Re-entry in a model of ischaemic ventricular tissue

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 GCa_L, 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.