From the Department of Medicine (C.W.T.), Cardiovascular Division, Beth Israel Deaconess Medical Center, Boston; Departments of Neurology (S.S., A.S.B., A.J.W., R.A., J.J.H., P.A.W.), Medicine (N.M.H., J.A.V., D.L., E.J.B., R.S.V.), and Biostatistics (A.S.B., J.J.H., M.G.L.), School of Public Health, School of Medicine and the Department of Mathematics (M.G.L.), Boston University, MA; Department of Neurology (C.D.), Center for Neuroscience and Division of Biostatistics, Department of Public Health Sciences, School of Medicine, University of California, Davis; National Heart Lung and Blood Institute (D.L.), NHLBI's Framingham Heart Study (C.W.T., S.S., A.S.B., R.A., D.L., M.G.L., E.J.B., P.A.W., R.S.V.), Framingham; and Cardiovascular Engineering Inc. (G.F.M.), Norwood, MA.
Neurology. 2013 Sep 10;81(11):984-91. doi: 10.1212/WNL.0b013e3182a43e1c. Epub 2013 Aug 9.
To determine the association of arterial stiffness and pressure pulsatility, which can damage small vessels in the brain, with vascular and Alzheimer-type brain aging.
Stroke- and dementia-free Framingham Offspring Study participants (n = 1,587, 61 ± 9 years, 45% male) underwent study of tonometric arterial stiffness and endothelial function (1998-2001) and brain MRI and cognition (1999-2002). We related carotid-femoral pulse wave velocity (CFPWV), mean arterial and central pulse pressure, and endothelial function to vascular brain aging by MRI (total cerebral brain volume [TCBV], white matter hyperintensity volume, silent cerebral infarcts) and vascular and Alzheimer-type cognitive aging (Trails B minus Trails A and logical memory-delayed recall, respectively).
Higher CFPWV was associated with lower TCBV, greater white matter hyperintensity volume, and greater prevalence of silent cerebral infarcts (all p < 0.05). Each SD greater CFPWV was associated with lower TCBV equivalent to 1.2 years of brain aging. Mean arterial and central pulse pressure were associated with greater white matter hyperintensity volume (p = 0.005) and lower TCBV (p = 0.02), respectively, and worse verbal memory (both p < 0.05). Associations of tonometry variables with TCBV and white matter hyperintensity volume were stronger among those aged 65 years and older vs those younger than 65 years (p < 0.10 for interaction). Brachial artery endothelial function was unrelated to MRI measures (all p > 0.05).
Greater arterial stiffness and pressure pulsatility are associated with brain aging, MRI vascular insults, and memory deficits typically seen in Alzheimer dementia. Future investigations are warranted to evaluate the potential impact of prevention and treatment of unfavorable arterial hemodynamics on neurocognitive outcomes.
确定动脉僵硬和压力脉动的相关性,这可能会损害大脑中的小血管,与血管和阿尔茨海默病型脑老化有关。
无中风和痴呆的弗雷明汉后代研究参与者(n=1587,61±9 岁,45%为男性)接受了血压计动脉僵硬和内皮功能研究(1998-2001 年)以及脑 MRI 和认知研究(1999-2002 年)。我们将颈股脉搏波速度(CFPWV)、平均动脉压和中心脉压以及内皮功能与脑 MRI 相关联,以评估血管性脑老化(总脑容量[TCBV]、脑白质高信号容积、无症状性脑梗死)和血管性及阿尔茨海默病型认知老化(Trails B 减去 Trails A 和逻辑记忆延迟回忆)。
较高的 CFPWV 与 TCBV 较低、脑白质高信号容积较大以及无症状性脑梗死发生率较高相关(均 p<0.05)。每增加一个标准差的 CFPWV 与 TCBV 降低 1.2 年的脑老化相当。平均动脉压和中心脉压与脑白质高信号容积较大(p=0.005)和 TCBV 较低(p=0.02)相关,与言语记忆较差相关(均 p<0.05)。在年龄在 65 岁及以上的参与者中,与在年龄小于 65 岁的参与者中,血压计变量与 TCBV 和脑白质高信号容积的相关性更强(交互作用的 p<0.10)。肱动脉内皮功能与 MRI 测量无关(均 p>0.05)。
动脉僵硬和压力脉动增加与脑老化、MRI 血管损伤以及阿尔茨海默病痴呆中常见的记忆缺陷相关。有必要进行进一步的研究,以评估不利的动脉血流动力学对神经认知结果的潜在影响。