## 3 Results  
Figure 2b shows the action potentials (AP) of endocardial cells, epicardial cells and midmyocardial cells which were simulated in the steady-state conditions. The APD of midmyocardial cells was the longest, the APD of epicardial cells was slightly shorter than that of endocardial cells [23]. Figure 2b also shows the APs of ischemic cardiomyocytes in the ICZ at different values of extracellular potassium concentrations. The APD of ischemic cardiomyocytes was significantly shortened and the resting potential increased. When the extracellular potassium concentration was 9 mm, 12 mm and 15 mm, respectively, APD shortened 49%, 55% and 66% and resting potential increased 15%, 23% and 32%, respectively [24]. Figure 3a shows the location of the ischemic tissue and the ventricular resting potential. The light blue area was ICZ, the dark blue area was BZ and the dark gray area was NZ. The ischemic tissue showed a high resting potential, which was caused by the increase of extracellular potassium concentration. Figure 3b shows the virtual electrocardiogram (ECG) results. The black curve and the red curve represented the lead II ECG under the normal ventricle and the ischemic ventricle, respectively. The red curve exhibited the ST depression and the T-wave elevation, which was consistent with the clinical ECG of subendocardial ischemia caused by distal occlusion of left anterior descending branch [25; 26]. In addition, the red curve also showed a wide QRS-wave, which was consistent with the clinical ECG of hyperkalemia [27]. So as to determine the effect of extracellular potassium concentration on arrhythmia vulnerability, this manuscript studied the relationship between extracellular potassium concentration and the size of vulnerability window of reentry. As presented in Figure 4, extracellular potassium concentration was found to have a significant effect on the size of the vulnerability window. For [K\({}^{+}\)]o = 9 mM, the vulnerability window was found to be 7 ms, with CIs originating reentry between 187 and 194 ms and the reentrant activation maintained 1900 ms. With the increase of extracellular potassium concentration, the vulnerability window also increased. For [K\({}^{+}\)]o = 12 mM, the vulnerability window increased  
Figure 2: (**a**) The position where S1 and S2 stimulation are applied; (**b**). Simulated action potentials under steady state for the endocardium cells, epicardium cells, midmyocardium cells and ischemic cardiomyocytes in the ICZ at three extracellular potassium concentrations. to a maximum of 12 ms (CIs between 181 and 193 ms). In this case, the reentry activity lasted for the longest time and ended spontaneously after 2100 ms. However, when the extracellular potassium concentration was further increased, the vulnerability window decreases. For [K\({}^{+}\)]\({}_{0}\) = 15 mM, the vulnerability window reduced to 6 ms (CIs between 191 ms and 197 ms) and the duration of reentrant activation was also reduced to 1100 ms. That is, in the range from 9 mM to 12 mM, the vulnerability window changed in the shape of a bell with the increase of extracellular potassium concentration, which was consistent with the results of animal experiments [20]. Figure 4: Coupling interval and vulnerability window size that could cause arrhythmia under different extracellular potassium concentration. Figure 3: (**a**) The location of the ischemic tissue and the ventricular resting potential; (**b**) Virtual electrocardiogram of normal ventricle (black) and virtual electrocardiogram of endocardial ischemia ventricle caused by left anterior descending branch occlusion (red). On the basis of the above work, this manuscript further analyzed the relationship between the mode of ventricular depolarization wave conduction and the location of the ischemic regions. After premature stimulation S2 was applied during the vulnerability window, the epicardium formed the macro-reentrant near the ischemic regions and the reentrant wavefront rotated around the ischemic regions.