Background
Recently, the concept of left bundle branch pacing (LBBP) has emerged in clinical practice, in an attempt to prevent the deteriorating effects of right ventricular pacing (Vp).
Purpose
The aim of this study is to compare the effect of Vp on left ventricular (LV) dyssynchrony in patients with atrioventricular block (AVB) and preserved ejection fraction (EF), subjected to either LBBP or right ventricular septal pacing (RVSP).
Methods
Patients with AVB are randomized 1:1 to LBBP or RVSP. The effect of Vp is evaluated by echocardiographic indices of dyssynchrony, such as global myocardial work efficiency (GWE) and peak systolic dispersion (PSD). GWE represents the ratio of constructive work divided by the sum of constructive and wasted work [1]. Successful LBBP is defined by the presence of right bundle branch block paced QRS morphology in lead V1 and stim to LV activation time <75 msec [2]. No back-up right Vp lead was used in LBBP group.
Results
We conducted a preliminary analysis of the first 20 patients. Enrollment is still ongoing and total follow-up period is one year. We sought to investigate the acute effect of Vp on LV dyssynchrony 24 hours post procedure. Patients' baseline characteristics were similar in both groups and are presented in Table 1.
One crossover was noted from LBBP to RVSP group, due to high ventricular capture threshold during implant. Implantation time was increased in LBBP arm (130±17.4 min in LBBP versus 47.7±4.5 min in RVSP group, p=0.004). Left bundle branch potential was recorded in 3 out of 10 LBBP patients. No statistically significant difference was demonstrated in GWE between the two groups (91.3% in LBBP versus 87.4% in RVSP group, p=0.052). PSD was numerically shorter in LBBP (53.3 msec) versus in RVSP (63.6 msec), p=0.114. There were no complications during both the acute perioperative phase and the running period of the follow-up. Moreover, no acute ventricular threshold capture rise, or lead dislodgement has been observed in neither group.
The increased implantation time may be attributed to the more demanding technique, or the learning curve period required in the arm of LBBP. In the present analysis, a remarkable difference regarding GWE in favor of the LBBP group was demonstrated, although statistically not significant. However, even in this initial phase of the study, there is a trend of better LV synchrony and less wasted myocardial work in the LBBP group. The final difference of these indices will be assessed at the end of the one-year follow-up, when comparative results will be available.
Conclusion
LBBP is a novel, safe pacing method. Despite the longer procedural time and the risk of crossover, LBBP seems to offer better – without however statistical significance – LV synchrony even in the acute postoperative phase compared to RVSP. Longer follow-up studies are required to test whether LBBP compared to RVSP confers substantial clinical benefit.
Funding Acknowledgement
Type of funding sources: None.
Coronary bifurcation is defined by the European Bifurcation Consensus as a
coronary artery stenosis adjacent to the origin of a significant side branch. Its
anatomy is composed of 3 different segments: proximal main vessel, distal main
vessel and side branch. Coronary artery bifurcation lesions are encountered in
approximately 15–20% of all percutaneous coronary interventions and constitute
a complex subgroup of lesions characterized by lower procedural success rates and
higher rates of adverse outcomes. In recent years, a growing focus in the European
and Japanese bifurcation club meetings has been the emerging role of
intravascular imaging, in guiding successful bifurcation percutaneous coronary
interventions (PCI). In this review we will present the main ways optical
coherence tomography (OCT) can be used to improve outcomes during bifurcation
PCI.
We present the case of a 68‐year‐old man with a cardiac resynchronization therapy‐defibrillator Medtronic device implanted 3 years ago, admitted to our hospital due to a wide complex tachycardia with unexpected pacing spikes inside QRS complexes. Although that could be easily attributed to ventricular undersensing, more complicated mechanisms are involved, including the origin of the tachycardia, the parameters of the device, and the position of the device and the leads.
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