TY - GEN
T1 - Arrhythmogenic Mechanism of the Enhanced Late Sodium Current in Human Ventricular Myocytes - A Simulation Study
AU - Wang, Wei
AU - Zhang, Shanzhuo
AU - Xu, Yong
AU - Wang, Kuanquan
AU - Zhang, Henggui
N1 - Publisher Copyright:
© 2019 Creative Commons.
PY - 2019/9
Y1 - 2019/9
N2 - The enhancement of the late sodium current (INaL) has been demonstrated to contribute to the cardiac arrhythmias. However, its arrhythmogenic mechanism at the cellular and tissue level remains incompletely elucidated. In this study, the O'Hara-Rudy model of human ventricular cells was implemented for multi-level simulations. At the cellular level, the influences of the pathological enhanced INaL on cardiac action potential characteristics, ion currents, intracellular concentration homeostasis and action potential duration (APD) restitution properties were simulated and analyzed. At the tissue level, a heterogeneous one dimensional (1D) strand was constructed to find out the impact of enhanced INaL on APD dispersion and the vulnerable windows (VWs). The simulations revealed the role of augmenting INaL in prolonging the APD, steepening the APD restitution curves, increasing the heterogeneity of the tissue and widening the VWs. Our simulation data provides a detailed mechanistic insight into the pro-arrhythmic role of the enhanced INaL at both cellular and tissue levels.
AB - The enhancement of the late sodium current (INaL) has been demonstrated to contribute to the cardiac arrhythmias. However, its arrhythmogenic mechanism at the cellular and tissue level remains incompletely elucidated. In this study, the O'Hara-Rudy model of human ventricular cells was implemented for multi-level simulations. At the cellular level, the influences of the pathological enhanced INaL on cardiac action potential characteristics, ion currents, intracellular concentration homeostasis and action potential duration (APD) restitution properties were simulated and analyzed. At the tissue level, a heterogeneous one dimensional (1D) strand was constructed to find out the impact of enhanced INaL on APD dispersion and the vulnerable windows (VWs). The simulations revealed the role of augmenting INaL in prolonging the APD, steepening the APD restitution curves, increasing the heterogeneity of the tissue and widening the VWs. Our simulation data provides a detailed mechanistic insight into the pro-arrhythmic role of the enhanced INaL at both cellular and tissue levels.
UR - https://www.scopus.com/pages/publications/85081127161
U2 - 10.22489/CinC.2019.277
DO - 10.22489/CinC.2019.277
M3 - 会议稿件
AN - SCOPUS:85081127161
T3 - Computing in Cardiology
BT - 2019 Computing in Cardiology, CinC 2019
PB - IEEE Computer Society
T2 - 2019 Computing in Cardiology, CinC 2019
Y2 - 8 September 2019 through 11 September 2019
ER -