TY - JOUR
T1 - Ventricular fibrillation mechanisms and cardiac restitutions
T2 - An investigation by simulation study on whole-heart model
AU - Zheng, Yi
AU - Wei, Daming
AU - Zhu, Xin
AU - Chen, Wenxi
AU - Fukuda, Koji
AU - Shimokawa, Hiroaki
N1 - Funding Information:
We would like to thank Dr. Osamu Okazaki from the National Center for Global Health and Medicine (Japan) for his precious advice. We also thank Dr. Xiaomei Wu, Dr. Cuiwei Yang, and Dr. Weijia Lu for their valuable assistances to the simulation study. This work is supported in part by the Grant-in-aid for Scientific Research, No. 24500369 Japan Society for the Promotion of Science ( JSPS ).
Publisher Copyright:
© 2014 Elsevier Ltd.
PY - 2015/8/1
Y1 - 2015/8/1
N2 - Background: The action potential duration (APD) and the conduction velocity (CV) restitution have been reported to be important in the maintenance and conversion of ventricular fibrillation (VF), whose mechanisms remain poorly understood. Multiple-wavelet and/or mother-rotor have been regarded as the main VF mechanisms, and APD restitution (APDR) and CV restitution (CVR) properties are involved in the mutual conversion or transition between VF and ventricular tachycardia (VT). Methods and results: The effects of APDR (both its slope and heterogeneity) and CVR on VF organization and conversion were examined using a "rule-based" whole-heart model. The results showed that different organizations of simulated VF were manifestations of different restitution configurations. Multiple-wavelet and mother-rotor VF mechanisms could recur in models with steep and heterogeneous APDR, respectively. Suppressing the excitability either decreased or increased the VF complexity under the steep or shallow APDR, respectively. The multiple-wavelet VF changed into a VT in response to a flattening of the APDR, and the VT degenerated into a mother-rotor VF due to the APDR heterogeneity. Conclusions: Our results suggest that the mechanisms of VF are tightly related to cardiac restitution properties. From a viewpoint of the "rule-based" whole-heart model, our work supports the hypothesis that the synergy between APDR and CVR contributes to transitions between multiple-wavelet and mother-rotor mechanisms in the VF.
AB - Background: The action potential duration (APD) and the conduction velocity (CV) restitution have been reported to be important in the maintenance and conversion of ventricular fibrillation (VF), whose mechanisms remain poorly understood. Multiple-wavelet and/or mother-rotor have been regarded as the main VF mechanisms, and APD restitution (APDR) and CV restitution (CVR) properties are involved in the mutual conversion or transition between VF and ventricular tachycardia (VT). Methods and results: The effects of APDR (both its slope and heterogeneity) and CVR on VF organization and conversion were examined using a "rule-based" whole-heart model. The results showed that different organizations of simulated VF were manifestations of different restitution configurations. Multiple-wavelet and mother-rotor VF mechanisms could recur in models with steep and heterogeneous APDR, respectively. Suppressing the excitability either decreased or increased the VF complexity under the steep or shallow APDR, respectively. The multiple-wavelet VF changed into a VT in response to a flattening of the APDR, and the VT degenerated into a mother-rotor VF due to the APDR heterogeneity. Conclusions: Our results suggest that the mechanisms of VF are tightly related to cardiac restitution properties. From a viewpoint of the "rule-based" whole-heart model, our work supports the hypothesis that the synergy between APDR and CVR contributes to transitions between multiple-wavelet and mother-rotor mechanisms in the VF.
KW - Action potential duration restitution
KW - Computer simulation
KW - Conduction velocity restitution
KW - Ventricular fibrillation
KW - Whole-heart model
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U2 - 10.1016/j.compbiomed.2014.06.014
DO - 10.1016/j.compbiomed.2014.06.014
M3 - Article
C2 - 25066787
AN - SCOPUS:84924256391
SN - 0010-4825
VL - 63
SP - 261
EP - 268
JO - Computers in Biology and Medicine
JF - Computers in Biology and Medicine
ER -