# A Computer Simulation Research of Two Types of Cardiac Physiological Pacing
## 3 Results
### Hbp  
The clinical ECG data before and after treatment of LBBB with HBP are both shown in Figure 4a,b for the comparison with the simulated results [25]. The reference study implemented NSHBP on 12 patients with LBBB and corrected their LBBB with a narrowing of QRS duration by 30%. The clinical ECG data were achieved from a typical patient with ischemic cardiomyopathy. the QRS complex was 55 ms in lead II, and the left ventricular activation time (LVAT) was 32 ms. The R waves in leads I, II, V5, and V6, were wide and large. Leads V1 and V2 were rS-shaped, with a much smaller R-wave and a deeper and wider S-wave compared with those in normal states. The T waves were inverted in leads I, II, V5, and V6, and were upright in leads V1 and V2. Figure 4d shows the conduction process of the electrical activity in LBBB at several specific moments that corresponded to the synthetic ECG characteristics. We used the QRS complex in lead II as a reference for detailed explanations. The activation sequences at 48.8 ms illustrated that the excitation of the PMJ was corresponding to the onset of the R-wave. The activation sequences at 62 ms showed that the wavefront in the right ventricle had fused and began to conduct to the left ventricle, which corresponded to the first R-wave peak. At 68.6 ms, the wavefront had excited the Purkinje network in the left ventricle and the PMJ. This time point corresponded to the onset of the second R-wave. Finally, at 77 ms (R-wave peak), the wavefront in the left ventricle fused. After the HBP was implemented, the LBB restored its conduction function, and the left ventricle was excited normally. Figure 4e shows the QRS complex of the synthetic ECG under HBP (blue line) compared with the synthetic ECG of the normal state from Figure 3 (red line). The duration of the QRS complex was 40 ms, narrowed by 28%, similar to that of the normal state. In the real ECG of the normal state, the Q wave is a reflection of the earliest excitation that occurs on the left side of the septum. Most of the myocardium depolarize synchronously, and correspond to the R-wave. Part of the left ventricular basal myocardium eventually depolarize, and thus generate the S-wave [26]. The simulated activation sequences of HBP are shown in Figure 4f. There was no Q wave in the synthetic ECG because the basal segment of the septum was excited first as soon as the NSHBP began. The pacing stimulus and the onset of the QRS complex were not discrete on the synthetic ECG because the excitation was conducted both through the His-Purkinje system and the myocardium. At 48.8 ms, the PMJ in the two ventricles were excited that indicated the LBB restored conduction function. At 58 ms, the two ventricles were excited synchronously. This corresponded to the R-wave peak in the synthetic ECG of lead II and lead V5, meaning the LVAT was 28 ms. Given that the pacing excited the basal segment of ventricular septum at the earliest, the left ventricular basal myocardium and most parts of the ventricles depolarized at the same time at 62 ms, and the amplitude of the corresponding S-wave peak was not as large as that in the normal state. The synthetic ECG of the HBP correcting LBBB-1 corresponded with the real ECG both statistically and morphologically. The proportion of QRS reduction was similar (28% vs. 30%). The R waves had physiological shapes. In the LBBB results, the polarities of the T waves were opposite to those in normal states. After the completion of HBP, the T wave polarities were corrected. The results indicated that the simulation method reproduced the bundle branch block and conduction system pacing well. This further proved the validity of our model and method. The synthetic ECG of HBP correcting AVB is shown in Figure 4g, which is also very similar to that in the normal state. HBP excited the conduction system at the distal His-bundle, and resynchronized the ventricles.