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      A database of virtual healthy subjects to assess the accuracy of foot-to-foot pulse wave velocities for estimation of aortic stiffness

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          Abstract

          This work presents a new methodology for the theoretical assessment of computed physiological indexes and algorithms based on pulse wave analysis. We created a database of virtual healthy subjects using a 1D model of the arterial hemodynamics. This study presents its application to central and peripheral foot-to-foot pulse wave velocities .

          Abstract

          While central (carotid-femoral) foot-to-foot pulse wave velocity (PWV) is considered to be the gold standard for the estimation of aortic arterial stiffness, peripheral foot-to-foot PWV (brachial-ankle, femoral-ankle, and carotid-radial) are being studied as substitutes of this central measurement. We present a novel methodology to assess theoretically these computed indexes and the hemodynamics mechanisms relating them. We created a database of 3,325 virtual healthy adult subjects using a validated one-dimensional model of the arterial hemodynamics, with cardiac and arterial parameters varied within physiological healthy ranges. For each virtual subject, foot-to-foot PWV was computed from numerical pressure waveforms at the same locations where clinical measurements are commonly taken. Our numerical results confirm clinical observations: 1) carotid-femoral PWV is a good indicator of aortic stiffness and correlates well with aortic PWV; 2) brachial-ankle PWV overestimates aortic PWV and is related to the stiffness and geometry of both elastic and muscular arteries; and 3) muscular PWV (carotid-radial, femoral-ankle) does not capture the stiffening of the aorta and should therefore not be used as a surrogate for aortic stiffness. In addition, our analysis highlights that the foot-to-foot PWV algorithm is sensitive to the presence of reflected waves in late diastole, which introduce errors in the PWV estimates. In this study, we have created a database of virtual healthy subjects, which can be used to assess theoretically the efficiency of physiological indexes based on pulse wave analysis.

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          Most cited references31

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          Clinical applications of arterial stiffness; definitions and reference values.

          Arterial stiffening is the most important cause of increasing systolic and pulse pressure, and for decreasing diastolic pressure beyond 40 years of age. Stiffening affects predominantly the aorta and proximal elastic arteries, and to a lesser degree the peripheral muscular arteries. While conceptually a Windkessel model is the simplest way to visualize the cushioning function of arteries, this is not useful clinically under changing conditions when effects of wave reflection become prominent. Many measures have been applied to quantify stiffness, but all are approximations only, on account of the nonhomogeneous structure of the arterial wall, its variability in different locations, at different levels of distending pressure, and with changes in smooth muscle tone. This article summarizes the methods and indices used to estimate arterial stiffness, and provides values from a survey of the literature, followed by recommendations of an international group of workers in the field who attended the First Consensus Conference on Arterial Stiffness, which was held in Paris during 2000, under the chairmanship of M.E. Safar and E.D. Frohlich.
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            Comparison between carotid-femoral and brachial-ankle pulse wave velocity as measures of arterial stiffness.

            Arterial stiffness is an important risk factor for cardiovascular disease. Carotid-femoral pulse wave velocity (cfPWV) is the most recognized and established index of arterial stiffness. An emerging automatic measure of PWV primarily used in the Asian countries is brachial-ankle PWV (baPWV). To systematically compare these two methodologies, we conducted a multicenter study involving a total of 2287 patients. There was a significant positive relation between baPWV and cfPWV (r = 0.73). Average baPWV was approximately 20% higher than cfPWV. Both cfPWV and baPWV were significantly and positively associated with age (r = 0.56 and 0.64), systolic blood pressure (r = 0.49 and 0.61), and the Framingham risk score (r = 0.48 and 0.63). The areas under the receiver operating curves (ROCs) of PWV to predict the presence of both stroke and coronary artery disease were comparable between cfPWV and baPWV. Collectively, these results indicate that cfPWV and baPWV are indices of arterial stiffness that exhibit similar extent of associations with cardiovascular disease risk factors and clinical events.
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              Noninvasive determination of age-related changes in the human arterial pulse.

              Arterial pressure waves were recorded noninvasively from the carotid, radial, femoral, or all three of these arteries of 1,005 normal subjects, aged 2-91 years, using a new transcutaneous tonometer containing a high fidelity Millar micromanometer. Waves were ensemble-averaged into age-decade groups. Characteristic changes were noted with increasing age. In all sites, pulse amplitude increased with advancing age (carotid, 91.3%; radial 67.5%; femoral, 50.1% from first to eighth decade), diastolic decay steepened, and diastolic waves became less prominent. In the carotid pulse, there was, in youth, a second peak on the downstroke of the waves in late systole. After the third decade, this second peak rose with age to merge with and dominate the initial rise. In the radial pulse, a late systolic wave was also apparent, but this occurred later; with age, this second peak rose but not above the initial rise in early systole, even at the eighth decade. In the femoral artery, there was a single systolic wave at all ages. Aging changes in the arterial pulse are explicable on the basis of both an increase in arterial stiffness with increased pulse-wave velocity and progressively earlier wave reflection. These two factors may be separated and effects of the latter measured from pressure wave-contour analysis using an "augmentation index," determined by a computer algorithm developed from invasive pressure and flow data. Changes in peak pressure in the central (carotid) artery show increasing cardiac afterload with increasing age in a normal population; this can account for the cardiac hypertrophy that occurs with advancing age (even as other organs atrophy) and the predisposition to cardiac failure in the elderly. Identification of mechanisms responsible offers a new approach to reduction of left ventricular afterload.
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                Author and article information

                Journal
                Am J Physiol Heart Circ Physiol
                Am. J. Physiol. Heart Circ. Physiol
                ajpheart
                ajpheart
                AJPHEART
                American Journal of Physiology - Heart and Circulatory Physiology
                American Physiological Society (Bethesda, MD )
                0363-6135
                1522-1539
                8 June 2015
                15 August 2015
                8 June 2015
                : 309
                : 4
                : H663-H675
                Affiliations
                [1] 1Division of Imaging Sciences and Biomedical Engineering, St. Thomas' Hospital, King's College London, London, United Kingdom; and
                [2] 2Department of Clinical Pharmacology, St Thomas' Hospital, King's College London, London, United Kingdom
                Author notes
                Address for reprint requests and other correspondence: M. Willemet, 3rd Floor Lambeth Wing, St Thomas' Hospital, SE1 7EH London, UK (e-mail: marie.willemet@ 123456gmail.com ).
                Article
                H-00175-2015
                10.1152/ajpheart.00175.2015
                4537944
                26055792
                4b2fadd6-934d-4920-bdd7-516c82d8acf4
                Copyright © 2015 the American Physiological Society

                Licensed under Creative Commons Attribution CC-BY 3.0: © the American Physiological Society.

                History
                : 10 March 2015
                : 5 June 2015
                Funding
                Funded by: 501100000266 Engineering and Physical Sciences Research Council (EPSRC)
                Award ID: EP/K031546/1
                Funded by: 501100004074 King's College London Medical Engineering Centre (Wellcome Trust EPSRC Centre of Excellence in Medical Engineering)
                Award ID: WT 088641/Z/09/Z
                Funded by: 501100000274 British Heart Foundation (BHF)
                Award ID: FS/09/030/27812
                Categories
                Integrative Cardiovascular Physiology and Pathophysiology

                Cardiovascular Medicine
                brachial-ankle pwv,carotid-femoral pwv,numerical 1d model,aortic stiffness,database of virtual subjects

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