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Arterial stiffness
Arterial stiffness occurs as a consequence of biological aging and arteriosclerosis. Increased arterial stiffness is associated with an increased risk of cardiovascular events such as myocardial infarction and stroke, the two leading causes of death in the developed world. The World Health Organisation predicts that in 2010, cardiovascular disease will also be the leading killer in the developing world and represents a major global health problem.
Several degenerative changes that occur with age in the walls of large elastic arteries are thought to contribute to increased stiffening over time, including the mechanical fraying of lamellar elastin structures within the wall due to repeated cycles of mechanical stress; changes in the kind and increases in content of 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).
==Background==
The arteries were once considered by the ancient Greeks as inert conduits within which air flowed; William Harvey is generally credited with being the first to describe the circulation of the blood through them. When the heart contracts it generates a pulse or energy wave that travels through the circulatory system. The speed of travel of this pulse wave (pulse wave velocity or PWV) is related to the stiffness of the arteries. Other terms that are used to described the mechanical properties of arteries include elastance, or the reciprocal (inverse) of elastance, compliance. The relationship between arterial stiffness and pulse wave velocity was first predicted by Thomas Young in his Croonian Lecture of 1808 〔(Young T: On the function of the heart and arteries: The Croonian lecture ). Phil Trans Roy Soc 1809;99:l-31〕 but is generally described by the Moens–Korteweg equation〔Nichols WW, O'Rourke MF. Vascular impedance. In: McDonald's Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. 4th ed. London, UK: Edward Arnold; 1998:54–97, 243–283, 347–395.〕 or the Bramwell–Hill equation. Typical values of PWV in the aorta range from approximately 5 m/s to >15 m/s.
Measurement of aortic PWV provides some of the strongest evidence concerning the prognostic significance of large artery stiffening. Increased aortic PWV has been shown to predict cardiovascular, and in some cases all cause, mortality in individuals with end stage renal failure,〔Blacher et al.,Circulation. 1999; 99: 2434–2439〕 hypertension,〔Laurent et al., Hypertension. 2001; 37: 1236–1241〕 diabetes mellitus〔Cruickshank et al., Circulation. 2002; 106: 2085–2090〕 and in the general population.〔Mattace-Raso et al. Circulation. 2006;113:657-663〕〔Hansen et al., Circulation. 2006;113:664-670〕 However, at present, the role of measurement of PWV as a general clinical tool remains to be established. Devices are on the market that measure arterial stiffness parameters (augmentation index, pulse wave velocity). These include the Complior, CVProfilor, PeriScope, Hanbyul Meditech, Mobil-O-Graph NG, Pulsecor, PulsePen, BPLab Vasotens, Arteriograph, and SphygmoCor.〔Avolio, A.; Butlin, M. & Walsh, A. (Arterial blood pressure measurement and pulse wave analysis - their role in enhancing cardiovascular assessment ). Physiol Meas, 2009, 31, R1-R47〕
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