Arterial Stiffness Assessed by Cardio-Ankle Vascular Index

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.

Keywords: arterial stiffness; cardio-ankle vascular index; endothelial dysfunction; heart failure.

Figure 1

Mechanism of arterial stiffness in each layer of arterial wall. The compound and structural changes caused by mechanical wall stress contribute to arterial stiffness. Additionally, endothelial dysfunction cause vasoconstriction and is a functional cause of arterial stiffness. Oxidative stress, inflammation, and traditional cardiovascular risk factors accelerate the progression. eNOS: endothelial nitric oxide synthesis, L-ADMA: L-asymmetric dimethylarginine, SIRT-1: Sirtuin-1, BH: tetrahydrobiopterin, MMP: matrix-metalloproteinases, AGE: advanced glycation end product.

Figure 2

Principle of stiffness parameter β. Stiffness parameter β represents arterial distensibility, which is derived from the measurements of diameters in one section. This index was originally used for cervical and carotid arteries. Ps: systolic blood pressure, Pd: diastolic blood pressure, D: diameter of the artery, ΔD: change in diameter.

Figure 3

Principles of the cardio-ankle vascular index (CAVI). CAVI is an index derived from arterial intraluminal volumetric change by combining stiffness parameter β and Bramwell-Hill formula. Heart-ankle pulse wave velocity (haPWV) is obtained by dividing L (the length from the aorta to the ankle) by T (the time for the pulse wave to propagate from the aortic valve to the ankle). CAVI: cardio-ankle vascular index, haPWV: heart-ankle pulse wave velocity, Ps: systolic blood pressure, Pd: diastolic blood pressure, ΔP is pulse pressure (Ps-Pd), ρ: blood density of 1.05 g/mL. a and b are constants.