There were 2 distinct groups-those awaiting a CRT and those prior to substrate mapping and VT ablation. It is important to review the group of patients who were studied here. However, the findings did dispute Narula’s concept of longitudinal dissociation with no evidence of differential conduction within the His bundle with the presence of intact fibres distal to the proximal conduction disease. Based on left septal Purkinje activation, patients with LBBB morphology can be divided into two groups-those with delayed septal conduction (who have a broader QRS duration) and those with normal septal activation and delayed myocardial conduction (i.e., the group with IVCD or IPA) ( 8). This study therefore confirmed key findings from previous studies that the majority of patients with broad LBBB (and low ejection fraction) have conduction disease at level of proximal His Purkinje system, associated with delayed transseptal conduction time ( 8) and that this can be successfully reversed with HBP. Multiple electrocardiography (ECG) criteria were compared to look for any predictors of response to HBP, though mid QRS notching had a 100% negative predictive value (NPV), presence of conduction block offered the same NPV with a much higher positive predictive value (85% vs. The majority of the patients with intra-hisian block responded to HBP (94%), compared to 64% of those with block in left bundle and none of the patients with IPA. Those with conduction block either had block at the level of the His bundle at the left septum (72%) or proximally within the left bundle (28%). The cause of LBBB was found to be localized conduction block in 64% of cohort and no specific block but intraventricular conduction delay (IVCD) with intact Purkinje activation (IPA) in the remainder of the cohort. In this study, left septal mapping was performed for the first time, to assess the presence and the level of block and the response to temporary HBP. In a group of 85 patients, half of whom were referred for a device implant and half of whom were referred for substrate mapping for ventricular tachycardia (VT) ablation, high-density intracardiac mapping of the left septum was performed ( 7). have re-examined the mechanisms underpinning LBBB. These include higher pacing thresholds and increased lead revision rate ( 1). Technical and patient related factors prevent HBP in reversing LBBB in many individuals. Localised lesions within the His bundle can therefore cause LBBB, and by pacing near or at a slightly more distal location within the His bundle can overcome the LBBB, and normalize conduction. The mechanism of how HBP reverses BBB for long had been based on a key study by OS Narula which developed the concept of longitudinal dissociation with specific fibres within the His bundle committed to the left bundle with asynchronous conduction leading to left bundle branch block (LBBB) pattern ( 4). Outcomes in general, have been positive with significant success in this group albeit in small non-randomised studies. This has enabled HBP to be studied in patients requiring biventricular pacing (BVP) for cardiac resynchronisation therapy (CRT) including those with failed left ventricular (coronary venous) lead placements or those who have not responded to BVP ( 5, 6). Furthermore, in some patients who have underlying bundle branch block (BBB), HBP has been able to narrow the QRS and reverse the conduction abnormality ( 4). It has therefore been used in variety of pacing indications including pacing for bradycardia pacing and in patients undergoing atrioventricular (AV) node ablation ( 2, 3). His bundle pacing (HBP) has the unique ability to deliver and replicate normal infra-nodal conduction ( 1). Intracardiac Delineation of Septal Conduction in Left Bundle-Branch Block Patterns. Email: This is an invited article commissioned by the Section Editor Fang-Zhou Liu (Guangdong Cardiovascular Institute, Guangdong, China).Ĭomment on: Upadhyay GA, Cherian T, Shatz DY, et al. Professor of Medicine, Director of Cardiac Electrophysiology, Geisinger Heart Institute, Geisinger Commonwealth School of Medicine, MC 36-10, 1000 E Mountain Blvd, M.c. Correspondence to: Pugazhendhi Vijayaraman, MD.
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