A case report of functional LV septal pacing

1. Clinical scenario

A 73-year-old male with ischemic heart failure with reduced ejection fraction and a history of paroxysmal atrial fibrillation underwent left bundle branch-optimized cardiac resynchronization therapy (LOT-CRT) implantation (Medtronic Serena MRI Quad W4TR05; Medtronic Secure Select 3830 LBB lead; Medtronic Attain Stability Quad 4798 LV lead), combined with Bachmann bundle area pacing (BBAP, Medtronic Secure Select 3830 lead). The indication was a symptomatic alternating right- and left bundle branch block (RBBB and LBBB respectively). The pre-implantation ECG showed sinus rhythm with a RBBB and left anterior fascicular block (LAFB).

To gain further insight of the level of conduction disease, temporary high-output His-bundle pacing was performed, which demonstrated correction of the RBBB and LAFB. Subsequently, the left bundle branch (LBB) pacing lead was implanted at a basal site, approximately 1.5cm distal to the His-bundle. Lead screwing through the septum was performed until a sudden drop in the amplitude of the myocardial current of injury was observed, consistent with reaching the left ventricular (LV) subendocardial area [1]. Decremental threshold testing was then performed to evaluate conduction system capture [2].

Criteria consistent with conduction system capture were an r’ pattern in lead V1 and a transition during decremental output pacing (1.6V@0.5ms) (Fig. 1). V6 R-wave peak time (V6RWPT) was 84 ms, and V6-V1 interpeak interval was 37 ms before the transition. In addition, a proximal left bundle branch potential was recorded at 48 ms before the onset of the QRS complex during intrinsic rhythm.

Fig. 1.

(A) QRS morphology transition during decremental output pacing, with shortening of V6 R-wave peak time (V6RWPT; 84 to 76 ms), an increase in the V6-V1 interpeak interval (37 to 80 ms) and a leftward axis shift. The intracardiac electrogram (LBBA lead – red) demonstrates a discrete electrogram after the transition. (B) Left bundle branch potential to QRS onset interval of 48 ms during intrinsic rhythm. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

1.1. Question

How should this output-dependent QRS transition be described and classified (Fig. 1)? Why does the V6 R-wave peak time appear shorter after the transition? How can the relatively wide QRS with leftward/superior axis and RBBB morphology be explained despite a long LBB potential-to-QRS onset interval of 48 ms? How can it be explained that the QRS axis and morphology change so considerably with the QRS transition?

2. Explanation

During LBB area (LBBA) lead implantation, careful evaluation of the 12-lead ECG is important to differentiate between different levels of conduction system capture. During decremental output pacing, a single transition from non-selective LBB pacing (nsLBBP; simultaneous capture of the LBB and septal myocardium) to either (i) selective-LBBP (sLBBP; loss of myocardial capture), or (ii) left ventricular septal pacing (LVSP; loss of conduction system capture) may be observed [2].

2.1. Classification of the output-dependent QRS transition and interpretation of the apparent V6 R-wave peak time shortening

In the present case, temporarily high-output His-bundle pacing (HBP) corrected both the RBBB and the LAFB (Fig. 2A and C). During LBBP, a QRS morphology transition occurred at 1.6V@0.5ms (Fig. 1). At higher output, V6RWPT was 84 ms and the V6-V1 interpeak interval 37 ms, with an intermediate QRS axis. When output was reduced to 1.5V@0.5ms, lead V1 changed from a QR-to R-wave morphology, coinciding with a complete leftward/superior QRS axis shift resembling baseline QRS (Fig. 2A, B, 2E) and a marked prolongation of the V6-V1 interpeak interval to 80 ms (Fig. 1). Although V6RWPT appeared near preserved (76 ms), this likely underestimated true LV activation because lead V6 developed an rS configuration. In this situation, RWPT in lead I is more reliable and was longer after the transition, indicating delayed LV activation (Fig. 2A) [3]. Importantly, following the transition the intracardiac electrogram demonstrated a discrete local ventricular component (Fig. 1A; indicated with red arrows), supporting selective conduction system capture after loss of myocardial capture and thus a transition from nsLBBP to sLBBP in this case (Fig. 2A, D, 2E) [2].

Fig. 2.

(A) 12-lead ECGs with lead V5 repositioned to the V8 location, shown during baseline intrinsic rhythm, His bundle pacing, non-selective left bundle branch pacing, and selective-left bundle branch pacing; (B-E) Schematic representation of ventricular activation during (B) Baseline intrinsic conduction; (C) His bundle pacing; (D) non-selective left bundle branch pacing (E) selective-left bundle branch pacing. Abbreviations: HB(P) = His bundle (pacing); LAF = left anterior fascicle; LBB = left bundle branch; LPF = left posterior fascicle; nsLBBP = non-selective left bundle branch pacing; RBB = right bundle branch; RWPT = R-wave Peak time; sLBBP = selective – left bundle branch pacing.

2.2. Explanation of the relatively wide QRS and leftward axis despite a long LBB potential-to-QRS onset

The pronounced axis shift could be misinterpreted as isolated left posterior fascicular pacing (LPFP) when judged from the surface ECG alone. However, an LBB potential preceding QRS onset by 48 ms during intrinsic rhythm (Fig. 1B) argues against selective LPFP and instead supports more proximal LBB (trunk) capture, as fascicular pacing is associated with much shorter potential-to-QRS intervals (<25 ms) [4]. This LPFP-like axis during sLBBP is also consistent with the patient's intrinsic conduction disease. In baseline RBBB with LAFB, anterograde conduction propagates via the posterior fascicle; selective capture of the LBB trunk in the setting of anterior fascicule block reproduces a similar activation sequence, leading to an LPFP-like axis (Fig. 2A, B, 2E).

2.3. Mechanism of the marked QRS axis and morphology change across the QRS transition

Although a single transition is typically observed during decremental output pacing, it has been shown that multiple transitions may occur with advanced conduction system disease and/or differential recruitment of other components (e.g. individual fascicules or the RBB) [1]. In our case, careful 12-lead ECG analysis demonstrated only one discrete transition, without stepwise morphology transitions suggestive of sequential loss of additional fascicular capture. This argues against high-output recruitment of an additional fascicular component and instead supports that output reduction resulted in loss of septal myocardial capture with preserved conduction system capture (i.e. nsLBBP to sLBBP). Accordingly, the intermediate axis at higher output is best explained by concomitant septal myocardial capture rather than additional capture of the anterior fascicle, which would be expected to produce an additional transition during decremental output pacing.

This nsLBBP to sLBBP transition also clarifies the mechanism of ventricular activation during nsLBBP. Despite confirmed conduction system capture, LV activation was slower during sLBBP than during nsLBBP, as reflected by longer limb-lead RWPTs (Fig. 2A). Because the only additional substrate stimulated during nsLBBP is LV septal myocardium, the shorter activation times imply that the dominant activation wavefront was myocardial rather than conduction system mediated. We therefore propose that the higher output configuration is best described as functional LVSP rather than nsLBBP: conduction system capture is present, but concomitant septal myocardial capture largely determines LV activation timing and QRS axis. Moreover, in this setting, a hypothetical transition from nsLBBP to ‘true’ LVSP (loss of conduction system capture with preserved septal myocardial capture) might not lead to a distinct QRS morphology transition, because the predominant myocardial activation pattern would remain unchanged.

3. Final programming

Bachmann bundle area pacing (BBAP) was performed as described by Lustgarten et al., resulting in shortening of the P-wave duration from 152 ms during intrinsic rhythm to 92 ms during BBAP, with preservation of a normal P-wave axis (Fig. 3A) [5]. Given that the narrowest QRS complex was obtained with nsLBBP, the coronary sinus lead was programmed off. The device was programmed in DDD mode with BBAP and nsLBBP only, using a paced AV-delay of 130 ms (Fig. 3B).

Fig. 3.

(A) 12-lead ECG demonstrating P-wave duration of 152 ms during intrinsic rhythm and shortening to 92 ms during Bachmann bundle area pacing. (B) final paced ECG in DDD mode with Bachmann bundle area pacing and non-selective left bundle branch pacing only, using a paced AV delay of 130 ms. Abbreviation: BBAP = Bachmann bundle area pacing.

4. Conclusion

Careful 12-lead ECG assessment during conduction system pacing is essential to define capture type [2]. In the present case, an output-dependent QRS morphology transition with leftward/superior axis change during LBBP mimicked isolated posterior fascicular pacing on the surface ECG. However, a long LBB potential-to-QRS interval supported proximal LBB (trunk) capture rather than true fascicular pacing. This axis shift was not explained by higher-output recruitment of additional conduction system components, but by loss of septal myocardial capture during the transition of nsLBBP to sLBBP, which unmasked slower conduction system-mediated LV activation. Accordingly, the higher-output state is best described as functional LVSP rather than nsLBBP, in which concomitant septal myocardial capture predominantly determines LV activation and QRS axis.

Editorial commentary (Haran Burri)

This case nicely illustrates the complexities of LBBAP ECG interpretation. There is no doubt that selective conduction system capture occurred with decrementing pacing output, due to the marked transition in QRS morphology, splitting of the intracardiac electrogram, and potential-V6RWPT equaling the stimulus-V6RWPT (this last criterion was not reported in the text but can be confirmed from figure 1). What is surprising is that with non-selective capture, the V6RWPT is shorter than with selective capture, whereas it would be expected to be identical. The authors provide the elegant explanation that this was due to slow conduction via the conduction system, meaning that with non-selective capture, myocardial activation dominated and resulted in functional LVSP.

As an analogy, conduction via the normal conduction system is similar to driving on the highway, whereas myocardial activation is more akin to driving on a country road to reach the same destination (the V6 electrode). The journal usually takes less time via the highway, unless: 1) there is a traffic jam on the highway with faster traffic via the country road or 2) the country road is a shortcut compared to the highway. In the present case, the duration of the fascicular potential to QRS onset was very long (48ms, instead of <25ms), indicating slow conduction.

Other examples of unusual findings with LBBAP may be found in the literature, for those readers who wish to dig deeper [6], [7], [8].

Informed consent

Written informed consent for publication of clinical details and electrocardiograms was obtained from the patient. All identifying information has been removed.

Authors’ contributions

All authors participated in writing and approved the final manuscript.

Ethical statement

Informed consent was obtained for publication of this case.

Declaration of competing interest

J. van Koll: no conflicts of interest. J. Luermans: consultancy agreement Medtronic. Research grant Medtronic ((all fees paid to institute)). J. Joza: holds an investigator-initiated external research grant from Medtronic, grants from Canadian Institutes of Health Research and Heart and Stroke Foundation and has consultancy agreements with Medtronic and Abbott. K. Vernooy: research/educational grants from Biosense Webster, Abbott, and Medtronic (all paid to institute), as well as from the Dutch Heart Foundation, the Moller Foundation and Dutch Scientific Organization (NWO), and is a consultant for Medtronic, Philips, Abbott, and Boston Scientific (all fees paid to institute).