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Could increased axial wall stress be responsible for the development of atheroma in the proximal segment of myocardial bridges?
BACKGROUND: A recent model describing the mechanical interaction between a stenosis and the vessel wall has shown that axial wall stress can considerably increase in the region immediately proximal to the stenosis during the (forward) flow phases, so that abnormal biological processes and wall damag...
Autores principales: | , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2007
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2020464/ https://www.ncbi.nlm.nih.gov/pubmed/17688694 http://dx.doi.org/10.1186/1742-4682-4-29 |
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author | Doriot, Pierre-André Dorsaz, Pierre-André Noble, Jacques |
author_facet | Doriot, Pierre-André Dorsaz, Pierre-André Noble, Jacques |
author_sort | Doriot, Pierre-André |
collection | PubMed |
description | BACKGROUND: A recent model describing the mechanical interaction between a stenosis and the vessel wall has shown that axial wall stress can considerably increase in the region immediately proximal to the stenosis during the (forward) flow phases, so that abnormal biological processes and wall damages are likely to be induced in that region. Our objective was to examine what this model predicts when applied to myocardial bridges. METHOD: The model was adapted to the hemodynamic particularities of myocardial bridges and used to estimate by means of a numerical example the cyclic increase in axial wall stress in the vessel segment proximal to the bridge. The consistence of the results with reported observations on the presence of atheroma in the proximal, tunneled, and distal vessel segments of bridged coronary arteries was also examined. RESULTS: 1) Axial wall stress can markedly increase in the entrance region of the bridge during the cardiac cycle. 2) This is consistent with reported observations showing that this region is particularly prone to atherosclerosis. CONCLUSION: The proposed mechanical explanation of atherosclerosis in bridged coronary arteries indicates that angioplasty and other similar interventions will not stop the development of atherosclerosis at the bridge entrance and in the proximal epicardial segment if the decrease of the lumen of the tunneled segment during systole is not considerably reduced. |
format | Text |
id | pubmed-2020464 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2007 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-20204642007-10-13 Could increased axial wall stress be responsible for the development of atheroma in the proximal segment of myocardial bridges? Doriot, Pierre-André Dorsaz, Pierre-André Noble, Jacques Theor Biol Med Model Research BACKGROUND: A recent model describing the mechanical interaction between a stenosis and the vessel wall has shown that axial wall stress can considerably increase in the region immediately proximal to the stenosis during the (forward) flow phases, so that abnormal biological processes and wall damages are likely to be induced in that region. Our objective was to examine what this model predicts when applied to myocardial bridges. METHOD: The model was adapted to the hemodynamic particularities of myocardial bridges and used to estimate by means of a numerical example the cyclic increase in axial wall stress in the vessel segment proximal to the bridge. The consistence of the results with reported observations on the presence of atheroma in the proximal, tunneled, and distal vessel segments of bridged coronary arteries was also examined. RESULTS: 1) Axial wall stress can markedly increase in the entrance region of the bridge during the cardiac cycle. 2) This is consistent with reported observations showing that this region is particularly prone to atherosclerosis. CONCLUSION: The proposed mechanical explanation of atherosclerosis in bridged coronary arteries indicates that angioplasty and other similar interventions will not stop the development of atherosclerosis at the bridge entrance and in the proximal epicardial segment if the decrease of the lumen of the tunneled segment during systole is not considerably reduced. BioMed Central 2007-08-09 /pmc/articles/PMC2020464/ /pubmed/17688694 http://dx.doi.org/10.1186/1742-4682-4-29 Text en Copyright © 2007 Doriot et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Doriot, Pierre-André Dorsaz, Pierre-André Noble, Jacques Could increased axial wall stress be responsible for the development of atheroma in the proximal segment of myocardial bridges? |
title | Could increased axial wall stress be responsible for the development of atheroma in the proximal segment of myocardial bridges? |
title_full | Could increased axial wall stress be responsible for the development of atheroma in the proximal segment of myocardial bridges? |
title_fullStr | Could increased axial wall stress be responsible for the development of atheroma in the proximal segment of myocardial bridges? |
title_full_unstemmed | Could increased axial wall stress be responsible for the development of atheroma in the proximal segment of myocardial bridges? |
title_short | Could increased axial wall stress be responsible for the development of atheroma in the proximal segment of myocardial bridges? |
title_sort | could increased axial wall stress be responsible for the development of atheroma in the proximal segment of myocardial bridges? |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2020464/ https://www.ncbi.nlm.nih.gov/pubmed/17688694 http://dx.doi.org/10.1186/1742-4682-4-29 |
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