Cerebral tomographic findings in patients undergoing carotid endarterectomy for asymptomatic carotid stenosis: short-term and long-term implications

Background and Purpose— Large randomized trials have demonstrated a net benefit of carotid endarterectomy (CEA) for asymptomatic carotid artery stenosis compared with best medical treatment. However, it takes years to overcome the perioperative risk and gain the reduction in stroke or death risk. Long-term survival after CEA for asymptomatic stenosis may be an important consideration in deciding on this prophylactic procedure, but is not well documented. The aim was to analyze long-term survival after CEA for asymptomatic stenosis and the impact of risk factors in a population-based study. Methods— The Swedish vascular registry (Swedvasc) covers all centers performing CEA. Data on all registered CEAs during 1994 to 2003 were retrieved. All patients were cross-matched with the Population-Registry for accurate data on mortality (date of death). Analyses with Kaplan-Meier curves for survival and relative odds ratio (OR) for predictors of survival were performed. Results— A total of 6169 CEAs in 5808 patients were registered, with a median time at risk of 5.1 (range, 0.1 to 11.8) years. The indication for CEA was asymptomatic stenosis in 10.8% of the patients. Survival after CEA for asymptomatic stenosis was 78.2% after 5 and 45.5% after 10 years. Previous vascular surgery (OR, 1.8; 1.1 to 3.0), cardiac disease (OR, 1.7; 1.0 to 2.8), diabetes mellitus (OR, 2.3; 1.3 to 4.1), and age (OR, 1.5; 1.1 to 2.1 per 10 years) were predictors of decreased 5-year survival. Conclusions— In this population-based study of patients operated on for asymptomatic stenosis, a substantial reduction in long-term survival was observed. Predictors of decreased longevity were age at operation, diabetes, cardiac disease, and previous vascular surgery.

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Long-Term Survival After Carotid Endarterectomy for Asymptomatic Stenosis

Kragsterman

Björck

Lindbäck

et al. 2006

“…Silent infarctions are found in about a quarter of patients with asymptomatic carotid stenosis but do not consistently appear to be more common on the side of the carotid stenosis. [100][101][102][103] As with AF, data relating silent infarction to subsequent risk are limited but suggest greater risk of subsequent stroke and mortality among those with preoperative silent infarction. A systematic review and meta-analysis found 2 studies that showed that a nonlacunar pattern of cortical and subcortical silent CT infarctions ipsilateral to the carotid stenosis was associated with future stroke risk (pooled odds ratio [OR], 4.6; 95% confidence interval [CI], 3.0-7.2), but there were no prospective MRI studies linking silent infarction and stroke risk in this setting.…”

Section: Investigations For Patients With Silent Brain Infarctsmentioning

confidence: 99%

Prevention of Stroke in Patients With Silent Cerebrovascular Disease: A Scientific Statement for Healthcare Professionals From the American Heart Association/American Stroke Association

Smith¹,

Saposnik²,

Biessels³

et al. 2017

316

297

Abstract-Two decades of epidemiological research shows that silent cerebrovascular disease is common and is associated with future risk for stroke and dementia. It is the most common incidental finding on brain scans. To summarize evidence on the diagnosis and management of silent cerebrovascular disease to prevent stroke, the Stroke Council of the American Heart Association convened a writing committee to evaluate existing evidence, to discuss clinical considerations, and to offer suggestions for future research on stroke prevention in patients with 3 cardinal manifestations of silent cerebrovascular disease: silent brain infarcts, magnetic resonance imaging white matter hyperintensities of presumed vascular origin, and cerebral microbleeds. The writing committee found strong evidence that silent cerebrovascular disease is a common problem of aging and that silent brain infarcts and white matter hyperintensities are associated with future symptomatic stroke risk independently of other vascular risk factors. In patients with cerebral microbleeds, there was evidence of a modestly increased risk of symptomatic intracranial hemorrhage in patients treated with thrombolysis for acute ischemic stroke but little prospective evidence on the risk of symptomatic hemorrhage in patients on anticoagulation. There were no randomized controlled trials targeted specifically to participants with silent cerebrovascular disease to prevent stroke. Primary stroke prevention is indicated in patients with silent brain infarcts, white matter hyperintensities, or microbleeds. Adoption of standard terms and definitions for silent cerebrovascular disease, as provided by prior American Heart Association/American Stroke Association statements and by a consensus group, may facilitate diagnosis and communication of findings from radiologists to clinicians. (Stroke. 2017;48:e44-e71.

“…When both nonlacunar and lacunar CT-demonstrated brain lesions were present, the infarcts were classified as nonlacunar lesions. 34 All CT brain scans were reported by an experienced neuroradiologist (J.M.S.) who was unaware of patients' clinical characteristics.…”

Section: Ct-demonstrated Brain Infarct Classificationmentioning

confidence: 99%

“…50 Because of the association of asymptomatic hypoechoic plaques with nonlacunar silent CT-demonstrated brain infarcts shown in this study, it is tempting to implicate carotid atheroembolism as the pathogenetic factor for these types of infarcts. On the other hand, although the presence of CTdemonstrated brain infarcts may predict the development of ischemic stroke in patients presenting with transient ischemic attacks 51,52 and is associated with significantly worse prognosis after carotid endarterectomy, 34,53,54 their role as a risk factor for atheroembolic stroke in patients with asymptomatic carotid stenosis is not certain and remains to be proven.…”

Section: Sabetai Et Al Reproducibility Of Computer-quantified Carotidmentioning

confidence: 99%

Reproducibility of Computer-Quantified Carotid Plaque Echogenicity

Sabetai

Tegos

Nicolaides

et al. 2000

187

113

Background and Purpose-We sought to assess the reproducibility, interobserver variability, and application to clinical studies of a new method for the quantitative assessment of carotid plaque echogenicity. Methods-Carotid plaques were scanned with the use of ultrasound, and their images were stored in a computer. They were normalized by assigning certain gray values to blood and adventitia, and the gray scale median (GSM) was used to quantify their echogenicity. The variability between storage media, between degrees of magnification, and between probes was assessed. The method was applied to 232 asymptomatic carotid plaques causing 60% to 99% stenosis in relation to the presence of ipsilateral CT-demonstrated brain infarcts. In all parts of the study the plaque GSM was measured before and after normalization to evaluate its effect. Interobserver agreement for the scanning process was assessed. Results-The GSM mean difference before and after normalization for variability studies of storage media, degrees of magnification, and probes was Ϫ14.5 and Ϫ0.12, 2.24 and 1.68, and Ϫ8.3 and Ϫ0.7, respectively. The median GSM of plaques associated with ipsilateral nonlacunar silent CT-demonstrated brain infarcts was 14, and that of plaques that were not so associated was 30 (Pϭ0.003). The interobserver GSM difference was Ϫ0.05 (95% CI, Ϫ1.7 to 1.6). Conclusions-Our method decreases the variability between storage media and between probes but not the variability between degrees of magnification. It separates echomorphologically the carotid plaques associated with silent nonlacunar CT-demonstrated brain infarcts from plaques that are not so associated.