without symptoms, and 34 patients without significant ICA lesions with either hemispheric ischaemia or no symptoms were studied. Magnetic resonance angiography (MRA) was used to investigate total cerebropetal flow (flow in the ICAs plus basilar artery) and the flow in the middle cerebral arteries. Cerebral metabolic changes in the flow territory of the middle cerebral artery were determined with proton MR spectroscopy. RESULTS: Low total cerebropetal flow (r=-0.15, p<0.05) and low middle cerebral artery flow (r=-0.31, p<0.001) were found in patients with an ICA occlusion, but did not correlate with the clinical syndrome. By contrast, patients with prior symptoms of hemispheric ischaemia had decreased cerebral N-acetylaspartate/choline ratios (r=-0.35, p<0.001). However, the presence of an ICA occlusion (and subsequent low flow) did not correlate with low N-acetylaspartate/choline ratios. CONCLUSION: Neurological deficit caused by (transient) hemispheric ischaemia is associated with low N-acetylaspartate/choline ratios, whereas prior clinical features are not associated with low cerebropetal blood flow, as measured with MR angiography. As a result, differences in cerebropetal flow cannot explain why patients with similar carotid artery disease experience different neurological features.
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Lack of evidence for a poor haemodynamic or metabolic state of the brain in patients with haemodynamic clinical features associated with carotid artery occlusion.
OBJECTIVE: To assess whether patients with carotid artery occlusion (CAO) who have clinical features suggesting a haemodynamic origin have a poor haemodynamic or metabolic state of the brain. METHODS: In 117 patients with ischaemic symptoms of the eye or brain that were transient or at most moderately disabling and associated with a CAO, we compared CO(2) reactivity, quantitative flow measurement by magnetic resonance (MR) angiography, metabolic ratios measured by (1)H-MR spectroscopy, collateral blood flow patterns and the presence of infarcts of the borderzone type between patients grouped by the following clinical features: (1) presence or absence of at least one of the 'classical' haemodynamic symptoms: limb shaking, retinal claudication, precipitation of symptoms by exercise, by rising from a sitting or lying position, by transition from a cold to a warm environment, or by documented hypotension, and (2) symptoms having occurred after demonstration of the CAO or only before the occlusion was documented. RESULTS: Patients with (n = 16) and without (n = 101) one of the 'classical' haemodynamic symptoms did not differ in any of the measured indices. Patients with recurrent symptoms after documentation of the CAO (n = 56) had lower CO(2) reactivity (difference 8.3%, 95% confidence interval 0.1-16.5) than those with symptoms only before documentation of the occlusion (n = 61), whereas no significant differences were found in any of the other measured indices. The difference in CO(2) reactivity was no longer significant after adjustment for the interval between the patients' last symptoms and the CO(2) reactivity measurement. CONCLUSION: In patients with CAO we could not find an association between symptoms that have been associated with hypoperfusion and a poor haemodynamic or metabolic state of the brain.
Adult↗
Outcome in patients with symptomatic occlusion of the internal carotid artery or intracranial arterial lesions: a meta-analysis of the role of baseline characteristics and type of antithrombotic treatment.
OBJECTIVES: We performed a systematic review of the literature to assess the impact of potential risk factors of recurrent stroke other than a compromised cerebral blood flow in patients with carotid occlusion or intracranial arterial lesions. In addition, we investigated the effect of treatment with aspirin or oral anticoagulation on recurrent stroke rate and assessed whether the incidence of recurrent stroke has decreased over the years. METHODS: We searched Medline (1966 and onwards) and reference lists of identified articles for papers reporting on the recurrent stroke risk in patients with carotid occlusion or intracranial arterial lesions. Two authors independently extracted information from all papers. The influence of study characteristics on the risk of the endpoints 'recurrent stroke', 'ipsilateral stroke' and 'vascular death' was determined by Poisson regression analysis. Rate ratios were calculated per 10 percentage points increase of a characteristic. RESULTS AND CONCLUSIONS: Patients with intracranial carotid stenosis or occlusion had a higher rate of recurrent stroke (rate ratio 1.09; 95% CI 1.05-1.14) than patients with extracranial carotid occlusion or middle cerebral artery stenosis or occlusion. In patients with bilateral carotid occlusion the rate was lower (rate ratio 0.82; 95% CI 0.68-0.98). No other vascular risk factors than hypertension (rate ratio 1.23; 95% CI 1.07-1.41) could be shown to increase the rate of recurrent stroke. Oral anticoagulation but not aspirin had a protective effect on the incidence of recurrent stroke (rate ratio 0.86; 95% CI 0.79-0.93). The reported rates of recurrent stroke in patients with symptomatic occlusion of the internal carotid artery or intracranial arterial lesions have not decreased over the years.
Administration, Oral↗
Reproducibility of measurements of cerebral infarct volume on CT scans.
BACKGROUND AND PURPOSE: Infarct volume is increasingly used as an outcome measure in clinical trials of therapies for acute ischemic stroke. We tested which of 5 different methods to measure infarct size or volume on CT scans has the highest reproducibility. METHODS: Infarct volume and total intracranial volume were measured with Leica Q500 MCP image analysis software, or with a caliper, on 38 CT scans of patients who participated in the Tirilazad Efficacy Stroke Study II (TESS II). The scans were performed 8 days (+/-2 days) after the onset of symptoms. The 5 methods tested were based on (1) semiautomated pixel thresholding, (2) manual tracing of the perimeter, (3) a stereological counting grid, (4) measurement of the 3 largest diameters, and (5) the single largest diameter. The measurements were performed independently by 2 observers; the first observer performed all measurements twice. RESULTS: The single largest diameter did not correlate well with infarct volume. Of the other methods, manual tracing of the perimeter of the infarct had the lowest intraobserver and interobserver variability: coefficients of variation were 8.6% and 14.1%, respectively. For total intracranial volume, manual tracing also provided the highest reproducibility: intraobserver and interobserver coefficients of variation were 3.3% and 4.9%, respectively. CONCLUSIONS: Manual tracing of the perimeter is the most reproducible method for measuring the volumes of the infarct and the total intracranial space in multicenter trials of therapies for acute ischemic stroke.
Adult↗
Sustained bilateral hemodynamic benefit of contralateral carotid endarterectomy in patients with symptomatic internal carotid artery occlusion.
BACKGROUND AND PURPOSE: We sought to investigate whether in patients with a symptomatic internal carotid artery (ICA) occlusion, endarterectomy of a severe stenosis of the contralateral carotid artery can establish long-term cerebral hemodynamic improvement. METHODS: Nineteen patients were studied on average 1 month before and 6 months after contralateral carotid endarterectomy (CEA). Volume flow in the main extracranial and intracranial arteries was measured with MR angiography. Collateral flow via the circle of Willis and the ophthalmic arteries was studied with MR angiography and transcranial Doppler sonography, respectively. Cerebral metabolism and CO(2) vasoreactivity were investigated with MR spectroscopy and transcranial Doppler sonography, respectively. Twelve nonoperated patients with a symptomatic ICA occlusion and contralateral ICA stenosis, who were matched for age and sex, served as control patients. RESULTS: In patients who underwent surgery, flow in the operated ICA increased significantly (P:<0.05) and flow in the basilar artery decreased significantly (P:<0.01) after CEA. On the occlusion side, mean flow in the middle cerebral artery increased significantly from 71 to 85 mL/min (P:<0.05) after CEA. The prevalence of collateral flow via the anterior communicating artery to the occlusion side increased significantly (47% before and 84% after CEA; P:<0.05), while the prevalence of reversed ophthalmic artery flow on the operation side decreased significantly (42% before and 5% after CEA; P:<0.05). In the hemisphere on the side of the ICA occlusion, lactate was no longer detected after CEA in 80% of operated patients, whereas it was no longer detected over time in 14% of nonoperated patients (P:<0.05). CO(2) reactivity increased significantly in operated patients in both hemispheres (P:<0.01). CONCLUSIONS: Contralateral CEA in patients with a symptomatic ICA occlusion induces cerebral hemodynamic improvement not only on the side of surgery but also on the side of the ICA occlusion.
Aspartic Acid↗
Effect of paracetamol (acetaminophen) on body temperature in acute ischemic stroke: a double-blind, randomized phase II clinical trial.
BACKGROUND AND PURPOSE: Body temperature is a strong predictor of outcome in acute stroke. However, it is unknown whether antipyretic treatment leads to early and clinically worthwhile reduction of body temperature in patients with acute stroke, especially when they have no fever. The main purpose of this trial was to study whether early treatment of acute ischemic stroke patients with acetaminophen (paracetamol) reduces body temperature. METHODS: Seventy-five patients with acute ischemic stroke confined to the anterior circulation were randomized to treatment with either 500 mg (low dose) or 1000 mg (high dose) acetaminophen or with placebo, administered as suppositories 6 times daily during 5 days. Body temperatures were measured with a rectal electronic thermometer at the start of treatment and after 24 hours and with an infrared tympanic thermometer at 2-hour intervals during the first 24 hours and at 6-hour intervals thereafter. The primary outcome measure was rectal temperature at 24 hours after the start of treatment. RESULTS: Treatment with high-dose acetaminophen resulted in 0.4 degrees C lower body temperatures than placebo treatment at 24 hours (95% CI 0.1 degrees C to 0.7 degrees C). The mean reduction from baseline temperature with high-dose acetaminophen was 0.3 degrees C (95% CI 0 degrees C to 0.6 degrees C) higher than that in placebo-treated patients. Treatment with low-dose acetaminophen did not result in lower body temperatures. After 5 days of treatment, no differences in temperature were found between the placebo and the high- or low-dose acetaminophen groups. CONCLUSIONS: Treatment with a daily dose of 6000 mg acetaminophen may result in a small, but potentially beneficial, decrease in body temperature shortly after ischemic stroke, even in normothermic and subfebrile patients. Further studies should determine whether this effect is reproducible and whether early reduction of body temperature leads to improved outcome.
Acetaminophen↗
Recurrent ischemia in symptomatic carotid occlusion: prognostic value of hemodynamic factors.
OBJECTIVE: To identify hemodynamic factors that predict recurrence of ipsilateral cerebral ischemic events in patients with symptomatic carotid artery occlusion (CAO). PATIENTS AND METHODS: The authors studied 117 consecutive patients with CAO and corresponding recent (</=6 months) ischemic symptoms of the brain or eye that were transient or at most mildly disabling. They determined, using Cox proportional hazards analysis, the prognostic value for recurrence of ipsilateral cerebral ischemic events of 1) clinical features believed to indicate hemodynamic compromise, 2) collateral blood flow pattern, and 3) transcranial Doppler CO(2)-reactivity. RESULTS: None of the 24 patients with symptoms of retinal ischemia alone had a recurrent cerebral ischemic event. In the 93 patients with cerebral ischemic symptoms on entry, recurrence of these symptoms was independently predicted by 1) the nature of the initial symptoms being of purported hemodynamic origin (limb-shaking, precipitation of symptoms by rising, exercise or low blood pressure, retinal claudication) (hazard ratio [HR] 3.8, 95% CI 1.5 to 9.5), 2) continuing symptoms after the CAO had been documented, but before inclusion in the study (HR 5.9, 95% CI 2.2 to 16.1), and 3) the presence of collateral blood flow via leptomeningeal vessels (HR 4.1, 95% CI 1.3 to 13.1). CO(2)-reactivity did not predict recurrence of cerebral ischemic events. CONCLUSIONS: Having cerebral in contrast to retinal ischemia, clinical features suggestive of hemodynamic compromise, continuing symptoms after demonstration of the CAO, and presence of leptomeningeal collaterals may help to identify patients with symptomatic CAO at high risk of future cerebral ischemia.
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