2020
Impact of Decreased Transmural Conduction Velocity on the Function of the Human Left Ventricle: A Simulation Study
VAVERKA, Jiri, Jiří MOUDR, Petr LOKAJ, Jiri BURSA, Michal PÁSEK et. al.Základní údaje
Originální název
Impact of Decreased Transmural Conduction Velocity on the Function of the Human Left Ventricle: A Simulation Study
Autoři
VAVERKA, Jiri (203 Česká republika), Jiří MOUDR (203 Česká republika, domácí), Petr LOKAJ (203 Česká republika), Jiri BURSA (203 Česká republika) a Michal PÁSEK (203 Česká republika, garant, domácí)
Vydání
Biomed Research International, London, Hindawi Publishing Corporation, 2020, 2314-6133
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
30105 Physiology
Stát vydavatele
Velká Británie a Severní Irsko
Utajení
není předmětem státního či obchodního tajemství
Odkazy
Impakt faktor
Impact factor: 3.411
Kód RIV
RIV/00216224:14110/20:00116020
Organizační jednotka
Lékařská fakulta
UT WoS
000528680300003
Klíčová slova anglicky
HEART; GENE; MYOCARDIUM; MUTATIONS; CHILDREN; DURATION; MODEL
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 17. 7. 2020 08:16, Mgr. Tereza Miškechová
Anotace
V originále
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.