GeroScience ( IF 5.3 ) Pub Date : 2024-06-20 , DOI: 10.1007/s11357-024-01254-5 Matthew K Armstrong 1 , Shivangi Jain 2 , Virginia Nuckols 3 , Ryan Pewowaruk 4 , Xinyu Zhang 5 , Lyndsey DuBose 6 , Matthew Sodoma 2 , Bryan Madero 2 , Michelle W Voss 2 , Gary L Pierce 1, 7
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Large central arterial stiffness is a risk factor for cerebrovascular damage and subsequent progression of neurodegenerative diseases, including Alzheimer’s disease and dementia. However, arterial stiffness is determined by both the intrinsic components of the arterial wall (structural stiffness) and the load (i.e., arterial blood pressure) exerted upon it by the blood (load-dependent stiffness). This study aimed to determine the degree to which structural and/or load-dependent mechanisms of central arterial stiffness are associated with cerebrovascular damage. Among 128 healthy individuals (aged 63±6, age range: 50-80 years, 42% men), aortic and carotid artery stiffness was measured via carotid-femoral pulse wave velocity and B-mode ultrasonography, respectively. Using participant-specific exponential models, both aortic and carotid artery stiffness were standardized to a reference blood pressure to separate their structural and load-dependent stiffness mechanisms. Magnetic resonance imaging was used to derive total, periventricular, and deep cerebral white matter lesion volume (WMLV) and global cortical thickness. After adjusting for common cardiovascular disease risk factors, a 1 m/s increase in structural aortic stiffness was associated with 15% greater total WMLV (95% confidence interval [CI] = 0.01, 0.27, P = 0.036), 14% greater periventricular WMLV (95%CI = 0.004, 0.25, P = 0.044) and 0.011mm lower cortical thickness (95%CI = -0.022, -1.18, P = 0.028). No association was observed between structural carotid stiffness and WMLVs (total, periventricular, and deep), and neither aortic nor carotid load-dependent stiffness was associated with WMLVs or cortical thickness. Structural, not load-dependent, mechanisms of aortic stiffness are related to cerebrovascular-related white matter damage.
中文翻译:
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结构性与负载依赖性大动脉僵硬度机制与人类脑血管损伤和皮质萎缩的关联
中央动脉僵硬度大是脑血管损伤和神经退行性疾病(包括阿尔茨海默病和痴呆症)后续进展的危险因素。然而,动脉硬度是由动脉壁的固有成分(结构硬度)和血液施加在其上的负荷(即动脉血压)(负荷相关的硬度)决定的。本研究旨在确定中央动脉僵硬度的结构和/或负载依赖性机制与脑血管损伤的相关程度。在 128 名健康个体(年龄 63±6 岁,年龄范围:50-80 岁,42% 男性)中,分别通过颈动脉-股动脉脉搏波速度和 B 型超声检查测量主动脉和颈动脉僵硬度。使用特定于参与者的指数模型,将主动脉和颈动脉硬度标准化为参考血压,以区分其结构性硬度和负载依赖性硬度机制。使用磁共振成像来获得总的、脑室周围的和深部的大脑白质病变体积(WMLV)和整体皮质厚度。调整常见心血管疾病危险因素后,结构性主动脉硬度增加 1 m/s 与总 WMLV 增加 15% 相关(95% 置信区间 [CI] = 0.01, 0.27, P = 0.036),心室周围 WMLV 增加 14% (95%CI = 0.004, 0.25, P = 0.044),皮质厚度降低 0.011mm (95%CI = -0.022, -1.18, P = 0.028)。未观察到结构性颈动脉硬度与 WMLV(总、心室周围和深部)之间存在关联,并且主动脉或颈动脉负荷依赖性硬度均与 WMLV 或皮质厚度无关。 主动脉僵硬度的结构性而非负荷依赖性机制与脑血管相关的白质损伤有关。