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].