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African Americans have one of the highest prevalence of hypertension in the United States. Impaired endothelial function has been implicated in the pathophysiology of hypertension in this group. We previously reported that brachial artery diameter increases from 3.9±0.14 to 4.1± 0.14 at 4 hours after ingestion of a high fat meal, suggesting vasodilation of conduit arteries. Considering that oral fat ingestion stimulates the release of gastrointestinal peptides with vasoactive properties, we aimed to isolate the vascular effect of fat on conduit artery and microvasculature by inducing an acute elevation of triglycerides and free fatty acids with an infusion of 20% intralipid® and heparin. To assess endothelial function we measured changes in the diameter of the brachial artery to hyperemia with a continuous edge detection and wall tracking software. Effect on microvasculature was obtained with contrast-enhanced ultrasonography (CEU) of the brachioradialis muscle with lipid-perflutren microbubbles infusion. We studied 14 obese healthy African American women, age 39± 10, BMI 38.7± 3.4 kg/m. 2 Triglycerides increased from 60.7±30.5 to 523.3±231 mg/dL at the end of the 4 h infusion. Brachial artery diameters were 3.6±0.16 and 3.9±0.18 mm at baseline, and 4-h, P=0.109, respectively. Flow mediated dilation improved at the end of the 4-h infusion period (4.3±0.95 to 6.2±1.21%, P=0.016), figure . Microvascular blood volume did not change with the intervention 5.8±4.9 vs. 5.9±3.6, P=0.55. In conclusion, IV acute hyperlipidemia did not increase brachial artery diameter nor microvascular circulation, however it potentiates vascular reactivity in conduit arteries.

Vascular health factors frequently co-occur with Alzheimer's disease (AD). A better understanding of how systemic vascular and cerebrovascular health intersects with clinical and pathological AD may inform prevention and treatment opportunities.To establish the Vanderbilt Memory & Aging Project, a case-control longitudinal study investigating vascular health and brain aging, and describe baseline methodology and participant characteristics.From September 2012 to November 2014, 335 participants age 60- 92 were enrolled, including 168 individuals with mild cognitive impairment (MCI, 73±8 years, 41% female) and 167 age-, sex-, and race-matched cognitively normal controls (NC, 72±7 years, 41% female). At baseline, participants completed a physical and frailty examination, fasting blood draw, neuropsychological assessment, echocardiogram, cardiac MRI, and brain MRI. A subset underwent 24-hour ambulatory blood pressure monitoring and lumbar puncture for cerebrospinal fluid (CSF) collection.As designed, participant groups were comparable for age (p = 0.31), sex (p = 0.95), and race (p = 0.65). MCI participants had greater Framingham Stroke Risk Profile scores (p = 0.008), systolic blood pressure values (p = 0.008), and history of left ventricular hypertrophy (p = 0.04) than NC participants. As expected, MCI participants performed worse on all neuropsychological measures (p-values < 0.001), were more likely to be APOEɛ4 carriers (p = 0.02), and had enhanced CSF biomarkers, including lower Aβ42 (p = 0.02), higher total tau (p = 0.004), and higher p-tau (p = 0.02) compared to NC participants.Diverse sources of baseline and longitudinal data will provide rich opportunities to investigate pathways linking vascular and cerebrovascular health, clinical and pathological AD, and neurodegeneration contributing to novel strategies to delay or prevent cognitive decline.

Background Flow‐mediated dilation ( FMD ) is used to assess endothelial function through changes in vascular diameter after hyperemia. High‐fat meal ( HFM ) has been shown to induce endothelial dysfunction; recent studies, however, reported conflicting results in obese African American women ( AAW ). Differences in the method used to analyze FMD may explain these discrepancies. Methods and Results In protocol 1, we assessed the time course of FMD and compared the repeatability of FMD using the individual maximum peak dilation ( FMD peak ) and the dilation at 60 seconds ( FMD 60 ). Sixteen AAW (age, 42±10.4 years; body mass index [ BMI], 39±5.8 kg/m 2 ) were studied on 2 occasions, 4 weeks apart, under fasting conditions (study 1 and study 2). In protocol 2, we used the most repeatable measurement from protocol 1 to assess changes in endothelial function after an HFM in 17 AAW (agen 42±11.1 years; BMIn 38±5.6 kg/m 2 ). We found that FMD peak was the most repeatable measurement (N=16; study 1, 5.31±3.12% and study 2, 5.80±2.91%; r =0.94). After an HFM , the baseline brachial artery diameter significantly increased at 2 hours (0.10 mm; 95% confidence interval [ CI ], 0.01–0.18; P =0.03) and at 4 hours (0.17 mm; 95% CI , 0.09–0.25; P FMD peak decreased compared with pre‐ HFM (−1.76; 95% CI , −3.55–0.02; P≤ 0.05). Conclusions The individual's maximum peak dilation after hyperemia is the most consistent measure to assess the effect of an HFM on endothelial function. Endothelial dysfunction occurred at 2 hours after an HFM in AAW . Clinical Trial Registration URL : https://clinicaltrials.gov/ Unique identifiers: NCT 01334554 and NCT 02126735.