1 Department of Epidemiology Gillings School of Global Public Health University of North Carolina at Chapel Hill NC.
2 Department of Epidemiology Johns Hopkins University Baltimore MD.
J Am Heart Assoc. 2019 Jan 22;8(2):e011045. doi: 10.1161/JAHA.118.011045.
Background Central arterial stiffening and increased pulsatility, with consequent cerebral hypoperfusion, may result in structural brain damage and cognitive impairment. Methods and Results We analyzed a cross-sectional sample of ARIC - NCS (Atherosclerosis Risk in Communities-Neurocognitive Study) participants (aged 67-90 years, 60% women) with measures of cognition (n=3703) and brain magnetic resonance imaging (n=1255). Central arterial hemodynamics were assessed as carotid-femoral pulse wave velocity and pressure pulsatility (central pulse pressure). We derived factor scores for cognitive domains. Brain magnetic resonance imaging using 3-Tesla scanners quantified lacunar infarcts; cerebral microbleeds; and volumes of white matter hyperintensities, total brain, and the Alzheimer disease signature region. We used logistic regression, adjusted for demographics, apolipoprotein E ɛ4, heart rate, mean arterial pressure, and select cardiovascular risk factors, to estimate the odds of lacunar infarcts or cerebral microbleeds. Linear regression, additionally adjusted for intracranial volume, estimated the difference in log-transformed volumes of white matter hyperintensities , total brain, and the Alzheimer disease signature region. We estimated the mean difference in cognitive factor scores across quartiles of carotid-femoral pulse wave velocity or central pulse pressure using linear regression. Compared with participants in the lowest carotid-femoral pulse wave velocity quartile, participants in the highest quartile of carotid-femoral pulse wave velocity had a greater burden of white matter hyperintensities ( P=0.007 for trend), smaller total brain volumes (-18.30 cm; 95% CI , -27.54 to -9.07 cm), and smaller Alzheimer disease signature region volumes (-1.48 cm; 95% CI , -2.27 to -0.68 cm). These participants also had lower scores in executive function/processing speed (β=-0.04 z score; 95% CI , -0.07 to -0.01 z score) and general cognition (β=-0.09 z score; 95% CI , -0.15 to -0.03 z score). Similar results were observed for central pulse pressure . Conclusions Central arterial hemodynamics were associated with structural brain damage and poorer cognitive performance among older adults.
中央动脉僵硬和脉动性增加,继而导致脑灌注不足,可能导致结构脑损伤和认知障碍。
我们分析了 ARIC-NCS(社区动脉粥样硬化风险研究-神经认知研究)参与者的一个横断面样本(年龄 67-90 岁,60%为女性),这些参与者的认知测量值(n=3703)和脑磁共振成像(n=1255)。中央动脉血液动力学评估为颈动脉-股动脉脉搏波速度和压力脉动性(中心脉搏压)。我们为认知域推导了因子得分。使用 3-Tesla 扫描仪进行脑磁共振成像,定量腔隙性梗死;脑微出血;以及白质高信号、总脑和阿尔茨海默病特征区域的体积。我们使用逻辑回归,调整了人口统计学、载脂蛋白 E ɛ4、心率、平均动脉压和一些心血管危险因素,以估计腔隙性梗死或脑微出血的比值比。线性回归,另外调整了颅内体积,估计白质高信号、总脑和阿尔茨海默病特征区域的对数转换体积差异。我们使用线性回归,根据颈动脉-股动脉脉搏波速度或中心脉搏压的四分位数,估计认知因子得分的平均差异。与颈动脉-股动脉脉搏波速度最低四分位的参与者相比,颈动脉-股动脉脉搏波速度最高四分位的参与者白质高信号负担更大(趋势 P=0.007),总脑体积更小(-18.30cm;95%CI,-27.54 至-9.07cm),阿尔茨海默病特征区域体积更小(-1.48cm;95%CI,-2.27 至-0.68cm)。这些参与者的执行功能/处理速度评分也较低(β=-0.04 标准分;95%CI,-0.07 至-0.01 标准分)和一般认知评分(β=-0.09 标准分;95%CI,-0.15 至-0.03 标准分)。对于中心脉搏压也观察到类似的结果。
中央动脉血液动力学与老年人的结构脑损伤和认知功能下降有关。