Department of Cardiology, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan.
Department of Intensive Care Medicine2, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan.
Int J Mol Sci. 2019 Jul 26;20(15):3664. doi: 10.3390/ijms20153664.
Arterial stiffness is an age-related disorder. In the medial layer of arteries, mechanical fracture due to fatigue failure for the pulsatile wall strain causes medial degeneration vascular remodeling. The alteration of extracellular matrix composition and arterial geometry result in structural arterial stiffness. Calcium deposition and other factors such as advanced glycation end product-mediated collagen cross-linking aggravate the structural arterial stiffness. On the other hand, endothelial dysfunction is a cause of arterial stiffness. The biological molecular mechanisms relating to aging are known to involve the progression of arterial stiffness. Arterial stiffness further applies stress on large arteries and also microcirculation. Therefore, it is closely related to adverse outcomes in cardiovascular and cerebrovascular system. Cardio-ankle vascular index (CAVI) is a promising diagnostic tool for evaluating arterial stiffness. The principle is based on stiffness parameter β, which is an index intended to assess the distensibility of carotid artery. Stiffness parameter β is a two-dimensional technique obtained from changes of arterial diameter by pulse in one section. CAVI applied the stiffness parameter β to all of the arterial segments between heart and ankle using pulse wave velocity. CAVI has been commercially available for a decade and the clinical data of its effectiveness has accumulated. The characteristics of CAVI differ from other physiological tests of arterial stiffness due to the independency from blood pressure at the time of examination. This review describes the pathophysiology of arterial stiffness and CAVI. Molecular mechanisms will also be covered.
动脉僵硬度是一种与年龄相关的疾病。在动脉的中膜层,由于脉动壁应变引起的疲劳失效导致机械断裂,从而引起中膜退化和血管重塑。细胞外基质组成和动脉几何形状的改变导致结构动脉僵硬度。钙沉积和其他因素,如晚期糖基化终产物介导的胶原交联,加重了结构动脉僵硬度。另一方面,内皮功能障碍是动脉僵硬度的一个原因。与衰老相关的生物学分子机制被认为涉及动脉僵硬度的进展。动脉僵硬度进一步对大动脉和微循环施加压力。因此,它与心血管和脑血管系统的不良后果密切相关。心血管-踝部血管指数(CAVI)是一种评估动脉僵硬度的有前途的诊断工具。其原理基于僵硬度参数β,该参数β是评估颈动脉可扩张性的指标。僵硬度参数β是通过脉搏在一个节段内改变动脉直径获得的二维技术。CAVI 将僵硬度参数β应用于心脏和脚踝之间所有动脉节段的脉搏波速度。CAVI 已经商业化了十年,其有效性的临床数据已经积累。由于检查时不受血压的影响,CAVI 的特点与其他动脉僵硬度的生理测试不同。这篇综述描述了动脉僵硬度和 CAVI 的病理生理学。还将涵盖分子机制。