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Journal of Healthcare Engineering
Volume 2018 (2018), Article ID 1364185, 9 pages
https://doi.org/10.1155/2018/1364185
Research Article

A Novel Interpretation for Arterial Pulse Pressure Amplification in Health and Disease

1Facultad Regional Buenos Aires, Grupo de Investigación en Bioingeniería (GIBIO) and Escuela de Estudios Avanzados en Ciencias de la Ingeniería (EEACI), Universidad Tecnológica Nacional, Medrano 951, C1179AAQ Buenos Aires, Argentina
2UMR 7190, Institut Jean Le Rond ∂'Alembert, CNRS and UPMC, Sorbonne Universités, 4 Place Jussieu, Boîte 162, 75005 Paris, France
3Universidad Tecnológica Nacional, Medrano 951, C1179AAQ Buenos Aires, Argentina
4Facultad Regional Buenos Aires, Centro de Procesamiento de Señales e Imagenes (CPSI) and Escuela de Estudios Avanzados en Ciencias de la Ingeniería (EEACI), Universidad Tecnológica Nacional, Medrano 951, C1179AAQ Buenos Aires, Argentina

Correspondence should be addressed to Manuel R. Alfonso; moc.liamg@0osnoflam

Received 22 May 2017; Revised 18 October 2017; Accepted 29 October 2017; Published 16 January 2018

Academic Editor: Andreas Maier

Copyright © 2018 Manuel R. Alfonso et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Arterial pressure waves have been described in one dimension using several approaches, such as lumped (Windkessel) or distributed (using Navier-Stokes equations) models. An alternative approach consists of modeling blood pressure waves using a Korteweg-de Vries (KdV) equation and representing pressure waves as combinations of solitons. This model captures many key features of wave propagation in the systemic network and, in particular, pulse pressure amplification (PPA), which is a mechanical biomarker of cardiovascular risk. The main objective of this work is to compare the propagation dynamics described by a KdV equation in a human-like arterial tree using acquired pressure waves. Furthermore, we analyzed the ability of our model to reproduce induced elastic changes in PPA due to different pathological conditions. To this end, numerical simulations were performed using acquired central pressure signals from different subject groups (young, adults, and hypertensive) as input and then comparing the output of the model with measured radial artery pressure waveforms. Pathological conditions were modeled as changes in arterial elasticity (E). Numerical results showed that the model was able to propagate acquired pressure waveforms and to reproduce PPA variations as a consequence of elastic changes. Calculated elasticity for each group was in accordance with the existing literature.