Abstract
Background: Between 9% and 23% of patients undergoing otherwise uncomplicated carotid endarterectomy (CEA) develop subtle cognitive decline 1 month postoperatively. The APOE-ε4 allele has been associated with worse outcome following stroke. Objective: To investigate the ability of APOE-ε4 to predict post-CEA neurocognitive dysfunction. Methods: Seventy-five patients with CEA undergoing elective CEA were prospectively recruited in this nested cohort study and demographic variables were recorded. Patients were evaluated before and 1 month after surgery with a standard battery of five neuropsychological tests. APOE genotyping was performed by restriction fragment length polymorphism analysis in all patients. Neuropsychological deficits were identified by comparing changes (before to 1 month post-operation) in individual performance on the test battery. Logistic regression was performed for APOE-ε4 and previously identified risk factors. Results: Twelve of 75 (16%) CEA patients possessed the APOE-ε4 allele. Eight of 75 (11%) patients experienced neurocognitive dysfunction on postoperative day 30. One month post-CEA, APOE-ε4-positive patients were more likely to be cognitively injured (42%) than APOE-ε4-negative patients (5%) (p = 0.002). In multivariate analysis, the presence of the APOE-ε4 allele increased the risk of neurocognitive dysfunction at 1 month 62-fold (62.28, 3.15 to 1229, p = 0.007). Diabetes (51.42, 1.94 to 1363, p = 0.02), and obesity (24.43, 1.41 to 422.9, p = 0.03) also predisposed to injury. Conclusion: The APOE-ε4 allele is a robust independent predictor of neurocognitive decline 1 month following CEA.
| Original language | English |
|---|---|
| Pages (from-to) | 1759-1763 |
| Number of pages | 5 |
| Journal | Neurology |
| Volume | 65 |
| Issue number | 11 |
| DOIs | |
| State | Published - Dec 1 2005 |
| Externally published | Yes |
Fingerprint
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
APOE-ε4 predisposes to cognitive dysfunction following uncomplicated carotid endarterectomy. / Heyer, E. J.; Wilson, D. A.; Sahlein, D. H.; Mocco, J.; Williams, S. C.; Sciacca, R.; Rampersad, A.; Komotar, Ricardo J; Zurica, J.; Benvenisty, A.; Quest, D. O.; Todd, G.; Solomon, R. A.; Connolly, E. S.
In: Neurology, Vol. 65, No. 11, 01.12.2005, p. 1759-1763.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - APOE-ε4 predisposes to cognitive dysfunction following uncomplicated carotid endarterectomy
AU - Heyer, E. J.
AU - Wilson, D. A.
AU - Sahlein, D. H.
AU - Mocco, J.
AU - Williams, S. C.
AU - Sciacca, R.
AU - Rampersad, A.
AU - Komotar, Ricardo J
AU - Zurica, J.
AU - Benvenisty, A.
AU - Quest, D. O.
AU - Todd, G.
AU - Solomon, R. A.
AU - Connolly, E. S.
PY - 2005/12/1
Y1 - 2005/12/1
N2 - Background: Between 9% and 23% of patients undergoing otherwise uncomplicated carotid endarterectomy (CEA) develop subtle cognitive decline 1 month postoperatively. The APOE-ε4 allele has been associated with worse outcome following stroke. Objective: To investigate the ability of APOE-ε4 to predict post-CEA neurocognitive dysfunction. Methods: Seventy-five patients with CEA undergoing elective CEA were prospectively recruited in this nested cohort study and demographic variables were recorded. Patients were evaluated before and 1 month after surgery with a standard battery of five neuropsychological tests. APOE genotyping was performed by restriction fragment length polymorphism analysis in all patients. Neuropsychological deficits were identified by comparing changes (before to 1 month post-operation) in individual performance on the test battery. Logistic regression was performed for APOE-ε4 and previously identified risk factors. Results: Twelve of 75 (16%) CEA patients possessed the APOE-ε4 allele. Eight of 75 (11%) patients experienced neurocognitive dysfunction on postoperative day 30. One month post-CEA, APOE-ε4-positive patients were more likely to be cognitively injured (42%) than APOE-ε4-negative patients (5%) (p = 0.002). In multivariate analysis, the presence of the APOE-ε4 allele increased the risk of neurocognitive dysfunction at 1 month 62-fold (62.28, 3.15 to 1229, p = 0.007). Diabetes (51.42, 1.94 to 1363, p = 0.02), and obesity (24.43, 1.41 to 422.9, p = 0.03) also predisposed to injury. Conclusion: The APOE-ε4 allele is a robust independent predictor of neurocognitive decline 1 month following CEA.
AB - Background: Between 9% and 23% of patients undergoing otherwise uncomplicated carotid endarterectomy (CEA) develop subtle cognitive decline 1 month postoperatively. The APOE-ε4 allele has been associated with worse outcome following stroke. Objective: To investigate the ability of APOE-ε4 to predict post-CEA neurocognitive dysfunction. Methods: Seventy-five patients with CEA undergoing elective CEA were prospectively recruited in this nested cohort study and demographic variables were recorded. Patients were evaluated before and 1 month after surgery with a standard battery of five neuropsychological tests. APOE genotyping was performed by restriction fragment length polymorphism analysis in all patients. Neuropsychological deficits were identified by comparing changes (before to 1 month post-operation) in individual performance on the test battery. Logistic regression was performed for APOE-ε4 and previously identified risk factors. Results: Twelve of 75 (16%) CEA patients possessed the APOE-ε4 allele. Eight of 75 (11%) patients experienced neurocognitive dysfunction on postoperative day 30. One month post-CEA, APOE-ε4-positive patients were more likely to be cognitively injured (42%) than APOE-ε4-negative patients (5%) (p = 0.002). In multivariate analysis, the presence of the APOE-ε4 allele increased the risk of neurocognitive dysfunction at 1 month 62-fold (62.28, 3.15 to 1229, p = 0.007). Diabetes (51.42, 1.94 to 1363, p = 0.02), and obesity (24.43, 1.41 to 422.9, p = 0.03) also predisposed to injury. Conclusion: The APOE-ε4 allele is a robust independent predictor of neurocognitive decline 1 month following CEA.
UR - http://www.scopus.com/inward/record.url?scp=33645080717&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33645080717&partnerID=8YFLogxK
U2 - 10.1212/01.wnl.0000184579.23624.6b
DO - 10.1212/01.wnl.0000184579.23624.6b
M3 - Article
C2 - 16207841
AN - SCOPUS:33645080717
VL - 65
SP - 1759
EP - 1763
JO - Neurology
JF - Neurology
SN - 0028-3878
IS - 11
ER -