%0 Journal Article
%T Cognitive impairment in asymptomatic carotid artery stenosis is associated with abnormal segments in the Circle of Willis.
%A Desikan SK
%A Brahmbhatt B
%A Patel J
%A Kankaria AA
%A Anagnostakos J
%A Dux M
%A Beach K
%A Gray VL
%A McDonald T
%A Crone C
%A Sikdar S
%A Sorkin JD
%A Lal BK
%J J Vasc Surg
%V 0
%N 0
%D 2024 May 6
%M 38710420
%F 4.86
%R 10.1016/j.jvs.2024.04.059
%X OBJECTIVE: Our group has previously demonstrated that patients with asymptomatic carotid artery stenosis (ACAS) demonstrate cognitive impairment. One proposed mechanism for cognitive impairment in patients with ACAS is cerebral hypoperfusion due to flow-restriction. We tested whether the combination of a high-grade carotid stenosis and inadequate cross-collateralization in the Circle of Willis (CoW) resulted in worsened cognitive impairment.
METHODS: Twenty-four patients with high-grade (≥70% diameter-reducing) ACAS underwent carotid duplex ultrasound, cognitive assessment, and 3D time-of-flight magnetic resonance angiography. The cognitive battery consisted of nine neuropsychological tests assessing four cognitive domains: learning and recall, attention and working memory, motor and processing speed, and executive function. Raw cognitive scores were converted into standardized T-scores. A structured interpretation of the magnetic resonance angiography images was performed with each segment of the CoW categorized as being either normal or abnormal. Abnormal segments of the CoW were defined as segments characterized as narrowed or occluded due to congenital aplasia or hypoplasia, or acquired atherosclerotic stenosis or occlusion. Linear regression was used to estimate the association between the number of abnormal segments in the CoW, and individual cognitive domain scores. Significance was set to P < .05.
RESULTS: The mean age of the patients was 66.1 ± 9.6 years, and 79.2% (n = 19) were male. A significant negative association was found between the number of abnormal segments in the CoW and cognitive scores in the learning and recall (β = -6.5; P = .01), and attention and working memory (β = -7.0; P = .02) domains. There was a trend suggesting a negative association in the motor and processing speed (β = -2.4; P = .35) and executive function (β = -4.5; P = .06) domains that did not reach significance.
CONCLUSIONS: In patients with high-grade ACAS, the concomitant presence of increasing occlusive disease in the CoW correlates with worse cognitive function. This association was significant in the learning and recall and attention and working memory domains. Although motor and processing speed and executive function also declined numerically with increasing abnormal segments in the CoW, the relationship was not significant. Since flow restriction at a carotid stenosis compounded by inadequate collateral compensation across a diseased CoW worsens cerebral perfusion, our findings support the hypothesis that cerebral hypoperfusion underlies the observed cognitive impairment in patients with ACAS.