Arterial wall stiffness is a highly relevant phenotype for cardiovascular medicine. Large artery stiffening is a key element in the pathogenesis of isolated systolic hypertension, a condition mainly affecting older adults, which is responsible for a high burden of cardiovascular disease worldwide. Arterial stiffening impairs the ability of conduit arteries to accommodate the stroke volume intermittently delivered by the left ventricle during systole, thus increasing the pulsatile hydraulic load impeding left ventricular ejection. There is increasing recognition of the adverse influence of increased pulsatile arterial load in conditions such as heart failure with preserved ejection fraction, heart failure with reduced ejection fraction, hypertensive heart disease, and valvular heart disease (particularly aortic stenosis). In addition, given the effect of arterial stiffness on pulsatile hemodynamics, increased large artery stiffness can also promote excessive penetration of pressure and flow pulsatility into the kidney and the brain, leading to target organ damage.

Arterial stiffness is affected by various risk factors and biologic processes that lead to cardiovascular disease. Arterial stiffness increases with aging and various disease states, such as hypertension, diabetes mellitus, obesity, smoking, hypercholesterolemia, subclinical inflammation, and kidney disease. Various long-term exposures lead to an accelerated stiffening of large arteries with aging over a period of decades. Therefore, measurements of arterial stiffness not only provide information about the effects of prevalent conditions but also reflect the cumulative history of exposure to risk factors over a period of decades, much like hemoglobin A _1c levels reflect the cumulative exposure to hyperglycemia over a period of months. Unlike hemoglobin A _1c , however, arterial stiffness is not only a “marker” of upstream abnormalities but also a causal mediator of various forms of cardiovascular disease. Not surprisingly, available studies demonstrate that carotid-femoral pulse-wave velocity (PWV), an index of large artery stiffness, independently predicts the risk for incident cardiovascular events in both clinical and community-based cohorts.

A precise in vivo characterization of the material properties of the arterial wall is not possible at present. However, arterial wall stiffness can be inferred or approximated using several indices derived from in vivo measurements of cyclic changes in pressure, diameter, and wall thickness at a given arterial location. These approaches yield intuitive metrics, such as cross-sectional compliance or distensibility coefficients. However, surface ultrasound can provide precise measurements of cyclic geometric changes only in superficial arteries, while ultrasound assessments of such changes in deeper, large arteries (such as the aorta), have limited accuracy. Furthermore, the estimation of arterial compliance or distensibility from cyclic arterial geometric changes also requires local arterial pulse pressure measurements. Unfortunately, differences in pulsatile pressure profiles along the arterial tree lead to systematic and variable bias in measurements of large artery distensibility or compliance, when only standard brachial blood pressure measurements are used.

Measurements of arterial PWV, in contrast, do not require knowledge of local pressure-volume, pressure-diameter, or pressure-strain relationships. PWV is a functional parameter affected by the stiffness of the arterial wall. The propagation velocity of a pulse wave in an elastic tube can be described by the Bramwell-Hill equation, which relates PWV to the inverse of the cross-sectional distensibility coefficient (which is the fractional area change divided by the pressure change):

Stay updated, free articles. Join our Telegram channel

Join