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Carotid artery stenosis as a cause of stroke.

ABSTRACT: Population-based studies have estimated that about 15% of ischemic strokes are caused by large-vessel cerebrovascular disease. We determined the types of large-vessel atherosclerosis responsible for ischemic strokes in a population-based stroke study.Patients with first-ever or recurrent ischemic stroke in the Greater Cincinnati area were identified during 2005 at all local hospitals. Study physicians assigned ischemic stroke subtypes. Overall event rates and incidence rates for first-ever events were calculated, and age-, race- and sex-adjusted to the 2000 US population.There were 2,204 ischemic strokes, including 365 strokes of large-vessel subtype (16.6% of all ischemic strokes). Extracranial internal carotid artery (ICA) stenosis was associated with 8.0% of all ischemic strokes, while extracranial ICA occlusion and intracranial atherosclerosis were each associated with 3.5% of strokes. The annual rate of first-ever and recurrent stroke attributed to extracranial ICA was 13.4 (11.4-15.4) per 100,000 persons. We conservatively estimate that about 41,000 strokes may be attributed to extracranial ICA stenosis annually in the United States.Large-vessel atherosclerosis is an important cause of stroke, with extracranial ICA stenosis being significantly more common than extracranial ICA occlusion or intracranial atherosclerotic disease.

SUBMITTER: Flaherty ML

PROVIDER: S-EPMC3626492 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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Carotid artery stenosis as a cause of stroke.

Flaherty Matthew L ML Kissela Brett B Khoury Jane C JC Alwell Kathleen K Moomaw Charles J CJ Woo Daniel D Khatri Pooja P Ferioli Simona S Adeoye Opeolu O Broderick Joseph P JP Kleindorfer Dawn D

Neuroepidemiology 20121011 1

<h4>Background</h4>Population-based studies have estimated that about 15% of ischemic strokes are caused by large-vessel cerebrovascular disease. We determined the types of large-vessel atherosclerosis responsible for ischemic strokes in a population-based stroke study.<h4>Methods</h4>Patients with first-ever or recurrent ischemic stroke in the Greater Cincinnati area were identified during 2005 at all local hospitals. Study physicians assigned ischemic stroke subtypes. Overall event rates and i ...[more]

PMID: 23075828

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Project description:Patients with contralateral carotid occlusion (CCO) have been excluded from randomized clinical trials because of a deemed high risk for adverse neurologic outcomes with carotid endarterectomy (CEA). Evidence for this rationale is limited and conflicting. Therefore, we aimed to compare outcomes after CEA between patients with and without CCO and varying degrees of contralateral carotid stenosis (CCS).We identified patients undergoing CEA from 2003 to 2015 in the Vascular Study Group of New England (VSGNE) registry. Patients were stratified by preoperative symptom status and presence of CCO. Multivariable analysis was used to account for differences in demographics and comorbidities. Our primary outcome was 30-day stroke/death risk.Of 15,487 patients we identified who underwent CEA, 10,377 (67%) were asymptomatic. CCO was present in 914 patients, of whom 681 (75%) were asymptomatic. Overall, the 30-day stroke/death was 2.0% for symptomatic patients (CCO: 2.6%) and 1.1% for asymptomatic patients (CCO: 2.3%). After adjustment, including symptom status, CCO was associated with higher 30-day stroke/death (odds ratio [OR], 2.1; 95% confidence interval [CI], 1.4-3.3; P = .001), any in-hospital stroke (OR, 2.8; 95% CI, 1.7-4.6; P < .001), in-hospital ipsilateral stroke (OR, 2.2; 95% CI, 1.2-4.0; P = .02), in-hospital contralateral stroke (OR, 5.1; 95% CI, 2.2-11.4; P < .001), and prolonged length of stay (OR, 1.6; 95% CI, 1.3-1.9; P < .001). CCS of 80% to 99% was only associated with a prolonged length of stay (OR, 1.3; 95% CI, 1.1-1.6; P = .01), not with in-hospital stroke. Neither CCO nor CCS was associated with 30-day mortality.Although CCO increases the risk of 30-day stroke/death, in-hospital strokes, and prolonged length of stay after CEA, the 30-day stroke/death rates in symptomatic and asymptomatic patients with CCO remain within the recommended thresholds set by the 14 societies' guideline document. Thus, CCO should not qualify as a high-risk criterion for CEA. Moreover, there is no evidence that patients with CCO have lower stroke/death rates after carotid artery stenting than after CEA. We believe that CEA remains a valid and safe option for patients with CCO and that CCO should not be applied as a criterion to promote carotid artery stenting per se.

Project description:ObjectiveWe have shown that almost 50% of patients with asymptomatic carotid stenosis (ACS) will demonstrate cognitive impairment. Recent evidence has suggested that cerebral hypoperfusion is an important cause of cognitive impairment. Carotid stenosis can restrict blood flow to the brain, with consequent cerebral hypoperfusion. In contrast, cross-hemispheric collateral compensation through the Circle of Willis, and cerebrovascular vasodilation can also mitigate the effects of flow restriction. It is, therefore, critical to develop a clinically relevant measure of net brain perfusion in patients with ACS that could help in risk stratification and in determining the appropriate treatment. To determine whether ACS results in cerebral hypoperfusion, we developed a novel approach to quantify interhemispheric cerebral perfusion differences, measured as the time to peak (TTP) and mean transit time (MTT) delays using perfusion-weighted magnetic resonance imaging (PWI) of the whole brain. To evaluate the utility of using clinical duplex ultrasonography (DUS) to infer brain perfusion, we also assessed the relationship between the PWI findings and ultrasound-based peak systolic velocity (PSV).MethodsStructural and PWI of the brain and magnetic resonance angiography of the carotid arteries were performed in 20 patients with ≥70% ACS. DUS provided the PSV, and magnetic resonance angiography provided plaque geometric measures at the stenosis. Volumetric perfusion maps of the entire brain from PWI were analyzed to obtain the mean interhemispheric differences for the TTP and MTT delays. In addition, the proportion of brain volume that demonstrated a delay in TTP and MTT was also measured. These proportions were measured for increasing severity of perfusion delays (0.5, 1.0, and 2.0 seconds). Finally, perfusion asymmetries on PWI were correlated with the PSV and stenosis features on DUS using Pearson's correlation coefficients.ResultsOf the 20 patients, 18 had unilateral stenosis (8 right and 10 left) and 2 had bilateral stenoses. The interhemispheric (left-right) TTP delays measured for the whole brain volume identified impaired perfusion in the hemisphere ipsilateral to the stenosis in 16 of the 18 patients. More than 45% of the patients had had ischemia in at least one half of their brain volume, with a TTP delay >0.5 second. The TTP and MTT delays showed strong correlations with PSV. In contrast, the correlations with the percentage of stenosis were weaker. The correlations for the PSV were strongest with the perfusion deficits (TTP and MTT delays) measured for the whole brain using our proposed algorithm (r = 0.80 and r = 0.74, respectively) rather than when measured on a single magnetic resonance angiography slice as performed in current clinical protocols (r = 0.31 and r = 0.58, respectively).ConclusionsInterhemispheric TTP and MTT delay measured for the whole brain using PWI has provided a new tool for assessing cerebral perfusion deficits in patients with ACS. Carotid stenosis was associated with a detectable reduction in ipsilateral brain perfusion compared with the opposite hemisphere in >80% of patients. The PSV measured at the carotid stenosis using ultrasonography correlated with TTP and MTT delays and might serve as a clinically useful surrogate to brain hypoperfusion in these patients.

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Carotid artery stenosis as a cause of stroke.

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Carotid artery stenosis as a cause of stroke.

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