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Published online before print October 5, 2005, doi:10.1212/01.wnl.0000184579.23624.6b)
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NEUROLOGY 2005;65:1759-1763
© 2005 American Academy of Neurology

APOE-{varepsilon}4 predisposes to cognitive dysfunction following uncomplicated carotid endarterectomy

E. J. Heyer, MD, PhD, D. A. Wilson, BS, D. H. Sahlein, MD, J. Mocco, MD, S. C. Williams, BS, R. Sciacca, EngScD, A. Rampersad, BA, R. J. Komotar, MD, J. Zurica, BA, A. Benvenisty, MD, D. O. Quest, MD, G. Todd, MD, R. A. Solomon, MD and E. S. Connolly, Jr, MD

From the Departments of Neurological Surgery (Drs. Mocco, Komotar, Quest, Solomon, and Connolly, and D.A. Wilson and S.C. Williams), Anesthesiology (Dr. Heyer, and A. Rampersad and J. Zurica), Neurology (Dr. Heyer), and Medicine (Dr. Sciacca), Columbia University, New York, NY; Department of Surgery (Drs. Benvenisty and Todd), Division of Vascular Surgery, Saint Luke’s Roosevelt Hospital, New York, NY; Department of Radiology (Dr. Sahlein), New York University, New York.

Address correspondence and reprint requests to Dr. Ricardo J. Komotar, Department of Neurosurgery, Columbia University, 630 West 168th Street, Room 5-454, New York, NY 10032; e-mail: rjk2103{at}columbia.edu

Background: Between 9% and 23% of patients undergoing otherwise uncomplicated carotid endarterectomy (CEA) develop subtle cognitive decline 1 month postoperatively. The APOE-{varepsilon}4 allele has been associated with worse outcome following stroke.

Objective: To investigate the ability of APOE-{varepsilon}4 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-{varepsilon}4 and previously identified risk factors.

Results: Twelve of 75 (16%) CEA patients possessed the APOE-{varepsilon}4 allele. Eight of 75 (11%) patients experienced neurocognitive dysfunction on postoperative day 30. One month post-CEA, APOE-{varepsilon}4–positive patients were more likely to be cognitively injured (42%) than APOE-{varepsilon}4–negative patients (5%) (p = 0.002). In multivariate analysis, the presence of the APOE-{varepsilon}4 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-{varepsilon}4 allele is a robust independent predictor of neurocognitive decline 1 month following CEA.

This article was previously published in electronic format as an Expedited E-Pub on October 5, 2005, at www.neurology.org.

This study was supported in part by the Irving Center for Clinical Research at Columbia University Medical Center. J.M. was supported in part by the Congress of Neurologic Surgeons Wilder Penfield Clinical Research Fellowship. D.A.W. was supported in part by the Doris Duke Clinical Research Fellowship. R.J.K. was supported in part by an NIH Research Training Fellowship. E.J.H. and E.S.C. were supported in part by a grant from the NIA (RO1 AG17604).

Disclosure: The authors report no conflicts of interest.

Received May 16, 2005. Accepted in final form August 23, 2005.


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