Relationship of Right Ventricular Apical Activation Time and V5/V6 RWPT for Rapid Recognition of Left Bundle Branch Area Pacing

Relationship of Right Ventricular Apical Activation Time and V5/V6 RWPT for Rapid Recognition of Left Bundle Branch Area Pacing | Authorea try { document.documentElement.classList.add('js'); } catch (e) { } var _gaq = _gaq || []; _gaq.push(['_setAccount', 'G-8VDV14Y67G']); _gaq.push(['_trackPageview']); (function() { var ga = document.createElement('script'); ga.type = 'text/javascript'; ga.async = true; ga.src = ('https:' == document.location.protocol ? 'https://ssl' : 'http://www') + '.google-analytics.com/ga.js'; var s = document.getElementsByTagName('script')[0]; s.parentNode.insertBefore(ga, s); })(); Skip to main content Preprints Collections Wiley Open Research IET Open Research Ecological Society of Japan All Collections About About Authorea FAQs Contact Us Quick Search anywhere Search for preprint articles, keywords, etc. Search Search ADVANCED SEARCH SCROLL This is a preprint and has not been peer reviewed. Data may be preliminary. 17 July 2025 V1 Latest version Share on Relationship of Right Ventricular Apical Activation Time and V5/V6 RWPT for Rapid Recognition of Left Bundle Branch Area Pacing Authors : Ryan Sanderson , Ram Amuthan 0000-0003-2904-6638 [email protected] , Mohammed Najeeb Osman 0000-0002-3205-6733 , Benzy Padanilam J , Anselma Intini , and Jayakumar Sahadevan Authors Info & Affiliations https://doi.org/10.22541/au.175277169.90022629/v1 418 views 148 downloads Contents Abstract Information & Authors Metrics & Citations View Options References Figures Tables Media Share Abstract Introduction: Confirming left bundle branch area pacing (LBBAP) during the procedure and reliably differentiating it from deep septal pacing (DSP) remains a challenge. The objective was to evaluate the utility of the relationship between right ventricular apical (RVA) activation timing and V5/V6 R-wave peak time (RWPT) in confirming LBBAP. Methods: This was a case series of five patients with varying degrees of conduction system disease and cardiomyopathy who underwent LBBAP at the Louis Stokes Cleveland Veterans Affairs Medical Center. During implantation, filtered bipolar RVA electrograms (EGMs) from the right atrial lead placed in the RVA for back up pacing with unipolar LBBAP lead EGMs were recorded alongside 12-lead ECG. RVA timing and V5/V6 RWPT were measured during stepwise lead advancement from RV septal positions to deep septal to LBBAP capture sites while varying the pacing output. Results: In all patients, pacing at progressively deeper septal positions led to increasing RVA activation time with decreasing V5/V6 RWPT. RVA activation on time with V5/V6 RWPT (“convergence”) or later than V5/V6 RWPT (“reversal”) while pacing at threshold was observed with successful LBBAP but not with DSP. These patterns were observed independent of underlying conduction system disease and/or cardiomyopathy. Conclusion: A ”reversal” or ”convergence” pattern between RVA activation and V5/V6 RWPT while pacing at threshold is a practical, real-time marker of LBBAP. This technique enhances procedural accuracy and may be integrated into standard implantation workflows without additional hardware. Larger studies are warranted to validate these findings and determine broader clinical applicability. Relationship of Right Ventricular Apical Activation Time and V5/V6 RWPT for Rapid Recognition of Left Bundle Branch Area Pacing Ryan Sanderson MD* 1,2 , Ram Amuthan MD* ², Mohammed Najeeb Osman MD 1,2 , Benzy J Padanilam MD, FACC, FHRS ³, Anselma Intini MD ², Jayakumar Sahadevan MD² ¹ Case Western Reserve University / University Hospitals Cleveland Medical Center, Cleveland, Ohio; ² Case Western Reserve University / Louis Stoked Cleveland Veterans Affairs Medical Center, Cleveland, Ohio; ³ Ascension St. Vincent Hospital, Indianapolis, Indiana *Ryan Sanderson MD and Ram Amuthan MD are co-first authors and contributed equally to the manuscript Financial support: None (all authors) Conflicts of Interest: None (all authors) Corresponding Authors: Ram Amuthan MD, and Jayakumar Sahadevan MD Louis Stokes Cleveland Veterans Affairs Medical Center, 10701 East Boulevard Cleveland, OH 44106. [email protected] Acknowledgments: We acknowledge Dr. Ivan Cakulev’s commitment to improving our understanding of conduction system pacing and for his critical appraisal of the manuscript Title: Relationship of Right Ventricular Apical Activation Time and V5/V6 RWPT for Rapid Recognition of Left Bundle Branch Area Pacing Introduction: Confirming left bundle branch area pacing (LBBAP) during the procedure and reliably differentiating it from deep septal pacing (DSP) remains a challenge. The objective was to evaluate the utility of the relationship between right ventricular apical (RVA) activation timing and V5/V6 R-wave peak time (RWPT) in confirming LBBAP. Methods: This was a case series of five patients with varying degrees of conduction system disease and cardiomyopathy who underwent LBBAP at the Louis Stokes Cleveland Veterans Affairs Medical Center. During implantation, filtered bipolar RVA electrograms (EGMs) from the right atrial lead placed in the RVA for back up pacing with unipolar LBBAP lead EGMs were recorded alongside 12-lead ECG. RVA timing and V5/V6 RWPT were measured during stepwise lead advancement from RV septal positions to deep septal to LBBAP capture sites while varying the pacing output. Results: In all patients, pacing at progressively deeper septal positions led to increasing RVA activation time with decreasing V5/V6 RWPT. RVA activation on time with V5/V6 RWPT (“convergence”) or later than V5/V6 RWPT (“reversal”) while pacing at threshold was observed with successful LBBAP but not with DSP. These patterns were observed independent of underlying conduction system disease and/or cardiomyopathy. Conclusion: A ”reversal” or ”convergence” pattern between RVA activation and V5/V6 RWPT while pacing at threshold is a practical, real-time marker of LBBAP. This technique enhances procedural accuracy and may be integrated into standard implantation workflows without additional hardware. Larger studies are warranted to validate these findings and determine broader clinical applicability. Key Words: Left bundle branch area pacing, V5/V6 R – wave peak time, Right ventricular apical activation timing, deep septal pacing, convergence, reversal Introduction Left bundle branch area (LBBA) pacing (LBBAP) has emerged in recent years as a preferred method of conduction system pacing. 1 This novel pacing technique has seen expanding indications over the past few years, including as a bail out or an alternative to cardiac resynchronization therapy (CRT). 2 During the implantation of LBBAP leads, it is essential to confirm conduction system capture, which can be challenging. LBBAP usually requires penetration of the lead tip electrode close to the left ventricular (LV) endocardial surface within the interventricular septum capturing the left bundle and or its fascicles. Various criteria have been used to differentiate LBBAP from deep septal pacing (DSP), however no single criterion has high sensitivity and specificity to confirm LBBA capture. 3,4 These are difficult to assess during the implantation procedure and therefore there is a need to develop criteria which can be easily appreciated during lead deployment. We present five cases using a two-lead technique using the relationship between the right ventricular (RV) apical (RVA) bipolar electrogram (EGM) activation time and the V5/V6 R Wave Peak Time (RWPT) to determine LBBAP independent of underlying conduction system and myocardial disease. Methods This is a case series of patients undergoing LBBAP at the Louis Stokes Cleveland Veterans Affairs Medical Center. All patients provided written informed consent for the procedure. All procedures were performed with 12 lead ECG and pacing lead EGMs displayed on the electrophysiology recording system. The right atrial lead was placed in the RVA for temporary back up pacing. LBBAP lead filtered and unfiltered unipolar EGMs with RVA lead filtered bipolar EGMs were displayed on the recording system. The apical position of the RVA lead was confirmed with fluoroscopy and paced QRS morphology. Left conduction system capture was confirmed according to the criteria described by guideline documents. 1,2 Successful LBBAP was defined as left conduction system capture which included both left bundle branch pacing and left fascicular pacing.DSP was defined as pacing from any septal location distinct from the RV aspect of the endocardium, but with no features of left conduction system capture. Case 1: LBBAP in patient with normal QRS duration and left anterior fascicular block in a structurally normal heart presenting with symptomatic high grade atrio-ventricular block (Figure1) Baseline ECG (a) demonstrated left anterior fascicular block (LAFB) narrow QRSd of 90ms with V6 RWPT of 33ms and time to RVa d from the earliest onset of surface QRS measured at 44ms. RV mid-septal position (b) was determined to be an optimal site for LBBAP by ECG morphology with a V6 RWPT of 110ms and time from pacing artifact to RVa d of 75ms. The lead was advanced in typical fashion to a position of DSP (c) with unchanged V6 RWPT at 110ms but with an increase in time from pacing stimulus artifact to RVa d measured at 91ms and accompanied by QRS morphology changes. The lead was then advanced further, and pacing was performed at threshold to demonstrate S-LBBAP (d) confirmed with an abrupt decrease in V6 RWPT, terminal R wave on V1, and stim – QRS latency. At this position a distinct ‘reversal’ pattern in the V6 RWPT was observed with a decrease in V6 RWPT to 78ms and an increase in time from pacing artifact to RVa d of 104ms. We recognized that the rS pattern on V6 may preclude accurate measurement of RWPT and thus we used lead I RWPT as has been previously described. The ‘reversal’ pattern was still observed. Case 2: LBBAP in patient with complete right bundle branch block and left anterior fascicular block in a structurally normal heart presenting with symptomatic high grade atrio-ventricular block (Figure 2) Baseline ECG (a) demonstrated right bundle branch block (RBBB) and LAFB wide QRSd of 161ms with V6 RWPT of 30ms and time to RVa d from the earliest onset of surface QRS measured at 43ms. The relatively early time to RVa d from the onset of surface QRS may indicate the presence of an atypical RBBB pattern supported by qR morphology on V1. RV mid-septal position (b) was determined to be an optimal site for LBBAP by ECG morphology with V6 RWPT measurement precluded by notching and time from pacing artifact to RVa d of 74ms. The lead was advanced in typical fashion to the position (c) with the loss of V6 notching and resultant V6 RWPT of 97ms accompanied by an increase in time from pacing artifact to RVa d measured at 91ms. The lead was further advanced to position (d) with an unchanged V6 RWPT, but with an increase in time from pacing stimulus artifact to RVa d measured at 110ms and QRS morphology changes of an increase in R wave amplitude on V1 with the development of subtle S wave on lead 1. This change in QRS morphology with an unchanged RWPT was characteristic of a transition from NS – LBBAP (c) to S – LBBAP (d). At position (d) with S – LBBAP while pacing at threshold, a distinct ‘reversal’ pattern was observed with the time from the pacing stimulus to the RVa d longer than V6 RWPT. Case 3: LBBAP in patient with complete left bundle branch block and left axis deviation in a structurally normal heart presenting with symptomatic high grade atrio-ventricular block (Figure 3) Baseline ECG (a) demonstrated left bundle branch block (LBBB) wide QRSd of 179ms and time to RVa d from the earliest onset of surface QRS measured at 48ms. Accurate measurement of V6 RWPT was precluded by the characteristic notching observed with LBBB. RV mid-septal position (b) was determined to be an optimal site for LBBAP by ECG morphology with V6 RWPT of 104 ms and time from pacing artifact to RVa d of 84 ms. The lead was advanced in typical fashion to position (c) with V6 RWPT of 99ms and time from pacing stimulus to RVa d measured at 80 ms. The lead was further advanced to position (d) with an unchanged V6 RWPT but with a change in the characteristic of the slope, an increase in time from pacing stimulus to RVa d measured at 106 ms, more prominent terminal R wave on V1, and other subtle QRS morphology changes. This change in QRS morphology with an unchanged V6 RWPT, and the development of Stim – QRS latency was characteristic of a transition from NS – LBBAP (c) to S – LBBAP (d). At position (d) with S – LBBAP and while pacing at threshold, a distinct ‘reversal’ pattern was observed with the time from the pacing stimulus to the RVa d longer than V6 RWPT. Case 4: LBBAP in patient with severe dilated ischemic cardiomyopathy and wide QRS duration non – specific intraventricular conduction delay as a bailout strategy for attempted CRT (Figure 4) Baseline ECG (a) demonstrated non-specific intraventricular conduction delay (IVCD) wide QRSd of 185ms and time to RVa d from the earliest onset of surface QRS measured at 24ms. Accurate measurement of V6 RWPT was precluded by mid QRS notching. RV mid-septal position (b) was determined to be an optimal site for LBBAP by ECG morphology with the time from pacing artifact to RVa d of 95ms and notches precluding measurement of V6 RWPT. The lead was advanced in typical fashion to position (c) with V6 RWPT of 144ms and time from pacing stimulus to RVa d measured at 121ms. The lead was further advanced to position (d) with a similar V6 RWPT of 138ms, an increase in time from pacing stimulus to RVa d measured at 133ms, and QRS morphology changes. Though the V6 RWPT was within measurement error between the two positions, position (d) had a steeper V6 RWPT slope, with similar steeper slopes also appreciated on leads V4 and V5. We also observed QRS morphology changes with the loss of notching and development of a prominent R wave on lead I and a change in precordial R wave transition from V4 to V3, both of which suggested earlier LV activation. This subtle but abrupt change in RWPT accompanied by QRS morphology changes was suggestive of a transition from DSP (c) to NS – LBBAP (d). At position (d) with NS – LBBAP and while pacing at threshold, a characteristic ’convergence’ pattern was observed with similar V6 RWPT and time from the pacing stimulus to the RVa d. We observed a sharp drop in the current of injury on the LBBAP lead unfiltered EGMs suggesting impending perforation, and thus we elected not to advance the lead any further. In this patient with severe cardiomyopathy and very wide QRS, we were unable to demonstrate any of the classical criteria for LBBAP. However, at position (d) the patient had an immediate improvement in hemodynamics with a mean blood pressure ranging between 75 – 80 mm Hg from a baseline range of 60 – 65 mm Hg. Case 5: LBBAP in patient with severe amyloid cardiomyopathy and complete heart block as a bail out strategy for attempted CRT (Figure 5) Baseline ECG (a) demonstrated incomplete LBBB QRSd 118ms with V6 RWPT of 52ms and time to RVa d from the earliest onset of surface QRS measured at 13ms. RV mid-septal position (b) was determined to be an optimal site for LBBAP by ECG morphology with V6 RWPT of 129ms and time from pacing artifact to RVa d of 48ms. The lead was advanced in typical fashion to position (c) with V6 RWPT of 110ms and time from pacing stimulus to RVa d measured at 44ms. The lead was further advanced to position (d) with a decrease in V6 RWPT measured at 96ms, an increase in time from pacing stimulus to RVa d measured at 104ms, and the development of R wave on V1 and S wave on leads V6/I. This change in QRS morphology with an abrupt decrease in V6 RWPT, and development of Stim – QRS latency was characteristic of a transition from DSP (c) to S – LBBAP (d). At position (d) with S – LBBAP and while pacing at threshold, a distinct ‘reversal’ pattern was observed with the time from the pacing stimulus to the RVa d longer than V6 RWPT. Discussion: We evaluated the relationship between RVA timing and V5/V6 RWPT in patients who underwent successful LBBAP, with both normal and abnormal conduction systems and substrates respectively. The main findings during unipolar pacing from the LBBAP lead tip are as follows: 1) Time to the RVA was shortest while pacing from the RV septum which progressively increased as the lead was advanced to the LV aspect of the septum with decreasing V5/V6 RWPT ;2) A sudden increase in timing to the RVA was observed with transition of QRS morphology from DSP or NS to S LBBAP; 3) The relationship (‘reversal’ or ‘convergence’ pattern) between the RVA timing and V5/V6 RWPT while pacing at threshold was useful for rapid and accurate intra-procedural confirmation of LBBAP. ; 3) The ‘reversal’ or ‘convergence’ patterns observed were independent of the presence or absence of conduction system disease and/or underlying cardiomyopathy. As far as we are aware, this is the first report describing the relationship between V5/V6 RWPT and RVA timing during LBBAP. Mechanistic rationale of right ventricular apical timing in confirming left bundle branch area capture: The findings of our case series are supported by the study by Ponnusamy et al 9 in which the authors used multi-electrode recordings to record from his bundle (HB), right bundle (RB) and the RV endocardial surface during LBBAP. They describe three patterns of RV activation. In type I pattern, the activation of the RV was mediated by retrograde activation of the HB followed by antegrade activation of the RB. This pattern was most observed in patients with normal QRS and intact retrograde HB activation. In their representative figure, local activation at the RVA occurred after V5 RWPT. This observation provides the framework for our ‘reversal’ pattern. Importantly, even in patients with no evidence of conduction system disease, activation of the RVA via the RB is delayed in comparison to the V5/V6 RWPT likely on account of the conduction time through the bundle branches. The delay in activation of the RVA in comparison to the RWPT can thus be taken as evidence of LBBAP. As illustrated in our examples above (Figures 1 and 5), during DSP the RVA timing is earlier than RWPT before the ‘reversal’ pattern is observed with S-LBBAP. The observation that the paced wavefront reached the RVA relatively late while utilizing the conduction system was intriguing. We speculate that this could be on account of conduction slowing or block as the wavefront curves across the acute angle between the LB and the RB. 10–13 However, though wavefront curvature mediated conduction slowing has been well described in the cardiac muscle, 12 it has not been specifically described in the His – Purkinje system. In type III pattern, the activation of the RV was suggested by the authors to be mediated by transseptal myocardial activation and/or possibly inter-bundle connections. In their representative figure, local activation at the RVA appears to have occurred at the same time as V5 RWPT. This provides a framework for our ’convergence’ pattern (Figure 4). Relationship between V6 RWPT and RVA timing during deep septal pacing and differentiation from non-selective left bundle branch area pacing: We recognize that unipolar pacing from a deep septal location may cause output dependent changes in V6 RWPT and time to RVA. Capture of a larger or a smaller area of septal myocardium could affect the relationship between V6 RWPT and time to RVA. In all our cases where we noticed a distinct change in timing during DSP, V6 RWPT was always later than the time to RVA. At high output DSP with capture of a larger area of the septal myocardium, there was a measurable decrease in both time to RVA and V6 RWPT when compared to low output DSP. Mechanistically, this can be explained by the paced wavefront reaching both the RVA and the LV apex faster at high output DSP. This phenomenon, in the absence of conduction system capture, did not affect the relationship between V6 RWPT and RVA timing. Figure 6 illustrates an example of this relationship. In contrast to this, with capture of both the septal myocardium and the left conduction system with NS – LBBAP, time to RVA can be earlier than V6 RWPT (Figure 3) possibly due to the multiple wavefronts activating the RVA (graphical abstract). However, with decreasing output and transition to S – LBBAP the relationship between V6 RWPT and RVA timing changes to the ‘reversal’ or ‘convergence’ pattern. This would not be the case with DSP. We illustrate plausible mechanisms of RVA activation and its relationship to V5/V6 RWPT during DSP and LBBAP in the graphical abstract. Clinical Implications: Observation of ‘reversal’ or ‘convergence’ pattern between the RVA and RWPT in V5/V6 suggests LBBAP and can be visualized easily by the operator during the procedure. The study can be incorporated into the procedural workflow without any additional leads or catheters. Importantly, these observations are independent of the presence or absence of cardiomyopathy and/or conduction system disease unlike the current criteria to establish LBBAP. Limitations: These are observations from a single center case series which limits the generalizability of our findings. In the absence of high-density mapping data, we can only postulate how the wavefront reaches the RV apex with LBBAP. It is also unclear how the RVA timing and its relationship to RWPT will be affected by direct RB or septal Purkinje network capture, though this has not been described with LBBAP to the best of our knowledge. While using our protocol to confirm LBBA capture, it is crucial to pace at threshold to be able to demonstrate the ‘convergence’ or ‘reversal’ relationship. As illustrated in Figure 3, during NS – LBBAP there was capture of the septal myocardium and hence the paced wavefront reached the RVA faster than V6 RWPT. The ‘reversal’ relationship was demonstrated only with S – LBBAP while pacing at threshold and with the loss of local septal myocardial capture. Conclusion: RVA activation on time with V5/V6 RWPT (‘convergence’) or later than V5/V6 RWPT (‘reversal’) while pacing at threshold is suggestive of LBBA capture rather than DSP. These patterns allow for rapid intra-procedural confirmation of LBBAP and are independent of underlying cardiomyopathy and or conduction system disease. Future studies are needed to validate our findings in a larger cohort of patients. References: 1. Burri H, Jastrzebski M, Cano Ó, et al. EHRA clinical consensus statement on conduction system pacing implantation: endorsed by the Asia Pacific Heart Rhythm Society (APHRS), Canadian Heart Rhythm Society (CHRS), and Latin American Heart Rhythm Society (LAHRS). Europace . 2023;25(4):1208-1236. doi:10.1093/europace/euad043 2. Chung MK, Patton KK, Lau CP, et al. 2023 HRS/APHRS/LAHRS guideline on cardiac physiologic pacing for the avoidance and mitigation of heart failure. Heart Rhythm . 2023;20(9):e17-e91. doi:10.1016/j.hrthm.2023.03.1538 3. Shengjie W, Xueying C, Songjie W, et al. Evaluation of the Criteria to Distinguish Left Bundle Branch Pacing From Left Ventricular Septal Pacing. JACC Clin Electrophysiol . 2021;7(9):1166-1177. doi:10.1016/j.jacep.2021.02.018 4. Jastrzębski M. ECG and Pacing Criteria for Differentiating Conduction System Pacing from Myocardial Pacing. Arrhythmia & Electrophysiology Review 2021;10(3):172–80 . Published online 2021. doi:10.15420/aer.2021.26 5. Huang W, Chen X, Su L, Wu S, Xia X, Vijayaraman P. A beginner’s guide to permanent left bundle branch pacing. Heart Rhythm . 2019;16(12):1791-1796. doi:10.1016/j.hrthm.2019.06.016 6. Wu S, Chen X, Wang S, et al. Evaluation of the Criteria to Distinguish Left Bundle Branch Pacing From Left Ventricular Septal Pacing. JACC Clin Electrophysiol . 2021;7(9):1166-1177. doi:10.1016/j.jacep.2021.02.018 7. Ponnusamy SS, Vijayaraman P. Electrocardiography guided left bundle branch pacing. J Electrocardiol . 2021;68:11-13. doi:10.1016/j.jelectrocard.2021.07.001 8. Ponnusamy SS, Vijayaraman P. Evaluation of Criteria for Left Bundle Branch Capture. Card Electrophysiol Clin . 2022;14(2):191-202. doi:10.1016/j.ccep.2021.12.011 9. Ponnusamy SS, Ganesan V, Ramalingam V, et al. Electrophysiologic characteristics and clinical correlation of right ventricular activation during left bundle branch area pacing (RV-LBBAP study). Heart Rhythm . Published online October 25, 2024. doi:10.1016/j.hrthm.2024.10.049 10. Syed FF, Hai JJ, Lachman N, DeSimone C V, Asirvatham SJ. The infrahisian conduction system and endocavitary cardiac structures: relevance for the invasive electrophysiologist. J Interv Card Electrophysiol . 2014;39(1):45-56. doi:10.1007/s10840-013-9858-7 11. Fast VG, Kléber AG. Role of wavefront curvature in propagation of cardiac impulse. Cardiovasc Res . 1997;33(2):258-271. doi:10.1016/s0008-6363(96)00216-7 12. Cabo C, Pertsov AM, Baxter WT, Davidenko JM, Gray RA, Jalife J. Wave-front curvature as a cause of slow conduction and block in isolated cardiac muscle. Circ Res . 1994;75(6):1014-1028. doi:10.1161/01.res.75.6.1014 13. Massing GK, James TN. Anatomical configuration of the His bundle and bundle branches in the human heart. Circulation . 1976;53(4):609-621. doi:10.1161/01.cir.53.4.609 Figures: Figure 1: Selective left bundle branch area pacing in patient with left anterior fascicular block and normal QRS duration demonstrating ‘reversal’ pattern. Each vertical panel (a) to (d) illustrates recordings of 12-lead ECGs with simultaneous bipolar EGMs from the RVa d during the deployment of the LBB lead. Displayed are recordings during (a) Baseline ECG; (b) RV mid-septal pacing; (c) DSP; and (d) S-LBBAP. All recordings are standardized with a sweep speed of 100 mm/s and signal amplification set to 2500, ensuring consistent temporal and amplitude comparisons across panels. Time scale is shown in the top left corner of panel (a). See text for explanation. EGMs = Electrocardiograms; RVa d = Right ventricle apex distal bipole; RV = right ventricle; DSP = Deep septal pacing; S-LBBAP = Selective left bundle branch area pacing. Figure 2: Selective left bundle branch area pacing in patient with complete right bundle branch block and left anterior fascicular block demonstrating ‘reversal’ pattern. Each vertical panel (a) to (d) illustrates recordings of 12-lead ECGs with simultaneous bipolar EGMs from the RVa d during the deployment of the LBB lead. Displayed are recordings during (a) Baseline ECG; (b) RV mid-septal pacing; (c) NS - LBBAP; and (d) S-LBBAP. All recordings are standardized with a sweep speed of 100 mm/s and signal amplification set to 2500, ensuring consistent temporal and amplitude comparisons across panels. Time scale is shown in the top left corner of panel (a). See text for explanation. EGMs = Electrocardiograms; RVa d = Right ventricle apex distal bipole; RV = right ventricle; NS – LBBAP = Non-selective left bundle branch area pacing; S-LBBAP = Selective left bundle branch area pacing. Figure 3: Selective left bundle branch area pacing in patient with complete left bundle branch block and left axis deviation demonstrating ‘reversal’ pattern. Each vertical panel (a) to (d) illustrates recordings of 12-lead ECGs with simultaneous bipolar EGMs from the RVa d during the deployment of the LBB lead. Displayed are recordings during (a) Baseline ECG; (b) RV mid-septal pacing; (c) NS - LBBAP; and (d) S-LBBAP. All recordings are standardized with a sweep speed of 100 mm/s and signal amplification set to 2500, ensuring consistent temporal and amplitude comparisons across panels. Time scale is shown in the top left corner of panel (a). See text for explanation. EGMs = Electrocardiograms; RVa d = Right ventricle apex distal bipole; RV = right ventricle; NS – LBBAP = Non-selective left bundle branch area pacing; S-LBBAP = Selective left bundle branch area pacing. Figure 4: Non – selective left bundle branch area pacing in patient with wide QRS non – specific intraventricular conduction delay and severe dilated cardiomyopathy demonstrating ‘convergence’ pattern. Each vertical panel (a) to (d) illustrates recordings of 12-lead ECGs with simultaneous bipolar EGMs from the RVa d during the deployment of the LBB lead. Displayed are recordings during (a) Baseline ECG; (b) RV mid-septal pacing; (c) DSP; and (d) NS-LBBAP. All recordings are standardized with a sweep speed of 100 mm/s and signal amplification set to 2500, ensuring consistent temporal and amplitude comparisons across panels. Time scale is shown in the top left corner of panel (a). See text for explanation. EGMs = Electrocardiograms; RVa d = Right ventricle apex distal bipole; RV = right ventricle; DSP = Deep septal pacing; NS – LBBAP = Non-selective left bundle branch area pacing. Figure 5: Selective left bundle branch area pacing in patient with severe cardiomyopathy and incomplete left bundle branch block demonstrating ‘reversal’ pattern. Each vertical panel (a) to (d) illustrates recordings of 12-lead ECGs with simultaneous bipolar EGMs from the RVa d during the deployment of the LBB lead. Displayed are recordings during (a) Baseline ECG; (b) RV mid-septal pacing; (c) DSP; and (d) S-LBBAP. All recordings are standardized with a sweep speed of 100 mm/s and signal amplification set to 2500, ensuring consistent temporal and amplitude comparisons across panels. Time scale is shown in the top left corner of panel (a). See text for explanation. EGMs = Electrocardiograms; RVa d = Right ventricle apex distal bipole; RV = right ventricle; S-LBBAP = Selective left bundle branch area pacing. Figure 6: Output dependent changes in timing during deep septal pacing in patient with structurally normal heart and baseline normal QRS duration of 90ms. All recordings are standardized with a sweep speed of 100 mm/s and signal amplification is set to 2500. Time scale is shown in the top left corner. The first two QRS complexes were obtained during high output DSP and the last two QRS complexes were obtained during low output DSP. V6 RWPT of 103ms and time to RVA of 93ms transition to a V6 RWPT of 117ms and time to RVA of 103ms. A distinct change in the RVa bipolar EGM was observed with the appearance of a signal shortly after the pacing spike on the LBBA F EGM which likely represents a local ventricular myocardial signal. Even with changes in V6 RWPT and time to RVA during DSP, the relationship between the RVA and V6 RWPT remained the same. DSP = Deep septal pacing; RWPT = R wave peak time; RVA = Right ventricular apex; RVa = Right ventricle apex distal bipole; LBBA F = Left bundle branch area filtered; EGM = Electrogram. Information & Authors Information Version history V1 Version 1 17 July 2025 Copyright This work is licensed under a Non Exclusive No Reuse License. Keyword clinical: implantable devices – physiologic pacing Authors Affiliations Ryan Sanderson UH Cleveland Medical Center View all articles by this author Ram Amuthan 0000-0003-2904-6638 [email protected] Louis Stokes Cleveland VA Medical Center View all articles by this author Mohammed Najeeb Osman 0000-0002-3205-6733 UH Cleveland Medical Center View all articles by this author Benzy Padanilam J Ascension St Vincent Hospital - Indianapolis View all articles by this author Anselma Intini Louis Stokes Cleveland VA Medical Center View all articles by this author Jayakumar Sahadevan Louis Stokes Cleveland VA Medical Center View all articles by this author Metrics & Citations Metrics Article Usage 418 views 148 downloads .FvxKWukQNSOunydq8rnd { width: 100px; } Citations Download citation Ryan Sanderson, Ram Amuthan, Mohammed Najeeb Osman, et al. Relationship of Right Ventricular Apical Activation Time and V5/V6 RWPT for Rapid Recognition of Left Bundle Branch Area Pacing. 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