Abstract
A 76-year-old woman with intermittent advanced atrioventricular block from a previous left septal accessory pathway and atrioventricular (AV) nodal slow pathway ablation for supraventricular tachycardia was referred for pacing. Her echocardiogram showed no structural abnormality and preserved left ventricular ejection fraction (LVEF). Left bundle branch area pacing (LBBaP) was achieved successfully, although frequent premature ventricular complexes (PVCs) were observed during the procedure. In the interrogation before discharge, asymptomatic ST-segment elevation on the precordial electrocardiogram (ECG) necessitated an emergent coronary angiography. No significant stenosis or spasm of coronary arteries was found, while left ventriculography revealed apical dyskinesis suggestive of Takotsubo cardiomyopathy. On closer inspection, frequent monomorphic PVCs developed after each pacing beat and formed a regular bigeminy pattern, indicating rapid LBB stimulation, and the facilitated slow conduction along the adjacent bundle branches induced the dual ventricular response. The resultant frequent desynchronized ventricular activation may have contributed to the stress for cardiac decompensation. Beta blocker was titrated to alter the critical time period matched for the repetitive activation pattern and to suppress sympathetic tension. The bigeminy was eliminated ultimately, and repositioning of the lead was avoided. The ventricular wall motion and LVEF recovered within months. This case highlights the importance of close observation of electrocardiographic monitoring after pacing. Despite the potential benefits for future cardiac function and lower pro-arrhythmic effect than routine pacing modalities, LBBaP may still be associated with new-onset arrhythmia and myocardial injury considering the baseline impairment of the electrical or anatomical substrate. Individualized management should be tailored according to specific scenarios.
Introduction
Conduction system pacing (CSP), in particular left bundle branch area pacing (LBBaP), has increasingly attracted interest as it preserves physiological left ventricular (LV) activation and generally has better pacing and sensing parameters than His-bundle pacing (HBP) (; Wang et al., 2022). At the same time, LBBaP has been shown to be associated with lower arrhythmia burden than biventricular (BiV) pacing (). Except for the establishment of physiological ventricular activation and effective resynchronization, ventricular pro-arrhythmia by epicardial coronary venous pacing used in conventional Bi-V cardiac resynchronization therapy (CRT) can be avoided during LBBaP (). However, we report here a rare case in which frequent “premature ventricular contractions” (PVCs) developed after LBBaP, and the so-called PVCs may have become a trigger for the stress of the cardiomyopathy.
Case description
A 76-year-old woman with intermittent syncope was referred for pacing. She underwent catheter ablation for supraventricular tachycardia 2 years prior. Advanced atrioventricular block (AVB) was recorded in the report from the left septal accessory pathway and atrioventricular (AV) nodal slow pathway ablation and partially resolved by cortisol infusion. At admission, her 12-lead electrocardiogram (ECG) demonstrated 2:1 AV conduction, occasional PVCs following a conducted sinus activation, and paroxysmal complete AVB. Echocardiogram showed no structural abnormality and preserved left ventricular ejection fraction (LVEF). LBBaP was achieved successfully by using a pre-shaped sheath (C315 His, Medtronic, Minneapolis, MN, USA) and a lumenless lead (SelectSecure 3830, Medtronic). Notably, increased PVCs were observed immediately after the lead implantation, mostly showing a regular pacing and PVC bigeminy pattern (Figure 1). As seen in the past implantation procedure, we took the PVCs as irritability of the myocardium. As no palpitation or chest pain symptoms were reported and with satisfactory pacing parameter measurements, as well as concerns about there being no better locations for qualified left bundle branch (LBB) capture, we made no further adjustment for the lead position. In the routine ECG before discharge, however, ST-segment elevation was noted in the precordial leads (Figure 1).
Figure 1
Diagnostic assessment, therapeutic intervention, and follow-up
Although no chest pain symptom could be recalled for this patient, acute coronary syndrome was suspected as widespread ST-elevation in the ECG was shown. Emergent coronary angiography was performed immediately, which showed no significant stenosis or spasm in her coronary arteries or branches, while left ventriculography showed apical dyskinesis and basal hyperkinesis suggestive of typical Takotsubo syndrome (TTS) (Figure 2). No evidence of inflammation and a persistent low-level increase of cardiac troponin I with no dynamic change also support the diagnosis.
Figure 2
TTS is commonly triggered by acute emotional or physical stressors. There are reports of TTS in the perioperative period or after implantation of cardiac implantable electronic devices (Yalta et al., 2026). A high sympathetic tone could drive both TTS and frequent PVCs. At the same time, the high burden of PVCs may become another form of stressor as a superimposed factor that could contribute to the TTS. Notably, PVCs occurring after the LBBaP were monomorphic, with consistent coupling intervals suggestive of the same origin and conduction routes, which is in support of the precursor role of PVCs rather than the consequence of TTS (majority of polymorphic PVCs). Upon review of the ECG and electrogram (EGM) recorded during the procedure, we noticed that the spontaneous PVCs before the lead implantation only occurred after the occasionally conducted native activations, but not during complete AVB. The PVCs after unipolar pacing beats showed a similar QRS morphology of the LBBB pattern to those of the spontaneous PVCs after the conducted sinus beats. The phenomenon suggests that the rapid activation of proximal LBB facilitated nearby impaired but slow conduction of His-RBB (right bundle branch), resulting in a dual activation of ventricles resembling to bigeminies. Bipolar pacing may have altered the exit of the slow activation and produced a similar precordial QRS pattern, but with a different frontal axis of the PVCs. Bipolar pacing may have also directly stimulated the RBB, resulting in a slightly earlier conduction through the RBB compared with unipolar pacing (Figure 3).
Figure 3
Another form of bigeminy with RBB-like PVCs provided evidence of an alternative dual activation introduced by LBBaP and facilitated slow conduction along the left anterior fascicular fiber (Figure 4).
Figure 4
Prior ablation-induced injury in multiple regions of the conduction system may have created a vulnerable environment for the multiple delays in the impulse conduction. Alternating bundle branch or fascicle activation with dual ventricular response and resultant frequent desynchronized ventricular activation may have contributed to the stress that induced cardiac dysfunction. The beta blocker was titrated to alter the critical time period matched for the repetitive activation pattern and to suppress sympathetic tension. The bigeminy was eliminated ultimately, and repositioning of the lead was avoided. The ventricular wall motion and cardiac function recovered within 4 months.
Discussion
We presented a rare case of dual bundle branch alternative activation-associated bigeminy and Takotsubo cardiomyopathy that occurred after a successful LBBaP procedure.
The patient was admitted for irreversible AV conduction block and symptomatic bradycardia. With the expected high percentage of ventricular pacing, physiological LBBaP was the preferred pacing modality for the potential protection of acute hemodynamic response, long-term synchronized and preserved LV function comparable to BiV pacing (; Wang et al., 2022). Successful capture of the LBB conduction system was demonstrated by typical RBBB morphology, a short and fixed peak time for the V6 R wave, and the LBB potentials in the EGM. However, the unexpected ST-elevation changes and the development of cardiac dysfunction were puzzling.
Although a unique risk of injury to the septal perforator arteries for LBBaP has been suggested, the absence of chest pain symptoms throughout the course made the possibility minimal. Diagnostic coronary angiography provided a direct denial demonstration. On the other hand, the frequent PVCs after the implantation raised concerns for PVC-induced cardiomyopathy presenting as an apical ballooning syndrome. In fact, cardiomyopathy induced by PVCs is mechanistically different from a tachycardia-mediated cardiomyopathy produced by regular ventricular tachy-pacing, with more severe LV systolic dysfunction due to the irregularity and dyssynchrony of the ventricles (Walters et al., 2018). The severity of the hemodynamic derangement associated with ectopic beats exhibits a dose effect on cardiomyopathy development (Walters et al., 2018). Although the majority of reports described cardiac dysfunction developing after a long time, continued PVC bigeminy after the procedure may have contributed to the rapid development of cardiac dysfunction.
On the other hand, we noted the significantly increased PVCs shortly after the device implantation that appeared to be triggered by pacing. Pacing-related pro-arrhythmia has been reported with conventional right ventricular (RV) pacing and LV epicardium (coronary sinus) pacing (; ; ). As the I-CLAS study showed that LBBAP led to fewer atrial and ventricular tachyarrhythmias than BiV pacing (), LBBAP-associated pro-arrhythmia has been increasingly reported in recent literature. One case described an electrical storm from monomorphic or pleomorphic ventricular tachycardia (VT) months after LBBaP, with the triggered PVC morphology suggestive of an origin from the proximal interventricular septum. The resolvent of the VTs required replacement of the LBBaP lead to routine RV endocardial pacing, upgrading to an implantable cardioverter defibrillator (ICD) device, and strengthened medication control (). Another case reported multiple episodes of VTs after LBBaP, attributed to the pacing stimulation and which necessitated removal of the LBBaP lead, upgrading of the device to CRT defibrillator (CRT-D), and ablation (). Both of the cases had structural heart disease, and LBBaP led to PVCs as triggers to initiate the VTs. Vijayaraman et al. presented an intra-procedural bundle branch reentry VT at the time of LBBaP lead implantation and eliminated it by BiV pacing afterwards (). The patient had cardiomyopathy and reduced LVEF. Recently, sustained bundle branch reentrant VT with two different morphologies was reported 1 month after LBBaP implantation in a patient without apparent structural heart disease. Repeated ablation at the lead location and repositioning of the lead to the RV septum comprised the final intervention for the VT (Zhang et al., 2026). Prior postulated mechanisms of pro-arrhythmia of pacing may be local irritability (), which is supported by a relatively higher incidence of VT occurring early after lead implantation. On the other hand, local fibrosis or scars provided a substrate for slow conduction and unidirectional conduction block and may lead to reentry. Pacing close to the critical region of slow conduction may have a pro-arrhythmic effect, known as pace-mapped induction of VT ().
Our presented case is in line with prior cases showing ventricular arrhythmia shortly after LBBaP, and the resultant PVCs appeared to be associated with the His–Purkinje system. However, our case is different from prior cases in that the so-called PVCs were not the direct consequence of LBBaP pacing, but facilitated slow conduction from the adjacent lesioned component of the conduction system by the rapid activation of LBB in an apparent structural normal heart. The dual bundle branch alternative activation was mechanically similar to the dual AV nodal non-reentrant tachycardias that happened in patients with AV nodal fast and slow pathway. In our case, the two different alternative activation modes of branches or fascicles suggested multiple impairments in the proximal conduction systems, which are assumed to be the complications of prior ablation. Notably, spontaneous “PVCs” before the pacemaker implantation only occurred after an occasional native conducted impulse, which also supports the pro-arrhythmic effect by stimulating the critical region of slow conduction. When we achieved the LBBaP successfully, each pacing stimulation acted as an initiation of dual fast and slow activation and created ventricular bigeminies. A significantly increased “PVC” burden may become the culprit for the exacerbation of cardiac dysfunction.
Titrated beta blockers and possible remodeling progress after the TTS may have changed the critical conditions for dual activations. From the patient’s perspective, she was fortunate because the arrhythmia was observed to have decreased and revision of the LBBaP lead was avoided.
Despite the favorable evolution of the course in our case, potential pro-arrhythmic risks of LBBaP remain a concern for future adverse outcomes. Considering that more patients with structural heart disease or significant conduction lesions may receive LBBaP as an important physiological pacing modality, our case stresses the need for careful observation of suspected new-onset arrhythmia during implantation and follow-up. For patients with a high burden of pacing-associated arrhythmia, the potential impact on cardiac function should be weighed against the benefits of CSP. Treatment strategies must be individualized for each patient.
Statements
Data availability statement
The original contributions presented in the study are included in the article/supplementary material. Further inquiries can be directed to the corresponding author.
Ethics statement
The studies involving humans were approved by Peking University First Hospital. The studies were conducted in accordance with the local legislation and institutional requirements. The participants provided their written informed consent to participate in this study. Written informed consent was obtained from the individual(s) for the publication of any potentially identifiable images or data included in this article. Written informed consent was obtained from the participant/patient(s) for the publication of this case report.
Author contributions
S-YC: Conceptualization, Data curation, Formal analysis, Investigation, Project administration, Writing – original draft, Writing – review & editing. YL: Investigation, Methodology, Writing – review & editing. L-TQ: Investigation, Methodology, Writing – review & editing. E-DC: Investigation, Project administration, Writing – review & editing. JZ: Investigation, Methodology, Supervision, Validation, Writing – review & editing.
Funding
The author(s) declared that financial support was not received for this work and/or its publication.
Conflict of interest
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Summary
Keywords
bundle branch block, case report, left bundle branch area pacing, Takotsubo cardiomyopathy, ventricular bigeminy
Citation
Chu S-Y, Li Y, Qi L-T, Chen E-D and Zhou J (2026) Left bundle branch area pacing induced dual bundle branches non-reentrant bigeminy and Takotsubo cardiomyopathy: a case report. Front. Physiol. 17:1915000. doi: 10.3389/fphys.2026.1915000
Received
21 June 2026
Revised
28 August 2026
Accepted
14 September 2026
Published
07 October 2026
Volume
17 - 2026
Edited by
Edward Joseph Vigmond, Université de Bordeaux, France
Reviewed by
Shota Ikeda, University of California, Los Angeles, United States
Ernest Lau, Belfast Health and Social Care Trust, United Kingdom
Updates
Copyright
© 2026 Chu, Li, Qi, Chen and Zhou.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Song-Yun Chu, cstellar@sina.com
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.