Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. Dependence of arterial stiffness on pressure quantified in the realm of the cardiac cycle: towards a patient-specific approach? Alberto Avolio and Mark Butlin See original paper on page 330 T he interaction of the structural and load-bearing components in the wall of arteries is a major deter- minant of the mechanical properties of the arterial vasculature [1]. At low strains, the load is borne by elastic fibres and becomes transferred to the stiffer collagen fibres with increasing strain. As the arterial wall is distended due to intravascular pressure, the inherent stiffness of the wall then becomes dependent on the distending pressure. This pressure-dependence of wall stiffness, due to the nonlinear stress-strain relationship, is an intrinsic property of all arteries. It is a fundamental evolutionary property of arterial design across all vertebrates and invertebrates with a closed circulatory system [2]. It enables the arteries to have a single value of wall tension to balance the distending pressure at all strains, as distinct from collapsible vessels wherein there may be more than a single operating point at different strains [2]. The measurement of intrinsic wall stiffness is not readily achievable in the intact circulation, and so, arterial pulse wave velocity (PWV) is generally used as a surrogate, due to the biophysical relationships between PWV and vessel stiffness and geometry [3]. Thus, when comparing measure- ments of arterial PWV across individuals, it is necessary to account for any difference in pressure for assessment of inherent differences in arterial stiffness. This has been important to differentiate age-related changes in popu- lations with different risk profiles or environmental factors [4]. The large numbers of studies conducted in this field confirm repeatedly that the main factors affecting PWV, and so wall stiffness, in large conduits arteries are age and arterial blood pressure. In population studies, the age and pressure-dependence of arterial stiffness is accounted for by statistical means employing multiregression techniques, and much has been gained by these methods to suggest that arterial stiffness is a strong independent predictor of cardiovascular risk [5]. Consequently, there is an increasing research effort in establishing whether arterial stiffness per se could precede the development of hyper- tension [6–9] and whether early structural changes may be causally related to age-related increase in arterial pressure and associated risk factors [10–13], or could be reversed or attenuated by treatment [14,15]. Thus, the inter-relationship of age and blood pressure with arterial stiffness is a highly significant factor for the proper interpretation of measure- ments of arterial stiffness in relation to levels of cardiovas- cular risk, and to align arterial stiffness measurements with emerging guidelines incorporating normal population val- ues of PWV as well as blood pressure [16,17]. However, although it is entirely feasible for this inter-relationship to be accounted for by statistical means in cohort studies, it does not necessarily follow that population normative values can always be extrapolated to individuals. The study by Spronck et al. [18] in the current issue of the Journal of Hypertension makes important advances in quantifying the degree of the pressure-dependence of arterial stiffness in individuals and can lead to important clinical applications of patient-specific assessment. In this study [18], arterial stiffness is measured as a regional parameter in the carotid artery by employing ultrasound measurement of arterial diameter and tonometric regis- tration of the arterial pressure pulse. The study uses tech- niques developed in earlier studies by some of the same group of investigators [19,20], wherein pressure-area curves are used to determine the values of stiffness at three specific points in the cardiac cycle: diastole, peak systole and end systole. The pressure-area curves are modelled by a single exponential function and carotid PWV (cPWV) is deter- mined using the established Bramwell–Hill relationship [cPWV ¼ (DP.Ad/DA.r) 1/2 ; where DP is pulse pressure; Ad: diastolic area; DA: change in area; r: blood density]. Spronck et al. [18] conducted the study in a small group of 23 hypertensive individuals. This was done essentially to demonstrate proof of principle and also to obtain ranges of variation of cPWV over the cardiac cycle with which to estimate broad values of pressure-dependence of cPWV. The overall conclusion is that in the human carotid artery, Journal of Hypertension 2015, 33:257–259 The Australian School of Advanced Medicine, Macquarie University, Sydney, New South Wales, Australia Correspondence to Alberto Avolio, 2 Technology Place, Macquarie University, NSW 2109, Australia. Tel: +61 2 9812 3500; fax: +61 2 9812 3600; e-mail: alberto.avolio @mq.edu.au J Hypertens 33:257–259 Copyright ß 2015 Wolters Kluwer Health, Inc. All rights reserved. DOI:10.1097/HJH.0000000000000443 Journal of Hypertension www.jhypertension.com 257 Editorial Comment