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Relative contributions from the ventricle and arterial tree to arterial pressure and its amplification: an experimental study

Arterial pressure is an important diagnostic parameter for cardiovascular disease. However, relative contributions of individual ventricular and arterial parameters in generating and augmenting pressure are not understood. Using a novel experimental arterial model, our aim was to characterize indivi...

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Autores principales: Gaddum, Nicholas, Alastruey, Jordi, Chowienczyk, Phil, Rutten, Marcel C. M., Segers, Patrick, Schaeffter, Tobias
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Physiological Society 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5625171/
https://www.ncbi.nlm.nih.gov/pubmed/28576835
http://dx.doi.org/10.1152/ajpheart.00844.2016
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author Gaddum, Nicholas
Alastruey, Jordi
Chowienczyk, Phil
Rutten, Marcel C. M.
Segers, Patrick
Schaeffter, Tobias
author_facet Gaddum, Nicholas
Alastruey, Jordi
Chowienczyk, Phil
Rutten, Marcel C. M.
Segers, Patrick
Schaeffter, Tobias
author_sort Gaddum, Nicholas
collection PubMed
description Arterial pressure is an important diagnostic parameter for cardiovascular disease. However, relative contributions of individual ventricular and arterial parameters in generating and augmenting pressure are not understood. Using a novel experimental arterial model, our aim was to characterize individual parameter contributions to arterial pressure and its amplification. A piston-driven ventricle provided programmable stroke profiles into various silicone arterial trees and a bovine aorta. Inotropy was varied in the ventricle, and arterial parameters modulated included wall thickness, taper and diameter, the presence of bifurcation, and a native aorta (bovine) versus silicone. Wave reflection at bifurcations was measured and compared with theory, varying parent-to-child tube diameter ratios, and branch angles. Intravascular pressure-tip wires and ultrasonic flow probes measured pressure and flow. Increasing ventricular inotropy independently augmented pressure amplification from 17% to 61% between the lower and higher systolic gradient stroke profiles in the silicone arterial network and from 10% to 32% in the bovine aorta. Amplification increased with presence of a bifurcation, decreasing wall thickness and vessel taper. Pulse pressure increased with increasing wall thickness (stiffness) and taper angle and decreasing diameter. Theoretical predictions of wave transmission through bifurcations werre similar to measurements (correlation: 0.91, R(2) = 0.94) but underestimated wave reflection (correlation: 0.75, R(2) = 0.94), indicating energy losses during mechanical wave reflection. This study offers the first comprehensive investigation of contributors to hypertensive pressure and its propagation throughout the arterial tree. Importantly, ventricular inotropy plays a crucial role in the amplification of peripheral pressure wave, which offers opportunity for noninvasive assessment of ventricular health. NEW & NOTEWORTHY The present study distinguishes contributions from cardiac and arterial parameters to elevated blood pressure and pressure amplification. Most importantly, it offers the first evidence that ventricular inotropy, an indicator of ventricular function, is an independent determinant of pressure amplification and could be measured with such established devices such as the SphygmoCor.
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spelling pubmed-56251712017-10-04 Relative contributions from the ventricle and arterial tree to arterial pressure and its amplification: an experimental study Gaddum, Nicholas Alastruey, Jordi Chowienczyk, Phil Rutten, Marcel C. M. Segers, Patrick Schaeffter, Tobias Am J Physiol Heart Circ Physiol Research Article Arterial pressure is an important diagnostic parameter for cardiovascular disease. However, relative contributions of individual ventricular and arterial parameters in generating and augmenting pressure are not understood. Using a novel experimental arterial model, our aim was to characterize individual parameter contributions to arterial pressure and its amplification. A piston-driven ventricle provided programmable stroke profiles into various silicone arterial trees and a bovine aorta. Inotropy was varied in the ventricle, and arterial parameters modulated included wall thickness, taper and diameter, the presence of bifurcation, and a native aorta (bovine) versus silicone. Wave reflection at bifurcations was measured and compared with theory, varying parent-to-child tube diameter ratios, and branch angles. Intravascular pressure-tip wires and ultrasonic flow probes measured pressure and flow. Increasing ventricular inotropy independently augmented pressure amplification from 17% to 61% between the lower and higher systolic gradient stroke profiles in the silicone arterial network and from 10% to 32% in the bovine aorta. Amplification increased with presence of a bifurcation, decreasing wall thickness and vessel taper. Pulse pressure increased with increasing wall thickness (stiffness) and taper angle and decreasing diameter. Theoretical predictions of wave transmission through bifurcations werre similar to measurements (correlation: 0.91, R(2) = 0.94) but underestimated wave reflection (correlation: 0.75, R(2) = 0.94), indicating energy losses during mechanical wave reflection. This study offers the first comprehensive investigation of contributors to hypertensive pressure and its propagation throughout the arterial tree. Importantly, ventricular inotropy plays a crucial role in the amplification of peripheral pressure wave, which offers opportunity for noninvasive assessment of ventricular health. NEW & NOTEWORTHY The present study distinguishes contributions from cardiac and arterial parameters to elevated blood pressure and pressure amplification. Most importantly, it offers the first evidence that ventricular inotropy, an indicator of ventricular function, is an independent determinant of pressure amplification and could be measured with such established devices such as the SphygmoCor. American Physiological Society 2017-09-01 2017-06-03 /pmc/articles/PMC5625171/ /pubmed/28576835 http://dx.doi.org/10.1152/ajpheart.00844.2016 Text en Copyright © 2017 the American Physiological Society http://creativecommons.org/licenses/by/4.0/deed.en_US Licensed under Creative Commons Attribution CC-BY 4.0 (http://creativecommons.org/licenses/by/4.0/deed.en_US) : © the American Physiological Society.
spellingShingle Research Article
Gaddum, Nicholas
Alastruey, Jordi
Chowienczyk, Phil
Rutten, Marcel C. M.
Segers, Patrick
Schaeffter, Tobias
Relative contributions from the ventricle and arterial tree to arterial pressure and its amplification: an experimental study
title Relative contributions from the ventricle and arterial tree to arterial pressure and its amplification: an experimental study
title_full Relative contributions from the ventricle and arterial tree to arterial pressure and its amplification: an experimental study
title_fullStr Relative contributions from the ventricle and arterial tree to arterial pressure and its amplification: an experimental study
title_full_unstemmed Relative contributions from the ventricle and arterial tree to arterial pressure and its amplification: an experimental study
title_short Relative contributions from the ventricle and arterial tree to arterial pressure and its amplification: an experimental study
title_sort relative contributions from the ventricle and arterial tree to arterial pressure and its amplification: an experimental study
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5625171/
https://www.ncbi.nlm.nih.gov/pubmed/28576835
http://dx.doi.org/10.1152/ajpheart.00844.2016
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