(3,18)
Moreover, restoration of ventricular synchrony by CRT resulted in
improved systolic function of LV and improved clinical outcomes.(19) This suggests that the abnormal
ventricular activation pattern during pacing may be the cause of LV
function deterioration. (20)
Based on the aforementioned studies regarding the consequences of RV
apical pacing on the heart and their effect on clinical outcomes, our
study investigated the effect of pacing of RV on global and regional LV
function using 2-D speckle tracking echocardiographic strain techniques,
in comparison to controls. In addition, we evaluated the change in
global LV longitudinal strain upon programming the DDD pacemaker from
AS-VP mode to AP- VP mode and to VVI mode.
When we measured the LV ejection fraction by M- Mode, we didn’t observe
any statistical difference between the controls and the patients during
AS-VP mode (group I) (P value > 0.05). on the contrary; we
found that LV ejection fraction measured by biplane 2D Simpson’s
technique was significantly lower in patients during AS-VP mode (group
I) than the controls (P value < 0.05). This can be explained
as EF by M Mode is measured across the basal septal and posterior walls
and is limited by excessive geometric simplification leading to
inaccurate values when abnormal wall motion is present especially in the
apical regions are present. (9) While
Simpson‘s method is based on the summation of the smaller volumes in
order to obtain the overall left ventricular volume which can provide a
better evaluation of left ventricular function especially in the
presence of abnormal motion of the septum during activation by RVA
pacing. (9)
Our results coincided with Burn et al who provided evidence
that mechanical dyssynchrony induced by RVA pacing was associated with
reduced LV function even when LV function was normal prior to pacing.(21) Pacing of RV acutely increases
intramural dyssynchrony in normal hearts. After chronic pacing,
intramural dyssynchrony persists and intraventricular dyssynchrony may
become evident. pacing induced LV dysfunction may be caused by
intramural dyssynchrony. (22)
By 2-D speckle tracking echocardiography; the patients during AS-VP mode
(group I) had statistically significant lower global LV longitudinal
systolic strain (LV LSS) when compared to the control (P Value
< 0.001). As regard regional LV longitudinal systolic strain;
most LV segments had significantly lower LSS in the patients during
AS-VP mode (group I) when compared to the controls. Moreover, the apical
segments showed the most significant difference in reduction (P value
< 0.001).
Similarly; Burn et al observed that LV longitudinal shortening
decreased acutely in a significant pattern in pacing of RV apex.
Affection of longitudinal strain were even more evident than
circumferential strain. Moreover, differences in strain were most
evident when measured at the apex and mid-ventricle, rather than at the
LV base. (21) Interestingly, the degree of
shortening in the early-activated regions of LV was lower than in the
other regions, causing a decrease in the global LV strain in pacing.(23) Liu et al studied the acute effects of
RVA on LV function using real-time three-dimensional echocardiography in
patients had sick sinus syndrome and they found that RVA pacing induced
interventricular and intraventricular mechanical delays that led to a
reduction of LV systolic function. (24)
Our results aligned with a study done by Liang et al ., who
showed that RV apical pacing resulted in a decrease in longitudinal
strain values near pacing sites (apical segments) compared to remote
regions (middle and base segments) indicating that RV apex pacing has an
unfavorable impact on the LV strain. (25)Chin et al used global longitudinal systolic strain as a
predictor of RVA pacing induced cardiomyopathy (PICM). In their study,
PICM was defined as LVEF decrease ≥10% from the preimplant EF that
results in LVEF <50%. They concluded that PICM was evidenced
by reduced global longitudinal strain values in patients with
subclinical LV systolic dysfunction. These patients warrant closer
follow-up with a lower threshold for biventricular pacing.