The relationships between the Hopf bifurcation in the cellular model and the Early Afterdepolarization(EAD)and the function of potassium channel are investigated for the EAD phenomenon of the voltage oscillation during the repolarizing phase of the cardiac action potential. A subsystem model is developed by removing the fast activated sodium current in the LR91 model and introducing control factors for time constants of calcium and potassium channels. Variables with different time scales are separated. A fast subsystem with 3 variables is formed and the variables are voltage
activation and inactivation gating variables of calcium channel. The relationship between the voltage and the steady state of the fast subsystem is analyzed by regarding the gating variable of the potassium channel as a bifurcation parameter. Simulation results show that the voltage approaches the attraction and Hopf bifurcation point more and more as the time constant of potassium channel gating variable increases. The action potential duration(APD)is prolonged to 1 060 ms and the voltage oscillation appears when the time constant is 6 times of its control value. The number of the oscillation waves increases to 15
when the time constant approaches 15 times. The results show that the Hopf bifurcation of the fast subsystem results in induction of EAD under the control of the potassium channel.
WANG Junkui, YU Zhongxiang, CUI Changcong. Mechanism of drug-induced torsade de pointes: an experimental study in dogs[J]. Journal of Southern Medical University, 2013, 33(7): 1093-1096.
ZHAO Zhenghang, WEN Hairuo, FEFELOVA N, et al. Revisiting the ionic mechanisms of early afterdepolarizations in cardiomyocytes: predominant by Ca waves or Ca currents[J]. American Journal of Physiology-Heart and Circulatory Physiology, 2012, 302(8): H1636-H1644.
VOLDERS P G, VOS M A, SZABO B, et al. Progress in the understanding of cardiac early afterdepolarizations and torsades de pointes: time to revise current concepts[J]. Cardiovascular Research, 2000, 46(3): 376-392.
LI Guirong, LAU C P, DUCHARME A, et al. Transmural action potential and ionic current remodeling in ventricles of failing canine hearts[J]. American Journal of Physiology-Heart and Circulatory Physiology, 2002, 283(3): H1031-H1041.
WEISS J N, GARFINKEL A, KARAGUEUZIAN H S, et al. Early afterdepolarizations and cardiac arrhythmias[J]. Heart Rhythm, 2010, 7(12): 1891-1899.
QU Zhilin, XIE Laihua, OLCESE R, et al. Early afterdepolarizations in cardiac myocytes: beyond reduced repolarization reserve[J]. Cardiovascular Research, 2013, 99(1): 6-15.
WANG Jiang, ZHANG Hua, ZENG Qiming. Analysis of Hopf bifurcation caused by sodium ions anti-electro-motive in the Hodgkin-Huxley model in muscles[J]. Journal of System Simulation, 2004, 16(10): 2276-2284.
LUO C H, RUDY Y. A model of the ventricular cardiac action potential depolarization, repolarization and their interaction[J]. Circulation Research, 1991, 68(6): 1501-1526.
TRAN D X, SATO D, YOCHELIS A, et al. Bifurcation and chaos in a model of cardiac early afterdepolarizations[J]. Physical Review Letters, 2009, 102(25): 2581031-2581034.
JIN Yinbin, YANG Lin, ZHANG Hong, et al. Numerical algorithm for conduction of action potential in two dimensional cardiac ventricle tissue[J]. Journal of Xi'an Jiaotong University, 2004, 38(8): 851-854.
IZHIKEVICH E M. Neural excitability, spiking and bursting[J]. International Journal of Bifurcation and Chaos, 2000, 10(6): 1171-1266.
LI Guoliang, CHENG Gong, WU Jing, et al. Drug-induced long QT syndrome in women[J]. Advances Therapy, 2013, 30(9): 793-802.
MARUYAMA M, XIAO Jianmin, ZHOU Qiang, et al. Carvedilol analogue inhibits triggered activities evoked by both early and delayed afterdepolarizations[J]. Heart Rhythm, 2013, 10(1): 101-107.