DocumentCode :
541517
Title :
Re-entry in a model of ischaemic ventricular tissue
Author :
Clayton, Richard H.
Author_Institution :
Dept. of Comput. Sci., Univ. of Sheffield, Sheffield, UK
fYear :
2010
fDate :
26-29 Sept. 2010
Firstpage :
181
Lastpage :
184
Abstract :
Ventricular fibrillation in the human heart results in global myocardial ischaemia. The aim of this study was to examine how ischaemia modulates the stability and period of re-entry in a computational model of human ventricular tissue. 2D tissue sheets were simulated using the monodomain equation with cellular electrophysiology described by the Ten Tusscher 2006 model. We modeled ischaemia by elevating [K+]o, reducing GCaL, and activating the ATP dependent K+ current. These changes acted to prolong the refractory period of tissue, to reduce conduction velocity, and to flatten restitution. In simulated normal tissue, re-entry had a period of between 230 and 300 ms, whereas in simulated ischaemic tissue the period was prolonged to around 400 ms. Elevating [K+]o to 8.0 mM converted unstable re-entry to stable re-entry. The mechanisms that sustain fibrillation in normal and globally ischaemic human ventricular tissue are likely to be different.
Keywords :
blood vessels; cellular transport; electrocardiography; haemorheology; muscle; physiological models; potassium; 2D tissue sheets; ATP dependent potassium current; K; Ten Tusscher 2006 model; cell model; cellular electrophysiology; computational model; conduction velocity; human heart; ischaemic ventricular tissue; monodomain equation; myocardial ischaemia; refractory period; time 230 ms to 300 ms; Biological system modeling; Cardiology; Computational modeling; Fibrillation; Heart; Humans; Mathematical model;
fLanguage :
English
Publisher :
ieee
Conference_Titel :
Computing in Cardiology, 2010
Conference_Location :
Belfast
ISSN :
0276-6547
Print_ISBN :
978-1-4244-7318-2
Electronic_ISBN :
0276-6547
Type :
conf
Filename :
5737939
Link To Document :
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