Delayed Carotid Surgery: What Are the Causes in the North West of England?

AbstractIntroductionCarotid endarterectomy (CEA) should be performed within two weeks of symptoms for patients with carotid stenosis >50%. Whether these standards are being achieved and causes of delay between symptoms and CEA were investigated.DesignAn analysis of prospectively collected multi-centre data.MaterialsConsecutive data for patients undergoing CEA between January-2006 and September-2010 were collected. Asymptomatic patients and those with no details on the timing of cerebral symptoms were excluded.Methods‘Delay’ from symptom to CEA was defined as more than two weeks and ‘prolonged-delay’ more than eight weeks. Univariable and multivariable analyses were used to identify factors associated with these delays.ResultsOf 2147 patients with symptoms of cerebral ischaemia, 1522(70.9%) experienced ‘delay’ and 920(42.9%) experienced ‘prolonged delay’. Patients with ischaemic heart disease were more likely to experience ‘delay’ (OR = 1.56; 95% CI 1.11–2.19, p = 0.011), whereas patients with stroke (OR = 0.77; 95%CI 0.63–0.94, p = 0.011) and those treated at hospitals with a stroke-prevention clinic (OR = 0.57; 95%CI 0.46–0.71, p < 0.001) were less likely to experience ‘delay’. Patients treated after the publication of National Institute for Health and Clinical Excellence (NICE) guidelines were less likely to experience ‘prolonged delay’ (OR = 0.77; 95%CI 0.65–0.91, p = 0.003) but not ‘delay’.ConclusionFew patients achieved CEA within two weeks of symptoms. Introducing stroke-prevention clinics with one-stop carotid imaging appears important

Cerebral injury during cardiopulmonary bypass: Emboli impair memory

AbstractObjectives: Cognitive deficits occur in up to 80% of patients after cardiac surgery. We investigated the influence of cerebral perfusion and embolization during cardiopulmonary bypass on cognitive function and recovery. Methods: Cerebrovascular reactivity was measured in 70 patients before coronary operations in which nonpulsatile bypass was used. Throughout the operations, middle cerebral artery flow velocity and embolization were recorded by transcranial Doppler and regional oxygen saturation was recorded by near-infrared spectroscopy. Cognitive function was measured by a computerized battery of tests before the operation and 1 week, 2 months, and 6 months after surgery. Elderly patients undergoing urologic surgery served as controls. Results: Cerebrovascular reactivity was impaired preoperatively in 49 patients. Median (interquartile range) regional cerebral oxygen saturation fell during bypass by 10% (6%-15%), indicating increased oxygen extraction, whereas mean middle cerebral flow velocity increased significantly by a median of 6 cm/s (both P <.0001, Wilcoxon), suggesting increased arterial tone. More than 200 emboli were detected in 40 patients, mainly on aortic clamping and release, when bypass was initiated, and during defibrillation. Cognitive function deteriorated more in patients having cardiopulmonary bypass than in control patients having urologic operations but recovered in most tests by 2 months. Measures of cerebral perfusion (poor cerebrovascular reactivity, low arterial pressures, and flow velocity in the middle cerebral artery) predicted poor attention at 1 week (r = 0.3, P <.01, Spearman). Emboli were associated with memory loss (r = 0.3, P <.02, Spearman). Conclusions: Cognitive deficits were common after cardiopulmonary bypass. Occult cerebrovascular disease was more severe than expected and predisposed to attention difficulties, whereas emboli caused memory deficits. We believe this to be the first report of differing cognitive effects from emboli and hypoperfusion. (J Thorac Cardiovasc Surg 2001;121:1150-60

Asymptomatic spontaneous cerebral emboli predict cognitive and functional decline in dementia.

Item does not contain fulltextBACKGROUND: Spontaneous cerebral emboli (SCE) are frequent in Alzheimer's disease (AD) and vascular dementia (VaD). We investigated the effect of SCE on the rates of cognitive and functional decline in AD and VaD. METHODS: One hundred thirty-two patients with dementia (74 AD, National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association [NINCDS/ADRDA] criteria; 58 VaD, National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche et l'Enseignement en Neurosciences [NINDS/AIREN] criteria) underwent 1-hour transcranial Doppler for detection of SCE (mean [SD] age 75.5 (7.4) years; 46% female). Neuropsychological tests (Mini-Mental State Examination [MMSE], Alzheimer's Disease Assessment Scale-Cognitive subscale [ADAS-Cog], and Neuropsychiatric Inventory [NPI]) and assessment of activities of daily living (Interview for Deterioration in Daily Living Activities in Dementia [IDDD]) were performed initially and 6 months later. SCE positive (SCE+ve, n = 47) and SCE negative (SCE-ve, n = 85) patients were compared using repeated measures analyses of variance (ANOVAs) adjusted for age, gender, and cardiovascular risk factors. RESULTS: SCE+ve patients with dementia, both AD and VaD, suffered a more rapid decline in cognitive functioning over 6 months (ADAS-cog, mean increase 7.1 for SCE+ve compared with 3.3 for SCE-ve, p = .006) and activities of daily living (IDDD, mean increase 24.4 for SCE+ve compared with 10.8 for SCE-ve, p = .014). CONCLUSIONS: Asymptomatic SCE are associated with an accelerated cognitive and functional decline in dementia. SCE may be a potentially treatable cause of disease progression in dementia