High-density mapping for AVNRT ablation with distorted conduction system anatomy post-ASD device closure-case report

Atrial septal defects (ASDs) are among the most common congenital heart defects, comprising about 10 % of cases in children. Transcatheter closure of ASDs has become a preferred treatment due to its minimally invasive nature, quicker recovery, and reduced risk compared to surgical closure. Despite its advantages, the procedure carries a risk of post-procedural arrhythmias, particularly bradyarrhythmias and tachyarrhythmias, occurring in approximately 7-10 % of patients. The development of these arrhythmias can be attributed to mechanical interference with conduction tissue or the formation of reentrant circuits around the closure device. These complications can present a challenge for long-term management and require careful monitoring and treatment.

We describe the case of an 8-year-old female who presented with recurrent palpitations after transcatheter closure of two ASDs using a 25 mm Gore Cardioform device. Her initial procedure was uneventful, with complete closure of both defects confirmed by echocardiography. However, one month after the procedure, the patient began experiencing episodes of palpitations and dizziness. Electrocardiographic monitoring revealed regular narrow complex tachycardia, and she was referred for further evaluation. An electrophysiology study confirmed the presence of AV nodal reentrant tachycardia (AVNRT). Detailed mapping revealed significant anatomical distortion of the slow pathway region of the AV node due to proximity to the implanted closure device. Using high-density electroanatomical mapping (HD mapping), we were able to precisely identify the critical pathways for reentry and perform successful slow pathway ablation, eliminating the tachycardia without damaging the closure device or surrounding conduction tissue. The fluoroscopy time was 0.126 mins.

This case highlights the potential complications that can arise following transcatheter ASD closure, particularly the development of arrhythmias like AVNRT. While arrhythmias following device closure are relatively rare, the mechanical interference caused by the device can result in structural changes to the heart's conduction system, predisposing patients to arrhythmias. In this case, the proximity of the Gore Cardioform device to the slow pathway in the AV node likely contributed to the development of AVNRT, as the device caused localized distortion of the anatomy, facilitating reentrant circuit formation. This case emphasizes the importance of long-term follow-up and the need for advanced mapping techniques in patients undergoing ASD closure who develop post-procedure arrhythmias. High-density electroanatomical mapping, in particular, was essential in this patient, allowing for the precise localization of the arrhythmogenic substrate while avoiding unnecessary damage to the closure device or surrounding healthy tissue. The use of this advanced technology not only improves spatial resolution but also enhances procedural safety by reducing radiation exposure and optimizing outcomes, particularly in pediatric patients with complex congenital heart conditions. Additionally in redo ablations performed after prior procedures at outside centers, high-density mapping has proved valuable in distinguishing patchy low-voltage scar from true slow pathway potentials. This approach enables us to target the functional slow pathway while avoiding ablation of scar tissue.

In conclusion, high-density mapping played a crucial role in managing this patient's AVNRT, demonstrating its importance in addressing complex arrhythmias in patients with prior transcatheter ASD closure. Continued advancements in mapping technology will likely further improve the management of arrhythmias associated with congenital heart disease interventions.