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Influence of LVAD function on mechanical unloading and electromechanical delay: a simulation study
This study hypothesized that a left ventricular assist device (LVAD) shortens the electromechanical delay (EMD) by mechanical unloading. The goal of this study is to examine, by computational modeling, the influence of LVAD on EMD for four heart failure (HF) cases ranging from mild HF to severe HF....
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Berlin Heidelberg
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5906510/ https://www.ncbi.nlm.nih.gov/pubmed/29098548 http://dx.doi.org/10.1007/s11517-017-1730-y |
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author | Heikhmakhtiar, Aulia Khamas Ryu, Ah Jin Shim, Eun Bo Song, Kwang-Soup Trayanova, Natalia A. Lim, Ki Moo |
author_facet | Heikhmakhtiar, Aulia Khamas Ryu, Ah Jin Shim, Eun Bo Song, Kwang-Soup Trayanova, Natalia A. Lim, Ki Moo |
author_sort | Heikhmakhtiar, Aulia Khamas |
collection | PubMed |
description | This study hypothesized that a left ventricular assist device (LVAD) shortens the electromechanical delay (EMD) by mechanical unloading. The goal of this study is to examine, by computational modeling, the influence of LVAD on EMD for four heart failure (HF) cases ranging from mild HF to severe HF. We constructed an integrated model of an LVAD-implanted cardiovascular system, then we altered the Ca(2+) transient magnitude, with scaling factors 1, 0.9, 0.8, and 0.7 representing HF1, HF2, HF3, and HF4, respectively, in order of increasing HF severity. The four HF conditions are classified into two groups. Group one is the four HF conditions without LVAD, and group two is the conditions treated with continuous LVAD pump. The single-cell mechanical responses showed that EMD was prolonged with the higher load. The findings indicated that in group one, the HF-induced Ca2 + transient remodeling prolonged the mechanical activation time (MAT) and decreased the contractile tension, which reduced the left ventricle (LV) pressure, and increased the end-diastolic strain. In group two, LVAD shortened MAT of the ventricles. Furthermore, LVAD reduced the contractile tension, and end-diastolic strain, but increased the aortic pressure. The computational study demonstrated that LVAD shortens EMD by mechanical unloading of the ventricle. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s11517-017-1730-y) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-5906510 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Springer Berlin Heidelberg |
record_format | MEDLINE/PubMed |
spelling | pubmed-59065102018-04-20 Influence of LVAD function on mechanical unloading and electromechanical delay: a simulation study Heikhmakhtiar, Aulia Khamas Ryu, Ah Jin Shim, Eun Bo Song, Kwang-Soup Trayanova, Natalia A. Lim, Ki Moo Med Biol Eng Comput Original Article This study hypothesized that a left ventricular assist device (LVAD) shortens the electromechanical delay (EMD) by mechanical unloading. The goal of this study is to examine, by computational modeling, the influence of LVAD on EMD for four heart failure (HF) cases ranging from mild HF to severe HF. We constructed an integrated model of an LVAD-implanted cardiovascular system, then we altered the Ca(2+) transient magnitude, with scaling factors 1, 0.9, 0.8, and 0.7 representing HF1, HF2, HF3, and HF4, respectively, in order of increasing HF severity. The four HF conditions are classified into two groups. Group one is the four HF conditions without LVAD, and group two is the conditions treated with continuous LVAD pump. The single-cell mechanical responses showed that EMD was prolonged with the higher load. The findings indicated that in group one, the HF-induced Ca2 + transient remodeling prolonged the mechanical activation time (MAT) and decreased the contractile tension, which reduced the left ventricle (LV) pressure, and increased the end-diastolic strain. In group two, LVAD shortened MAT of the ventricles. Furthermore, LVAD reduced the contractile tension, and end-diastolic strain, but increased the aortic pressure. The computational study demonstrated that LVAD shortens EMD by mechanical unloading of the ventricle. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s11517-017-1730-y) contains supplementary material, which is available to authorized users. Springer Berlin Heidelberg 2017-11-03 2018 /pmc/articles/PMC5906510/ /pubmed/29098548 http://dx.doi.org/10.1007/s11517-017-1730-y Text en © The Author(s) 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. |
spellingShingle | Original Article Heikhmakhtiar, Aulia Khamas Ryu, Ah Jin Shim, Eun Bo Song, Kwang-Soup Trayanova, Natalia A. Lim, Ki Moo Influence of LVAD function on mechanical unloading and electromechanical delay: a simulation study |
title | Influence of LVAD function on mechanical unloading and electromechanical delay: a simulation study |
title_full | Influence of LVAD function on mechanical unloading and electromechanical delay: a simulation study |
title_fullStr | Influence of LVAD function on mechanical unloading and electromechanical delay: a simulation study |
title_full_unstemmed | Influence of LVAD function on mechanical unloading and electromechanical delay: a simulation study |
title_short | Influence of LVAD function on mechanical unloading and electromechanical delay: a simulation study |
title_sort | influence of lvad function on mechanical unloading and electromechanical delay: a simulation study |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5906510/ https://www.ncbi.nlm.nih.gov/pubmed/29098548 http://dx.doi.org/10.1007/s11517-017-1730-y |
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