Abstract
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.
Highlights
Arterial stiffness increases with age [1]
Cardio-ankle vascular index (CAVI) improves the dependency of measurement value on blood pressure (BP) at measurement, which exists in brachial-ankle pulse wave velocity
CAVI is closely related to left ventricular (LV) systolic and diastolic function measured by echocardiography, whereas central blood pressure (CBP) is more associated with LV hypertrophy
Summary
Arterial stiffness increases with age [1]. Arterial stiffness augments pulse wave reflection by increasing peripheral arterial resistance and central arterial wall stiffness. Arterial stiffness increases cardiac afterload, which can cause left ventricular hypertrophy, diastolic dysfunction, and heart failure even though systolic function is preserved. Inhibition, or slowdown, of the progression of arterial stiffness is an ideal way to prevent cardiovascular disease (CVD) and heart failure. For this purpose, appropriate evaluation for arterial stiffness is necessary. Cardio-ankle vascular index (CAVI) as an index of arterial stiffness was first proposed in 2006 [2]. CAVI improves the dependency of measurement value on blood pressure (BP) at measurement, which exists in brachial-ankle pulse wave velocity (baPWV). J.cMlionl.iSccai.l2p01r9a, 2c0t,icxeF.OTR hPEisERreRvEiVeIwEWaims to summarize the pathophysiology of arterial sti2ffonfe1s8s and the fuenvadlaumateedntianlcslionficCaAl pVrIa.cWticee.bTehliiesvreevaieswsesasiminsgtothseumremlaatiroiznesthhieppsabthetowpheyensioCloAgVyIo, fbairotmeraiarlksetirfsf,naesnsd clinical praongdntohseisfuonfdhaemaernt tfaalisluorfeCwAVillI.leWaedbteoliaevbeetatsesresusnindgetrhsetarnedlaitniognoshfiaprstebreitawl esetniffCnAesVsI., biomarkers, and clinical prognosis of heart failure will lead to a better understanding of arterial stiffness
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