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Impact of Decreased Transmural Conduction Velocity on the Function of the Human Left Ventricle: A Simulation Study
J. Vaverka, J. Moudr, P. Lokaj, J. Burša, M. Pásek
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články
NLK
Free Medical Journals
od 2013
Hindawi Publishing Open Access
od 2001-01-01
PubMed Central
od 2013
Europe PubMed Central
od 2013
ProQuest Central
od 2013
Open Access Digital Library
od 2001-01-01
Open Access Digital Library
od 2012-12-04
Open Access Digital Library
od 2013-01-01
CINAHL Plus with Full Text (EBSCOhost)
od 2013-01-01
Medline Complete (EBSCOhost)
od 2013-01-01
Health & Medicine (ProQuest)
od 2013
ROAD: Directory of Open Access Scholarly Resources
od 2013
PubMed
32337235
DOI
10.1155/2020/2867865
Knihovny.cz E-zdroje
- MeSH
- fibrilace síní patofyziologie MeSH
- hemodynamika fyziologie MeSH
- lidé MeSH
- modely kardiovaskulární * MeSH
- počítačová simulace * MeSH
- převodní systém srdeční fyziologie MeSH
- srdce - funkce komor fyziologie MeSH
- srdeční komory patofyziologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
This study investigates the impact of reduced transmural conduction velocity (TCV) on output parameters of the human heart. In a healthy heart, the TCV contributes to synchronization of the onset of contraction in individual layers of the left ventricle (LV). However, it is unclear whether the clinically observed decrease of TCV contributes significantly to a reduction of LV contractility. The applied three-dimensional finite element model of isovolumic contraction of the human LV incorporates transmural gradients in electromechanical delay and myocyte shortening velocity and evaluates the impact of TCV reduction on pressure rise (namely, (dP/dt)max) and on isovolumic contraction duration (IVCD) in a healthy LV. The model outputs are further exploited in the lumped "Windkessel" model of the human cardiovascular system (based on electrohydrodynamic analogy of respective differential equations) to simulate the impact of changes of (dP/dt)max and IVCD on chosen systemic parameters (ejection fraction, LV power, cardiac output, and blood pressure). The simulations have shown that a 50% decrease in TCV prolongs substantially the isovolumic contraction, decelerates slightly the LV pressure rise, increases the LV energy consumption, and reduces the LV power. These negative effects increase progressively with further reduction of TCV. In conclusion, these results suggest that the pumping efficacy of the human LV decreases with lower TCV due to a higher energy consumption and lower LV power. Although the changes induced by the clinically relevant reduction of TCV are not critical for a healthy heart, they may represent an important factor limiting the heart function under disease conditions.
Department of Internal Medicine and Cardiology University Hospital Brno Brno Czech Republic
Department of Physiology Faculty of Medicine Masaryk University Brno Czech Republic
Institute of Thermomechanics Czech Academy of Science Prague Czech Republic
Citace poskytuje Crossref.org
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