The importance of anisotropy in modeling ST segment shift in subendocardial ischaemia.
In this paper, a simple mathematical model of a slab of cardiac tissue is presented in an attempt to better understand the relationship between subendocardial ischaemia and the resulting epicardial potential distributions. The cardiac tissue is represented by the bidomain model where tissue anisotropy and fiber rotation have been incorporated with a view to predicting the epicardial surface potential distribution. The source of electric potential in this steady-state problem is the difference between plateau potentials in normal and ischaemic tissue, where it is assumed that ischaemic tissue has a lower plateau potential. Simulations with tissue anisotropy and no fiber rotation are also considered. Simulations are performed for various thicknesses of the transition region between normal and ischaemic tissue and for various sizes of the ischaemic region. The simulated epicardial potential distributions, based on an anisotropic model of the cardiac tissue, show that there are large potential gradients above the border of the ischaemic region and that there are dips in the potential distribution above the region of ischaemia. It could be concluded from the simulations that it would be possible to predict the region of subendocardial ischaemia from the epicardial potential distribution, a conclusion contrary to observed experimental data. Possible reasons for this discrepancy are discussed. In the interests of mathematical simplicity, isotropic models of the cardiac tissue are also considered, but results from these simulations predict epicardial potential distributions vastly different from experimental observations. A major conclusion from this work is that tissue anisotropy and fiber rotation must be included to obtain meaningful and realistic epicardial potential distributions.
Johnston
P R
PR
School of Science, Griffith University, Nathan, Queensland 41 11, Australia. P.Johnston@mailbox.gu.edu.au
Kilpatrick
D
D
Li
C Y
CY
D000818:Animals; D016880:Anisotropy; D004562:Electrocardiography; D006321:Heart / Q000503:physiopathology; D006801:Humans; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000175:diagnosis* / Q000503:physiopathology*