This manuscript adopted the cardiac modeling and simulation method to study the problems of physiological pacing in clinical application. A multiscale rabbit ventricular electrophysiological model was constructed. We simulated His-bundle pacing (HBP) treatment for left bundle branch block (LBBB) and atrioventricular block (AVB), and left bundle branch pacing (LBBP) treatment for LBBB by setting various moments of the stimulus. The synthetic ECGs and detailed electrical activities were analyzed. Our electrophysiological model accurately simulated the normal state, HBP, and LBBP. The synthetic ECG showed that QRS duration was narrowed by 30% after HBP correction for LBBB. For LBBB correction with LBBP, the synthetic ECGs of LBBP starting before 30 ms (if the end of atrial excitation is set as 0 ms) presented right bundle branch block (RBBB), and those of LBBP starting at 30–38 ms were synchronous, while those of LBBP starting after 42 ms possessed LBBB morphologies. The best pacing results were obtained when LBBP started at 34 ms. This manuscript verified the feasibility of the constructed ventricular model, and studied the physiological pacing mechanism. The results showed that HBP realized correction for AVB and high LBBB. The performance of LBBP can be improved by applying the stimulus within a specific period of time (0–8 ms) after atrial excitation.

Myocardial ischemia could induce arrhythmias such as ventricular tachycardia and ventricular fibrillation, leading to sudden death and other serious consequences. This manuscript adopted the cardiac modeling and simulation method to study the activity pattern of myocardial ischemia-related ventricular tachycardia and the effect of increased extracellular potassium concentration on arrhythmia vulnerability. A whole ventricular electrophysiological model of endocardial ischemia caused by distal occlusion of left anterior descending coronary artery was established. The simulation results suggested that the relationship between the vulnerability of ventricular arrhythmias and extracellular potassium concentration was bell shaped with a peak in susceptibility at 12 mM. This result was caused by the effect of extracellular potassium concentration on the dispersion of repolarization and the effective refractory period of cardiomyocytes. The extension of the effective refractory period was due to the electrical remodeling of the ventricle. Specifically, it was because of the delayed recovery of the I_Na current. In addition, the regularity of endocardial/epicardial reentrant pattern during non-transmural ischemia was also analyzed. The endocardium formed micro-reentrant, while the epicardium established macro-reentrant rotating around the ischemic regions provided a new idea for the determination of clinical ablation targets.