(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.