Increased procoagulant platelet levels are predictive of death in COVID-19.

Prior research has identified abnormal platelet procoagulant responses in COVID-19. Coated-platelets, a form of procoagulant platelets, support thrombin formation and are elevated in ischemic stroke patients with increased risk for recurrent infarction. Our goal was to examine changes in coated-platelet levels over the course of COVID-19 infection and determine their association with disease severity, thrombosis, and death. Coated-platelet levels were assayed after admission and repeated weekly in COVID-19 patients, and in COVID-19 negative controls. Receiver operator characteristic (ROC) analysis was used to calculate area under the curve (AUC) values for a model including baseline coated-platelets to predict death. Kaplan-Meier and Cox proportional hazards analysis was used to predict risk for death at 90 days. We enrolled 33 patients (22 with moderate and 11 with severe infection) and 20 controls. Baseline coated-platelet levels were lower among moderate (mean ± SD; 21.3 ± 9.8%) and severe COVID-19 patients (28.5 ± 11.9%) compared to controls (38.1 ± 10.4%, p < 0.0001). Coated-platelet levels increased during follow-up in COVID-19 patients by 7% (relative) per day from symptom onset (95% CI 2-12%, p = 0.007). A cut-off of 33.9% for coated-platelet levels yielded 80% sensitivity and 96% specificity for death at 90 days, with resulting AUC of 0.880 (95% CI 0.680-1.0, p = 0.0002). The adjusted hazard ratio for death in patients with coated-platelet levels > 33.9% was 40.99 when compared to those with levels ≤ 33.9% (p < 0.0001). Platelet procoagulant potential is transiently decreased in most patients during COVID-19; however, increased baseline platelet procoagulant levels predict death. Defining the mechanisms involved and potential links with aging may yield novel treatment targets.

High rates of undiagnosed vascular cognitive impairment among American Indian veterans.

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), non-amnestic 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.

Cognitive impairment is associated with medication nonadherence in asymptomatic carotid stenosis.

OBJECTIVE: Adherence to medical management of vascular risk is vital for stroke prevention in patients with asymptomatic carotid stenosis. Because carotid disease is a risk factor for cognitive impairment, we sought to determine whether undiagnosed cognitive impairment affects medication adherence in this setting. METHODS: Sixty patients with asymptomatic ≥50% internal carotid artery stenosis without known dementia or stroke were screened for evidence of cognitive impairment using the Montreal Cognitive Assessment. Medication adherence was monitored using electronic pharmacy prescription refills. Medications studied included antiplatelet agents, statins, antihypertensives, and diabetes medications. Nonadherence was defined as a refill lag of ≥3 months during the 12 months before cognitive screening. RESULTS: Sixty percent of patients (36/60) had evidence of cognitive impairment (Montreal Cognitive Assessment <26). Medication adherence was noted in 31% (11/36) of cognitively impaired patients and 88% (21/24) of patients without cognitive impairment (P < .0001). Antiplatelet therapy adherence was significantly lower among cognitively impaired patients compared with those without cognitive impairment (P = .009). A trend toward decreased adherence to statins (P = .09) and antihypertensives (P = .06) was observed. CONCLUSIONS: Medication adherence in patients with asymptomatic carotid stenosis is significantly reduced among those with undiagnosed cognitive impairment. Cognitive screening of asymptomatic patients with carotid stenosis identifies those who may benefit from increased supervision to improve medication adherence.

Reduced high-density lipoprotein level is linked to worse ankle brachial index and peak oxygen uptake in postmenopausal women with peripheral arterial disease.

Women with peripheral arterial disease (PAD) have more limited physical function than men but the mechanisms involved are not clear. We determined whether alterations in lipid components, such as decreased high-density lipoprotein cholesterol (HDL-C), are associated with worsening intermittent claudication (IC) in postmenopausal women with PAD. Our cross-sectional cohort study included 69 postmenopausal women with IC (Fontaine stage II). A treadmill test was used to measure initial claudication distance (ICD), absolute claudication distance (ACD), peak oxygen uptake, and ankle systolic blood pressure. High-density lipoprotein cholesterol correlated with ankle brachial index ([ABI]; R = .29, P = .019). No other lipid profile components were associated with exercise performance and hemodynamic measures. Among women with HDL-C <50 mg/dL (n = 43), the median peak oxygen uptake level was significantly lower (P = .021) relative to women with normal HDL-C >50 mg/dL (n = 26). Lower HDL-C levels are associated with worse ABI and decreased peak oxygen uptake in postmenopausal women with PAD.