Septal Radiofrequency Ablation for Sigmoid Ventricular Septum-Related Dynamic Obstruction: First Mechanistic Evidence of Left Bundle Branch Block as a Therapeutic Collaborator

Technical Summary: Septal Radiofrequency Ablation for Sigmoid Ventricular Septum-Related Dynamic Obstruction

Problem Statement
Sigmoid ventricular septum (SVS), characterized by basal septal thickening and a reduced aortoseptal angle, can induce dynamic left ventricular outflow tract obstruction (LVOTO) during stress via systolic anterior motion (SAM) of the mitral valve. While medical therapy is the first-line treatment, some patients remain refractory. Established interventions like surgical myectomy and alcohol septal ablation face limitations in SVS cases due to the thinner mid-septum and lack of suitable septal perforators. Although radiofrequency ablation (RFA) has been utilized for septal reduction in hypertrophic obstructive cardiomyopathy, its application in SVS is limited to only two prior reports, and the specific mechanisms of action, particularly regarding iatrogenic conduction disturbances, remain poorly understood.

Methodology
This study presents a case report of a 77-year-old woman with symptomatic dynamic LVOTO secondary to SVS who failed medical therapy. The patient underwent endocardial RFA of the basal septum. The procedural endpoint was defined as the induction of a new-onset complete left bundle branch block (CLBBB) on surface electrocardiography.

The study employed multimodality imaging to evaluate the mechanistic effects of the ablation:

• Dobutamine Stress Echocardiography (DSE): Performed pre- and post-ablation to assess LVOT gradients and SAM.
• Blood Speckle Imaging (BSI): Used to visualize flow dynamics, specifically looking for systolic vortices and laminar flow restoration.
• Strain Analysis: Measured regional contractility, time-to-peak strain, and post-systolic index (PSI). To account for inter-study variations in heart rate and loading, the basal inferior wall (INF) was used as an internal reference to compare changes in the basal anterior septum (ANT_SEPT).

Key Results

• Pre-Ablation Status: Baseline echocardiography showed no resting obstruction. However, DSE (20 µg/kg/min) provoked severe obstruction with a peak gradient of 210 mmHg, significant SAM, and a large systolic vortex on BSI. Strain analysis revealed hypercontractility of the basal anterior septum (−29%) with synchronous contraction relative to the inferior wall.
• Procedural Outcome: The RFA successfully induced a new-onset CLBBB, increasing QRS duration from 68 ms to 138 ms.
• Post-Ablation Status:
  • Hemodynamics: Resting gradients normalized (2 mmHg). Repeat DSE (30 µg/kg/min) showed resolution of SAM with a peak gradient of only 14 mmHg.
  • Flow Dynamics: BSI demonstrated a transition from a large systolic vortex to laminar flow.
  • Mechanical Changes: Strain analysis indicated that the targeted septal segments exhibited reduced contractility (strain reduced to −9% to −13%), markedly delayed contraction (time-to-peak delay increased from +33 ms to +166 ms relative to INF), and a significant increase in post-systolic shortening (PSI rose from −4% to +25%).
• Follow-up: At 3 months, the patient remained asymptomatic off beta-blockers, with a peak gradient of 30 mmHg under high-dose stress (40 µg/kg/min) and no recurrent syncope.

Key Contributions and Claims
The primary contribution of this work is the provision of the first mechanistic evidence suggesting that iatrogenic CLBBB can act as a "therapeutic collaborator" rather than a mere complication in the RFA treatment of SVS-related LVOTO.

The authors propose a dual mechanism for therapeutic success:

1. Reduction of Regional Hypercontractility: RFA directly reduced the hypercontractile state of the basal septum.
2. Timing Shift via CLBBB: The induced CLBBB shifted septal contraction out of the early-systolic window. By delaying contraction and rendering it post-systolic (occurring after aortic valve closure), the septum lost its ability to propel the anterior mitral leaflet into the LVOT during the critical period of SAM initiation.

The paper references a 1995 hypothesis by Dalvi regarding RFA-induced LBBB altering contraction timing in hypertrophic cardiomyopathy, noting that this case provides the first clinical support for that concept. The authors also highlight the safety profile of this approach, noting that while CLBBB carries theoretical risks, large cohort studies suggest it does not adversely affect long-term survival in post-myectomy patients, and the risk of CLBBB-induced cardiomyopathy is low in patients with preserved baseline LVEF.

Significance and Limitations
The paper claims significance in redefining the role of conduction disturbances in septal reduction therapy, suggesting that for SVS, the induction of CLBBB may be a desired therapeutic endpoint that synergizes with tissue ablation to resolve obstruction.

The authors maintain a modest stance regarding the generalizability of these findings, explicitly acknowledging the following limitations:

• The study is a single case report.
• The relative contributions of direct tissue injury versus CLBBB-induced dyssynchrony cannot be fully separated.
• Long-term outcomes beyond 3 months are unknown.
• The risk of late atrioventricular block, while low, remains a consideration for informed consent.