Cognitive Impairment Risk Increases With Carotid Stenosis Severity

My right carotid artery was at 80% blockage at time of stroke and then thankfully fully closed up 3 years later. Remained closed for 10 years and I cognitively functioned quite well with no episodes of fainting or poor executive functioning. Eventually collaterals grew around the blockage. Since my Circle of Willis is complete, I still had 3 fully functioning arteries supplying blood to the brain, obviously enough to keep me highly functioning. I'm glad that my doctors were so incompetent they never found that 80% blockage, otherwise they probably would have insisted I undergo either stenting or endarterectomy, both of which they couldn't guarantee no problems. And I didn't find out about those problems until years later researching for this blog.

Cognitive Impairment Risk Increases With Carotid Stenosis Severity

 Increased severity of carotid stenosis is significantly associated with poorer executive function and slower processing speed, independent of traditional vascular risk factors and history of stroke. Patients with greater carotid stenosis demonstrate significantly worse processing speed and executive function performance compared with those who have less severe disease, according to results of a study published in Alzheimer’s & DementiaAsymptomatic extracranial carotid atherosclerotic disease (aECAD) has been associated with a 22% increased risk for Alzheimer disease, but previous studies evaluating the effect of aECAD on cognitive outcomes have been limited by methodological biases.To better characterize early cognitive changes associated with aECAD, researchers from the University of Arizona examined data from the Carotid and Mind (CAM) clinical study. The researchers evaluated data from the first 182 individuals enrolled in CAM between 2022 and 2024, of whom 167 were included in the final analysis. Participants were aged 50 to 85 years and were recruited from vascular surgery and cardiology clinics. All participants underwent magnetic resonance imaging (MRI), carotid stenosis assessment using North American Symptomatic Carotid Endarterectomy Trial criteria, and comprehensive neurocognitive testing. The researchers defined aECAD as greater than 50% carotid stenosis without a history of stroke or transient ischemic attack in the previous 6 months. This work builds momentum for clinical management changes and future studies with a long-term goal of dementia prevention.

The study population had a mean (SD) age of 72 (7) years, 57% were men, 96% were White, 49% had 13 to 16 years of education, 36% had less than 50% carotid stenosis, and 26% carried the apolipoprotein E (APOE) ε4 allele.

After adjusting for age, sex, race, and ethnicity, increasing carotid stenosis severity was significantly associated with slower processing speed (adjusted b [ab], -0.20; 95% CI, -0.34 to -0.07; P =.004) and poorer executive function (ab, -0.19; 95% CI, -0.33 to -0.05; P =.009).

At the individual test level, greater carotid stenosis was associated with worse performance on the Wechsler Adult Intelligence Scale (ab, -0.26; 95% CI, -0.40 to -0.12; P <.001), Stroop Color-Word Interference (ab, -0.21; 95% CI, -0.35 to -0.07; P =.003), and Trail Making Test part A (ab, -0.21; 95% CI, -0.36 to -0.06; P =.007). Using these 3 tests, a composite Carotid Cognitive Index (CCI) was formulated.

The CCI was also inversely related with phosphorylated tau217 (p-tau217; r, -0.33; P <.001). This relationship was independent of white matter lesion volume (ab, -0.27; P =.006); demographic factors of age, gender, race, ethnicity, and education (ab, -0.24; P =.005); vascular risk factors (ab, -0.22; P =.01); APOE ε4 status (ab, -0.21; P =.01); and vascular disease history (ab, -0.21; P =.02). Higher p-tau217 levels were independently associated with APOE ε4 carriership (b, 0.57; P <.001).

Study limitations include a lack of racial and ethnic diversity.

The study authors concluded, “Although patients with carotid disease are not regularly evaluated clinically for cognitive impairment or dementia, this work builds momentum for clinical management changes and future studies with a long-term goal of dementia prevention.”

Disclosures: One study author declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.