A novel method for septal reduction therapy by three-dimensional guided transvenous intraseptal pulsed-field ablation
Rongxuan Chang1, Duan Luo2, Wei He3
1Department of Cardiology, The First Affiliated Hospital of Sun Yat-sen University, Key Laboratory on Assisted Circulation, Guangzhou, Guangdong, China.
Background:
Pulsed-field ablation (PFA) is a nonthermal method for achieving selective cell death with little inflammation response. However, there are no reports of PFA for septal reduction therapy (SRT).
Objective:
The purpose of this study was to investigate the effectiveness and safety of PFA for SRT.
Methods:
A novel transvenous intraseptal PFA method with 3-dimensional (3D) guidance was introduced in Yorkshire pigs. Electrocardiographic parameters, transthoracic echocardiography, and histopathology were used to evaluated.
Results:
The maximum injury diameter of intramyocardial PFA increased with electric field intensity. After PFA, bipolar electrogram amplitude and pacing threshold measured by the PFA electrodes significantly decreased (F = 6.945, P = .007) or increased (F = 5.842, P = .024), respectively. In the ablated septal region, motion amplitude and systolic wall thickening rate significantly decreased and remained at low levels (motion amplitude: F = 20.793, P = .000; systolic wall thickening rate: F = 14.343, P = .000); however, septal thickness did not significantly change after PFA (F = 1.503, P = .248). Histologic examination showed specific cardiomyocyte death with gradually increased hyperchromatic cytoplasm and nuclear pyknosis, without obvious inflammatory cell infiltration in acute phase. TUNEL stain for fragmented DNA showed extensively positive in the ablation region 24 hours after PFA. During PFA, no sustained ventricular arrhythmia or atrioventricular conduction block occurred.
Conclusion:
A novel intraseptal PFA method with 3D guidance was described. Intraseptal PFA resulted in effective myocardial injury and local hypokinesis without significant acute edema. Histologic examination showed widely programmed cardiomyocyte death with little inflammatory cell infiltration.
