As data on prevalence and etiology of dementia in American Indians are limited, we sought to determine rates and patterns of memory loss among American Indian veterans with vascular risk factors. Sixty consecutive outpatient American Indian veterans with a mean age of 64 years (range 50-86), without prior dementia or mild cognitive impairment (MCI), and with ≥ 2 vascular risk factors were enrolled. The Montreal Cognitive Assessment (MoCA) and the Beck Depression Inventory-II were used to screen for cognitive impairment and depression. Patients with MoCA scores < 26 were referred for additional evaluation, including imaging, serology, and neuropsychological testing. Overall rates, types, and distribution of cognitive impairment were determined. Most prevalent vascular risk factors included hypertension (92%), hyperlipidemia (88%), diabetes (47%), and smoking (78%). Eight patients (13%) with severe depression were excluded, leaving 23/52 with abnormal MoCA scores (44%, 95%CI 30%-59%). Fifteen completed additional evaluation for memory loss, including four with normal MoCA scores who requested evaluation based on symptoms. Results were adjudicated as normal (4), nonamnestic MCI (4), vascular MCI (5), and vascular dementia (2). These results show that rates of undiagnosed cognitive impairment among American Indian veterans with vascular risk factors exceed rates previously published in non-American Indian cohorts. The most common etiology is vascular. Our findings support the need to improve vascular risk reduction in this understudied population.

Background: Rates of cardiovascular disease and stroke are elevated in Native Americans, and a greater propensity to develop vascular cognitive impairment (VCI) rather than Alzheimer-type dementia has been inferred, supporting a need for further research in VCI in this population. We determined rates and patterns of memory loss among Native American veterans with multiple vascular risk factors. Methods: Native American veterans ≥50 years old with ≥2 vascular risk factors, including smoking history, hyperlipidemia, diabetes, coronary artery disease, or peripheral arterial disease, were recruited between September 2015 and May 2016. The Montreal Cognitive Assessment (MoCA) and the Beck Depression Inventory-II were used to screen for cognitive impairment and depression. Patients with MoCA scores <26 were referred for imaging studies, memory loss serology, neuropsychiatric testing and clinical assessment by a memory loss physician. Final cognitive status was assigned by blinded adjudication. Results: We recruited 60 Native Americans aged 50-86 (mean±SD: 64±7.1 years); 90% were male, 95% had at least high-school education, and 69% had some college or advanced degrees. Risk factors included hypertension (92%), hyperlipidemia (88%), diabetes (47%), and prior/current smoking (78%). Eight (13%) with severe depression were excluded, leaving 23/51 with abnormal MoCA scores (44%, 95%CI 30%-59%). All with cognitive impairment were male compared to 83% among non-impaired subjects (p=0.059). Fifteen completed additional evaluation for memory loss, including 4/15 with normal MoCA scores who requested evaluation based on symptoms. Results were adjudicated as normal (4), or as having non-amnestic MCI (4), vascular MCI (5), and vascular dementia (2). MoCA correctly identified cognitive status in 86% (Kappa 0.66, 95%CI 0.23-1.00). Conclusions: Native American veterans have high rates of vascular cognitive impairment, which exceed rates of cognitive impairment documented in previously published older non-Native American cohorts. These results highlight the need for improved vascular risk reduction among Native American veterans. Further study is needed to identify ways to improve care in this underserved and understudied population.

Background: Coated-platelets, a subset of activated platelets observed with dual-agonist stimulation with collagen and thrombin, represent 30% of the platelet population in normal controls. In recently published work, we have shown that elevated coated-platelet levels (>45%) are predictive of stroke in asymptomatic carotid stenosis. We now investigate if platelet count and mean platelet volume (MPV) are related to coated-platelet levels. Methods: Coated-platelet levels were measured in a cohort of asymptomatic outpatients referred for carotid ultrasound studies. Platelet count and mean platelet volume for each subject were recorded from the VA electronic medical record at the closest possible time period (within ≤6 months) to the date of coated-platelet sample. Correlations between each parameter and coated-platelet levels were determined and those reaching significance at p≤0.1 were included in a multiple regression model with LDL and systolic blood pressure (SBP), variables previously known to correlate with coated-platelet levels. Results: Platelet count and mean platelet volume data were available within the specified period for 289 patients (96% male, mean age 66 years). On univariate analysis, coated-platelet levels correlated with platelet count (r = 0.15, p=0.01), but not with MPV (r=-0.04, p=0.53). When platelet count was included in a multiple regression analysis with LDL and SBP, platelet count was no longer significantly associated with coated-platelet levels. In the final model, higher coated-platelet levels were associated with LDL (p=0.008) and SBP (p=0.007) after controlling for all potentially confounding variables, including medications and comorbidities. Conclusions: Among asymptomatic patients with carotid atherosclerosis, neither MPV, which has been previously shown to correlate with platelet aggregation, nor platelet count are significantly associated with coated-platelet levels after accounting for all potential confounding variables. These findings support the notion of coated-platelets as a unique measure of platelet procoagulant potential.