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...

Background Systemic inflammation has been implicated in the development of cognitive dysfunction following carotid endarterectomy (CEA). Neutrophil-lymphocyte ratio (NLR) is a reliable measure of systemic inflammation. We hypothesize that patients with elevated preoperative NLR have increased risk of cognitive dysfunction 1 day after CEA. Methods Five hundred fifty-one (551) patients scheduled for CEA were enrolled at Columbia University in New York, NY from 1995 to 2012. NLR was retrospectively reviewed; only 432 patients had preoperative NLR values available within 2 weeks of CEA. NLR was analyzed as a continuous variable and categorically with a cutoff of ≥5 and <5 and equal tertiles, as done in previous studies. Results Patients with cognitive dysfunction had significantly higher NLR than those without cognitive dysfunction (4.5±4.0 vs. 3.2±2.6, P<0.001). The incidence of cognitive dysfunction was significantly higher in patients with NLR ≥5 than NLR <5 (34.7% vs. 12.8%, P<0.001). Significantly fewer patients in the low tertile had cognitive dysfunction than in the high tertile (6.9% vs. 25.9%, P<0.001) and middle tertile (6.9% vs. 17.4%, P=0.006). In the final multivariate model, diabetes mellitus (OR: 2.03 [1.08–3.75], P=0.03) and NLR ≥5 (OR: 3.38 [1.81–6.27], P<0.001) were significantly associated with higher odds of cognitive dysfunction, while statin use was significantly associated with lower odds (OR: 0.48 [0.27–0.84], P=0.01). Conclusions Preoperative NLR is associated with cognitive dysfunction 1 day after CEA. NLR ≥5 and diabetes mellitus are significantly associated with increased odds of cognitive dysfunction while statin use is significantly associated with decreased odds.

OBJECTIVE-Neurocognitive dysfunction has been shown to occur in roughly 25% of patients undergoing carotid endarterectomy (CEA). Despite this, little is known about the mechanism of this injury. Recently, several groups have shown that new diffusion weighted imaging (DWI)-positive lesions are seen in 20% of patients undergoing CEA. We investigated to what degree neurocognitive dysfunction was associated with new DWI lesions.METHODS-Thirty-four consecutive patients undergoing CEA were subjected to preand postoperative cognitive evaluation with a battery of neuropsychological tests. Postoperative magnetic resonance imaging was performed in all patients within 24 hours of surgery. Lesions that showed high signal on DWI and restricted diffusion on apparent diffusion coefficient maps but no abnormal high signal on the fluid-attenuated inversion recovery images were considered hyperacute. RESULTS-Cognitive dysfunction was seen in eight (24%) patients. New hyperacute DWI lesions were seen in three (9%). Only one (13%) of the patients with cognitive dysfunction had a new DWI lesion. Two thirds of the new DWI lesions occurred in the absence of cognitive deterioration. Patients with cognitive dysfunction had significantly longer carotid cross-clamp times.CONCLUSION-Neurocognitive dysfunction after CEA does not seem to be associated with new DWI positive lesions.Correspondence to: Eric J. Heyer. Carotid endarterectomy (CEA) is an effective means of preventing future stroke (1,6,11,14). The low occurrence of perioperative complications such as stroke makes this a very safe procedure. However, subtle cognitive decline occurs in 28% of patients undergoing CEA when they are evaluated by a battery of neuropsychometric (NP) tests 1 day after surgery (5). This functional change in performance reflects a significant alteration in the brain because patients who have cognitive dysfunction also have a statistically significant increase in S100B, a glial protein serum marker of brain injury, at 24 and 48 hours after surgery (2).Cognitive dysfunction may arise because of multiple reasons. The two most evident relate to ischemic events caused by emboli or global hypoperfusion. Gaunt et al. (4) have shown that the majority of patients having CEA have an average of five emboli per procedure. Furthermore, these emboli, at least when generated during preclamp dissection, may lead to diffusion weighted imaging (DWI) or T1-weighted contrast-enhanced magnetic resonance imaging (MRI) lesions of cerebral infarct (17). On the other hand, upon clamping the carotid artery, there may be a decrease in cerebral blood flow determined by xenon, transcranial Doppler ultrasonography, and electroencephalography (EEG). In fact, there can be as much as a 50% decline in cerebral blood flow before significant changes become evident on the electroencephalogram (15).Therefore, we wanted to determine whether patients having CEA and neurocognitive changes also have acute ischemic lesions on MRI associated with the surgical procedure. To identify these les...

BackgroundMany acute coronary syndrome (ACS; myocardial infarction and unstable angina) patients are rehospitalized within 30 days of discharge, and recent US health policy initiatives have tied hospital Medicare reimbursement to 30-day readmission rates. Patient-perceived psychological stress is thought to impact prognosis after ACS. A recently offered “posthospital syndrome” model of 30-day readmissions posits that the stress level at the time of the index hospitalization itself may increase 30-day risk for readmission in ACS patients. We tested whether self-reported stress in the days surrounding the ACS hospitalization was associated with increased risk for readmission within 30 days.MethodsA mean of 8.5 days after discharge, 342 consecutively hospitalized ACS patients reported on how often they felt stress during the past two weeks. Readmission within 30 days of hospital discharge for any cause was determined by follow-up telephone calls to patients and confirmed by hospital records.ResultsOverall, 40 (11.7%) participants were readmitted within 30 days, and 22 (6.4%) reported high stress. Readmission within 30 days was more common in patients with high stress (5 admissions, 23%) than in patients with low stress (35 admissions, 11%). After adjustment for demographic and clinical factors, as well as depression, high stress was associated with a 3-fold increased risk of 30-day readmission (HR = 3.21, 95% CI = 1.13, 9.10).ConclusionsPrevious research has shown that stress in the days surrounding a hospitalization can mark long-term cardiovascular risk, but this is the first study to test a hypothesis of the posthospital syndrome model of early readmission. Further research is needed to confirm the association between stress and readmission risk, and to identify the processes of hospitalization that could be modified to both reduce the stress experienced and that would also be effective for reducing readmissions.