Arterial stiffness occurs as a consequence of biological aging, arteriosclerosis and genetic disorders, such as Marfan, Williams, and Ehlers-Danlos syndromes.
[6] Degenerative changes that occur with age in the walls of large elastic arteries are thought to contribute to increased stiffening over time, including the disruption of lamellar elastin structures within the wall, possibly due to repeated cycles of mechanical stress; inflammation;[7] changes in arterial collagen proteins, partially as a compensatory mechanism against the loss of arterial elastin and partially due to fibrosis; and crosslinking of adjacent collagen fibers by advanced glycation endproducts (AGEs).
Increased aortic PWV has been shown to predict cardiovascular, and in some cases all-cause, mortality in individuals with end stage kidney disease,[15] hypertension,[16] diabetes mellitus[17] and in the general population.
Devices are on the market that measure arterial stiffness parameters (augmentation index, pulse wave velocity).
These include Complior, CVProfilor, PeriScope, Hanbyul Meditech, Mobil-O-Graph NG, BP Plus (Pulsecor), PulsePen, BPLab Vasotens, Arteriograph, Vascular Explorer, and SphygmoCor.
[23][24] This effect may be exaggerated if the increase in arterial stiffness results in reduced wave reflection and more propagation of the pulsatile pressure into the microcirculation.
The speed of propagation (i.e. PWV[10]) is increased in stiffer arteries and consequently reflected waves will arrive at the heart earlier in systole.