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Effect of Transmural Differences in Excitation-Contraction Delay and Contraction Velocity on Left Ventricle Isovolumic Contraction: A Simulation Study
J. Vaverka, J. Burša, J. Šumbera, M. Pásek,
Language English Country United States
Document type Journal Article
NLK
Free Medical Journals
from 2013
PubMed Central
from 2013
Europe PubMed Central
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ProQuest Central
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Open Access Digital Library
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Open Access Digital Library
from 2012-12-04
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from 2013-01-01
CINAHL Plus with Full Text (EBSCOhost)
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Wiley-Blackwell Open Access Titles
from 2001
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from 2013
PubMed
29862273
DOI
10.1155/2018/4798512
Knihovny.cz E-resources
- MeSH
- Myocardial Contraction physiology MeSH
- Humans MeSH
- Models, Cardiovascular * MeSH
- Computer Simulation * MeSH
- Ventricular Function physiology MeSH
- Heart Ventricles * MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
Recent studies have shown that left ventricle (LV) exhibits considerable transmural differences in active mechanical properties induced by transmural differences in electrical activity, excitation-contraction coupling, and contractile properties of individual myocytes. It was shown that the time between electrical and mechanical activation of myocytes (electromechanical delay: EMD) decreases from subendocardium to subepicardium and, on the contrary, the myocyte shortening velocity (MSV) increases in the same direction. To investigate the physiological importance of this inhomogeneity, we developed a new finite element model of LV incorporating the observed transmural gradients in EMD and MSV. Comparative simulations with the model showed that when EMD or MSV or both were set constant across the LV wall, the LV contractility during isovolumic contraction (IVC) decreased significantly ((dp/dt)max was reduced by 2 to 38% and IVC was prolonged by 18 to 73%). This was accompanied by an increase of transmural differences in wall stress. These results suggest that the transmural differences in EMD and MSV play an important role in physiological contractility of LV by synchronising the contraction of individual layers of ventricular wall during the systole. Reduction or enhancement of these differences may therefore impair the function of LV and contribute to heart failure.
References provided by Crossref.org
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