UHF-ECG dyssynchrony during myocardial RV pacing
The shortest LVLWd was observed with mSp, follow by RV apical capture and was similar during RV lateral and anterior wall captures. Interestingly, the V5-8d, which reflects the speed of depolarization in the LV lateral wall, was similar during RV apical, anterior and lateral wall pacings, but in all of them significantly longer compared to mSp capture. This is likely a reflection of the differences in electrical wavefront propagation in the LV during RV pacing. RV apical wall capture relies mostly on cell-to-cell LV activation, contrary to RV septal capture, which also uses (after trans-septal signal transition) the left ventricular Purkinje system to activate the left ventricular mass [14]. Our results suggest that similar to RV apical capture, during both RV anterior and lateral wall captures, the left ventricular mass under V5-V8 is being activated mainly through slower myocardial conduction. However, the longer distance from the RV lateral wall and anterior wall to the LV lateral wall under V8 is responsible for the significantly longer time delay between the first activation and activation under the V8 compared to RV apical capture. This accented electrical LV dyssynchrony may be the cause of worse outcomes in patients observed in some clinical studies in which the pacing lead was placed in the RV anterior wall or lateral wall [3, 15]. The LVLWd during RV apical capture was only slightly longer compared to all mSp captures, but as was discussed before, significant differences exist between septal locations (RVIT vs RVOT). Noteworthy was that significant RVLWd, during RV apical pacing, was documented. It is a reflection of concomitant RV dyssynchrony during apical pacing; our observation was very similar to the one documented using an ECGi in patients with heart failure [16].