Unprecedented Complication of Left Bundle Branch Pacing

Abstract

Background

Left bundle branch pacing (LBBP) is increasingly used for physiological pacing in bradyarrhythmias and is generally safe, though rare complications may arise.

Case Summary

A 72-year-old woman with sick sinus syndrome underwent LBBP with multiple challenging lead placement attempts. One attempt caused resistance during lead withdrawal. Imaging later revealed a 1.5-mm ventricular septal defect, severe mitral regurgitation from anterior mitral leaflet prolapse, and severe tricuspid regurgitation. Histopathology showed valvular tissue on the lead, suggesting chordal entrapment and septal perforation during manipulation.

Discussion

This case highlights a unique, previously unreported combination of ventricular septal rupture and valvular injury after LBBP.

Take-Home Messages

Although rare, conduction system pacing can result in mechanical complications such as septal injury and mitral chordal entrapment. Monitoring of pacing parameters, including abrupt impedance changes or resistance during lead manipulation, may aid in early recognition of tissue entrapment and prevent structural damage.

Visual Summary

Left bundle branch pacing (LBBP) is increasingly being adopted as a more physiological pacing modality, especially in patients with symptomatic bradyarrhythmias. By directly engaging the conduction system, LBBP preserves ventricular synchrony and avoids some of the adverse effects associated with chronic right ventricular (RV) pacing. Although considered relatively safe, certain complications—though infrequent—have been reported, including ventricular septal perforation.

Take-Home Messages

• •Although rare, conduction system pacing can result in mechanical complications such as septal injury and mitral chordal entrapment.
• •Monitoring of pacing parameters, including abrupt impedance changes or resistance during lead manipulation, may aid early recognition of tissue entrapment and prevent structural damage.

Here, we describe a rare and, to the best of our knowledge, previously unreported complication of LBBP. During the procedure, the patient developed a ventricular septal defect (VSD), which was further complicated by entrapment of the mitral chordae in the conduction system pacing lead, resulting in structural mitral valve injury. This case underscores the importance of procedural vigilance and careful anatomical assessment during LBBP.

Case Presentation

A 72-year-old woman presented with episodes of syncope. Clinical evaluation, electrocardiogram, and Holter monitoring confirmed a diagnosis of sick sinus syndrome. Preprocedural echocardiography revealed a dilated left atrium with grade I diastolic dysfunction, preserved left ventricular (LV) systolic function (LV ejection fraction: 60%), and mild mitral regurgitation (MR) and tricuspid regurgitation with structurally normal valves. Informed consent was received from the patient.

Procedure

The patient was scheduled for left bundle branch area pacing dual-chamber (DDDR) pacemaker with a 49-cm, 9-F CPS Locator sheath and Tendril 2088TC stylet-driven lead (Abbott) under fluoroscopic guidance. Coronary angiography via right radial access showed normal coronary arteries. Subclavian venous access was obtained without difficulty. During the procedure, we went from the RV side of the septum. The CPS Locator sheath was going into the coronary sinus every time, even after multiple maneuvers, so we took 0.35 Teflon wire and negotiated the sheath into the RV with its support. We then progressed the sheath to the RV outflow tract, but while withdrawing, the sheath position was unstable, and it was again falling into the RV cavity. We removed the sheath and gave it an extra bend manually, then took it over the wire once again. The CPS Locator sheath was taken below-upwards slowly over the Teflon wire support, and during the fourth attempt, we obtained a good fluoroscopic position. We took the stylet-driven lead inside the sheath after obtaining a positive lead II and inferior lead discordance. After 8 turns, deep septal pacing was achieved, with a current of injury (COI) of 26 mA and impedance of 764 Ω. A few additional rotations were made under fluoroscopy, after which the impedance abruptly dropped to 368 Ω and COI to 7 mA, suggesting perforation into the LV cavity. An attempt was made to retract the lead using counterclockwise rotation, but resistance was encountered, and the lead could not be extracted, even with considerable force (Figure 1). The sheath was telescoped over the lead up to the helix tip, and with careful manipulation, the lead was successfully removed. Notably, it came out with a sizable amount of attached tissue (Figure 2). A new conduction system pacing lead was implanted at a different site, with satisfactory pacing parameters. Final pacing parameters were satisfactory: pseudo–right bundle branch block pattern in V₁, V₁ to V₆ R-wave peak time difference of 46 ms, early R/S transition, and LV activation time of 68 ms. Atrial lead placement and wound closure were uneventful. Postprocedural electrocardiogram showed a QRS duration of 118 ms (Figure 3A).

Figure 1.

Conduction System Pacing Lead Stuck in Cardiac Tissue

Figure 2.

Tissue Retrieved From Conduction System Pacing Lead

Figure 3.

Postprocedural Electrocardiogram and 2-Dimensional Echocardiography

(Top Left) Post-procedural electrocardiogram. (Top Right) Two-dimensional echocardiography parasternal short-axis view showing septal rupture. (Bottom Left) Two-dimensional echocardiography apical 4-chamber view (Bottom Right) apical 4-chamber (zoomed) view showing the ventricular septal defect.

Postprocedural 2-dimensional echocardiography revealed a 1.5-mm VSD with moderate to severe MR (Figure 3B). Repeat echocardiography the following day confirmed the VSD and revealed moderate to severe eccentric MR. Floating tissue over the anterior mitral leaflet suggested chordal rupture, likely due to mechanical entrapment by the lead during extraction (Figure 4). The patient remained asymptomatic and hemodynamically stable over the next 48 hours. She was discharged in stable condition with an angiotensin-converting enzyme inhibitor and a low-dose diuretic. Histopathology of the extracted tissue revealed fibromuscular tissue, consistent with chordae tendineae. The middle image in Figure 5 shows rows of collagen bundles and few elastic fibers. It is avascular and is lined by endothelium; all of these features are suggestive of chordae tendineae. Along with this, the absence of cells disposed in syncytial interconnecting fibers with oval nuclei (ie, myocardial fibers) differentiates it from the papillary muscle.

Figure 4.

Floating Tissue Over Anterior Mitral Leaflet (Suspected Chordal Rupture) and Subsequent Mitral Regurgitation

Figure 5.

Histopathological Section of the Tissue Caught on the Helix of the Lead Showing Fibromuscular Swirl (Suggestive of Chordae Tissue)

Hypothesis

Although initial parameters suggested appropriate septal engagement, it is likely that the lead traversed into the LV cavity and simultaneously entrapped mitral chordal tissue. Further manipulation led to chordal rupture and damage to the mitral valve apparatus. The patient's pre-existing dilated left atrium may have mitigated the clinical expression of acute volume overload.

Discussion

LBBP has gained traction as a superior physiological pacing approach compared to RV pacing. Yet, with increasing adoption, understanding its associated procedural risks becomes imperative.

Epidemiology of septal perforation in LBBP

Septal perforation is a recognized complication of LBBP. The MELOS study, a multicenter European registry involving 2,533 patients, reported an acute perforation rate of 3.67% and a delayed perforation rate of 0.08%.¹ Despite improvements in procedural technique and lead design, pacemaker lead placement has a 3% to 9% complication rate, largely owing to lead displacement, myocardial perforation, and pneumothorax.² Another study observed septal perforation during lead deployment in 14.1% of patients, emphasizing the need for vigilance during the procedure.³

Mechanisms of injury

The transseptal approach of LBBP necessitates deep penetration of the interventricular septum. Factors such as multiple lead positioning attempts, operator experience, and patient-specific anatomical variations can increase the risk of complications.⁴ In our case, various anatomical factors associated with septal anatomy, such as decreased thickness or scarring, could have played a detrimental role. Also, lead factors, such as the sturdiness of the lead, can also be implicated. Additionally, inadvertent entanglement of the lead with mitral valve chordae could explain the subsequent valvular injuries. Another mechanism by which the septal and valvular apparatus were injured could be the burrowing of the sheath until the lead tip, which was stuck. This was done to try and manipulate the lead to come out but might have contributed to the persistence of VSD. Hence, we advise against such manipulation to avoid any structural complications.

Valvular injury: an overlooked complication

Although septal perforations are documented, direct mitral valve injury during LBBP has not been reported. Lead-induced chordal injury may result from mechanical shearing or torsion. Our finding of valvular tissue on the retrieved lead confirms this as the most plausible etiology. Such injuries, while rare, can result in clinically significant MR. While septal perforations are documented, valvular injuries, particularly involving the mitral and tricuspid valves, are almost unreported. The mechanical trauma from lead manipulation can damage valvular structures, leading to regurgitation. In our patient, the histopathological finding of valvular tissue on the lead supports this mechanism. Entrapment of active fixation leads in cardiac tissue is usually resolved by counterrotation and gentle traction, which was tried but failed in our case. Another novel technique described by Seow⁵ is the use of electrocautery delivered at the distal pin tip to cause microablation of the tissue in which the lead is entrapped. But the use of electrocautery, even a short burst, can lead to further damage if the lead tip is trapped in a valvular structure, as was suspected in our case.

Clinical outcome

Despite moderate to severe MR and VSD, the patient remained stable. The compensatory capacity of her dilated left atrium may have buffered acute symptoms. Long-term monitoring remains crucial to assess MR progression or development of LV volume overload.

Preventive strategies

• •Preprocedural imaging: Use of echocardiography or cardiac magnetic resonance imaging to assess septal anatomy and thickness can be helpful in high-risk patients.⁶
• •Intraprocedural monitoring: Sudden changes in impedance or COI should trigger reassessment.
• •Operator training: Adequate training, fluoroscopic experience, and gentle manipulation are vital to avoid complications.
• •Avoiding excessive rotations: Once optimal thresholds and COI are achieved, avoid additional rotations that may breach septal integrity.

Conclusions

This case illustrates a rare but important complication of LBBP involving ventricular septal rupture and mitral valve apparatus injury. It reinforces the importance of close procedural monitoring, careful technique, and a high index of suspicion for atypical resistance or postprocedural valvular pathology. As LBBP becomes more common, documenting and sharing such complications is essential to refine best practices and improve patient safety.

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Visual Summary.

Timeline of Case Presentation

Time	Events
Day 0 (presentation)	A 72-year-old woman presented with recurrent syncope. ECG and Holter monitoring confirmed sick sinus syndrome. Baseline echocardiography showed preserved LVEF (60%) with mild mitral and tricuspid regurgitation and structurally normal valves.
Day 1 (procedure)	The patient underwent LBBAP using a St Jude CSP DDDR pacemaker.
During lead placement	Deep septal pacing was initially achieved. Additional lead rotations resulted in an abrupt drop in impedance and current of injury, raising suspicion of left ventricular cavity perforation.
Intraprocedural complication	Counterclockwise lead rotation for retraction encountered marked resistance. The lead could not be withdrawn with gentle traction. The sheath was telescoped over the lead, allowing successful removal. A sizable amount of tissue was noted attached to the extracted lead.
Reimplantation	A new CSP lead was implanted at an alternative septal site, with satisfactory pacing parameters.
Postprocedure imaging	Echocardiography revealed a 1.5-mm VSR, moderate to severe mitral regurgitation, and findings suggestive of anterior mitral leaflet injury.
Day 2 (repeat imaging)	Repeat echocardiography confirmed the VSR and eccentric mitral regurgitation. Floating tissue over the anterior mitral leaflet suggested chordal rupture.
Hospital course	The patient remained asymptomatic and hemodynamically stable. Conservative management was pursued.
Day 3 (discharge)	The patient was discharged in stable condition on medical therapy.
Histopathology	Histopathological analysis of the retrieved tissue demonstrated fibromuscular tissue consistent with chordae tendineae.

CSP = conduction system pacing; ECG = electrocardiogram; LBBAP = left bundle branch area pacing; LVEF = left ventricular ejection fraction; VSR = ventricular septal rupture.