Predictors of Neurocognitive Decline after Carotid Endarterectomy

Abstract

OBJECTIVE-Although the incidence of stroke after carotid endarterectomy (CEA) is low (1-3%), approximately 25% of patients experience subtle declines in postoperative neuropsychometric function. No studies have investigated the risk factors for this neurocognitive change. We sought to identify predictors of postoperative neurocognitive dysfunction.METHODS-We enrolled 186 CEA patients, with both symptomatic and asymptomatic stenosis, to undergo a battery of neuropsychometric tests preoperatively and on postoperative Days 1 and 30. Neurocognitive dysfunction was defined as a two standard deviation decline in performance compared with a similarly aged control group of lumbar laminectomy patients. Univariate logistic regression was performed for age, sex, obesity, smoking, symptomatology, diabetes mellitus, hypertension, hypercholesterolemia, use of statin medication, previous myocardial infarction, previous CEA, operative side, duration of surgery, duration of carotid cross-clamp, and weightadjusted doses of midazolam and fentanyl. Variables achieving univariate P < 0.10 were included in a multivariate analysis. Data is presented as (odds ratio, 95% confidence interval, P-value). CONCLUSIONS-Advanced age and diabetes predispose to neurocognitive dysfunction after CEA. These results are consistent with risk factors for neurocognitive dysfunction after coronary bypass and major stroke after CEA, supporting an underlying ischemic pathophysiology. Further work is necessary to determine the role these neurocognitive deficits may play in appropriately selecting patients for CEA. KeywordsCarotid endarterectomy; Cerebral ischemia; Neuropsychological tests; Risk factorsCarotid endarterectomy (CEA) reduces the risk of future stroke in patients with high-grade stenosis (5,10,15,25). However, approximately 25% of CEA patients experience declines in postoperative neurocognitive function that are detected by a battery of neuropsychometric tests (NPMTs) (12,13). Although the mechanism of post-CEA neurocognitive decline is poorly understood, it is thought to be ischemic in nature, and may be owing to hypoperfusion during carotid artery cross-clamping or the dislodgement of microemboli during vessel dissection and plaque removal.To date, no studies have thoroughly investigated the risk factors for these neurocognitive changes after CEA. With nearly 100,000 CEAs performed annually (5,25), many for borderline indications with small absolute benefit (11,35), understanding the variables that predispose to subtle changes in cerebral function is crucial in appropriate patient selection. We sought to identify factors that predict postoperative neurocognitive dysfunction. PATIENTS AND METHODS Study PopulationOne hundred and eighty six consecutive patients undergoing elective CEA for both symptomatic and asymptomatic carotid artery stenosis were prospectively enrolled in this institutional review board-approved study. All CEA patients had 60% or greater stenosis of the operative carotid artery. After obtaining written informed conse...

Elevation of monocyte chemoattractant protein-1 in patients experiencing neurocognitive decline following carotid endarterectomy

“…The association between diabetes mellitus and post-operative injury was rein-forced by our data. Additionally, we found smoking history to be linked with favorable outcome, although this relationship was not observed in prior, larger studies [17]. Percent change in peri-operative MCP-1 levels, however, demonstrated the strongest correlation with outcome in our multivariate analysis.…”

“…Chronic inflammation and small vessel disease likely render patients susceptible to neuronal injury following global cerebral hypoperfusion. Our group has demonstrated that advanced age and history of diabetes mellitus are independent predictors of neurocognitive outcome following CEA [17]. We have also shown that elevated preoperative monocyte count independently predicts neuropsychological decline [16].…”

“…As stated, our previous studies demonstrate that age and history of diabetes mellitus also predict neurocognitive decline following CEA [17]. In order to control for the former, we selected an age-and sex-matched cohort of injured and uninjured patients for comparison in our analysis.…”

“…Recent studies suggest that preexisting microvascular disease may render CEA patients susceptible to cerebral hypoperfusion, initiating neuronal injury during a brief episode of ischaemia. We have previously shown that advanced age, pre-operative monocyte count and history of diabetes mellitus all independently predict neuropsychological decline following CEA [16,17]. We have also demonstrated that neuropsychological changes are not associated with positive lesions on diffusion weighted imaging (DWI), further implicating a role for regional hypoxia and hypoperfusion [9].…”

“…All patients were assessed pre-operatively and on POD 1 by a trained full-time research assistant using a battery of 5 neuropsychological tests chosen to represent a range of cognitive domains as we have described previously [9,10,12,16,17]. These tests are representative of the outcome measures recommended by a consensus group [19] along with tests used in previous studies of neuropsychological testing after carotid endarterectomy to better elucidate neurocognitive changes [1,13].…”