Mechanisms of the acute ischemia-induced arrhythmogenesis--a simulation study.
The underlying ionic mechanisms of ischemic-induced arrhythmia were studied by the computer simulation method. To approximate the real situation, ischemic cells were simulated by considering the three major component conditions of acute ischemia (elevated extracellular K(+) concentration, acidosis and anoxia) at the level of ionic currents and ionic concentrations, and a round ischemic zone was introduced into a homogeneous healthy sheet to avoid sharp angle of the ischemic tissue. The constructed models were solved using the operator splitting and adaptive time step methods, and the perturbation finite difference (PFD) scheme was first used to integrate the partial differential equations (PDEs) in the model. The numerical experiments showed that the action potential durations (APDs) of ischemic cells did not exhibited rate adaptation characteristic, resulting in flattening of the APD restitution curve. With reduction of sodium channel availability and long recovery of excitability, refractory period of the ischemic tissue was significantly prolonged, and could no longer be considered as same as APD. Slope of the conduction velocity (CV) restitution curve increased both in normal and ischemic region when pacing cycle length (PCL) was short, and refractory period dispersion increased with shortening of PCL as well. Therefore, dynamic changes of CV and dispersion of refractory period rather than APD were suggested to be the fundamental mechanisms of arrhythmia in regional ischemic myocardium.
Zhang
Hong
H
The Key Laboratory of Biomedical Information Engineering of Ministry of Education of China, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, PR China.
Zhang
Zhen-Xi
ZX
Yang
Lin
L
Jin
Yin-Bin
YB
Huang
Yi-Zhuo
YZ
D000138:Acidosis / Q000503:physiopathology; D000200:Action Potentials / Q000502:physiology; D003198:Computer Simulation; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000503:physiopathology*; D011188:Potassium / Q000502:physiology; D014693:Ventricular Fibrillation / Q000209:etiology* / Q000503:physiopathology
D011188:Potassium