Arterial Stiffness and Wave Reflection: Biomarkers of Cardiovascular Risk

Abstract

Arterial stiffness and excessive pressure pulsatility have emerged as important risk factors for cardiovascular disease. Arterial stiffness increases with age and in the presence of traditional cardiovascular disease risk factors, such as hypertension, diabetes and lipid disorders. Pathologic stiffening of large arteries with advancing age and risk factor exposure predominantly involves the elastic aorta and carotid arteries, whereas stiffness changes are relatively limited in muscular arteries. Aortic stiffening is associated with increased pulse wave velocity and pulse pressure, which are related but distinct measures of the pulsatile energy content of the pressure waveform. A dramatic increase in pulsatile energy content of pressure and flow waves in the arterial system places considerable pulsatile stress on the heart, large arteries and distal circulation. Large artery stiffening is associated with abnormalities in microvascular structure and function that may contribute to tissue damage, particularly in susceptible high flow organs such as the brain and kidneys. This brief review summarizes results of recent research on risk factors for and adverse effects of large artery stiffening.

Figure 1

Measurement of PWV. Transit time, ΔT, between the foot of the carotid (red waveform) and femoral waveforms is measured with a tonometer. Carotid-femoral transit distance (CFTD) is estimated by measuring the distance from the suprasternal notch (SSN, ) to the carotid (SSN-C) and femoral (SSN-F) sites and taking the difference to account for parallel transmission along the brachiocephalic and carotid arteries and around the aortic arch (red shading). This corrected distance is divided by transit time delay to give PWV. Note that carotid-femoral PWV fails to assess stiffness of the proximal aorta (red shading). (Reproduced from (62).)

Figure 2

Potential effects of alterations in aortic diameter on pulsatile hemodynamics. PWV increases monotonically during the full lifespan, whereas characteristic impedance (Z_c) falls slightly during early adulthood and then increases to high levels in older people. Changes in aortic diameter may mediate these disparate relations between PWV and Z_c. The solid line in the aortic diameter plot approximates the known change in aortic diameter with advancing age. A rapid increase in aortic diameter prior to 60 years of age may account for the reduction in Z_c even as PWV increases. The broken line in the diameter plot represents a hypothetical aortic diameter trajectory that would produce the accelerated rise in Z_c shown with a broken line in the Z_c plot. Thus, attenuation of an age-related increase in aortic diameter could manifest as increased Z_c and pulse pressure in older individuals, giving rise to the inverse relation between pulse pressure and aortic diameter. Eh, elastance-wall thickness product.