The impact of contralateral carotid artery stenosis on outcomes after carotid endarterectomy

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 afte...

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Veröffentlicht in:Journal of vascular surgery 2017-12, Vol.66 (6), p.1727-1734.e2
Hauptverfasser: Pothof, Alexander B., Soden, Peter A., Fokkema, Margriet, Zettervall, Sara L., Deery, Sarah E., Bodewes, Thomas C.F., de Borst, Gert J., Schermerhorn, Marc L.
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container_end_page 1734.e2
container_issue 6
container_start_page 1727
container_title Journal of vascular surgery
container_volume 66
creator Pothof, Alexander B.
Soden, Peter A.
Fokkema, Margriet
Zettervall, Sara L.
Deery, Sarah E.
Bodewes, Thomas C.F.
de Borst, Gert J.
Schermerhorn, Marc L.
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.
doi_str_mv 10.1016/j.jvs.2017.04.032
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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 &lt; .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 &lt; .001), and prolonged length of stay (OR, 1.6; 95% CI, 1.3-1.9; P &lt; .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. 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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 &lt; .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 &lt; .001), and prolonged length of stay (OR, 1.6; 95% CI, 1.3-1.9; P &lt; .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. 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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 &lt; .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 &lt; .001), and prolonged length of stay (OR, 1.6; 95% CI, 1.3-1.9; P &lt; .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. 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title The impact of contralateral carotid artery stenosis on outcomes after carotid endarterectomy
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