Electrocardiographic Change in VI, V5 and V6 Leads in Patients with Pulmonary Hypertension who are Receiving Effective Treatment

Introduction: Local conduction abnormalities at the right ventricular outflow tract epicardium (RVOT-Epi) are one of the potent arrhythmogenic substrates in the structural and non-structural heart diseases. However, how much delay at RVOT-Epi develops ventricular arrhythmias (VAs) is not quantitatively investigated. Methods: We constructed a three-dimensional human ventricular model (including approximately 20 million units) to investigate the role of conduction delay in the RVOT-Epi on initiation and maintenance of the ventricular tachyarrhythmias. Degree and location of conduction delay and its size in the RVOT-Epi could freely be changed by alteration of the gap junction (Gj) conductance. To compute activation sequence, simulation program was conducted on a supercomputer (SX-ACE, NEC, Japan). Results: No spontaneous arrhythmias occurred in the mild to moderate (Gj>15% of normal) conduction delay of 2.3 cm diameter in the RVOT-Epi, but in the severe delay (Gj=5%), propagation of the wave front was broken up into the multiple waves in the RVOT-Epi, thus maintained the VAs. The VAs inducibility is much easier in the larger delayed size (3.0 cm diameter). The wave fronts rotated around filaments that bent spontaneously and occasionally fragmented. Many filaments were located on the border between ventricular septum and RVOT-Epi. On the other hand, these findings could not be reproduced in the delayed conduction set at right ventricular free wall (RVFW). Conclusion: Arrhythmic substrate of RVOT-Epi depends on the size and degree of conduction delay, furthermore, these findings are only observed at the RVOT-Epi but not RVFW, suggesting that the structural vulnerability for VAs in RVOT-Epi as an arrhythmic risk.