Catheter Ablation -> Ventricular Arrhythmias -> Experimental methods D-PO01 - Featured Poster Session (ID 11) Poster

D-PO01-174 - Intracardiac Mapping And Ablation Of Ventricular Arrhythmias In Boxer Dogs (ID 128)


Background: Boxer dogs are known to develop ventricular arrhythmias and sudden cardiac death, often due to arrhythmogenic right ventricular cardiomyopathy (ARVC).
Objective: We sought to characterize the electroanatomic substrate and VT mechanisms in Boxer dogs with drug refractory sustained VT to investigate if this naturally occurring disease in dogs is similar to the clinical manifestation of ARVC seen in humans.
Results: Two Boxer dogs with a history of VT and syncope/collapse underwent detailed ENDO RV voltage mapping using CARTO with a 3.5mm Smart-Touch catheter. Programmed stimulation (PES) was performed to attempt induction of sustained VT. Pt 1 (9 y/o female, 36kg) had a normal RV bipolar (Bi: 0.5-1.5mV) and unipolar (Uni: <5.5mv) voltage map. PES did not induce any VT. A spontaneous left bundle inferiorly directed PVC was localized with pace mapping and ablated at the RV free-wall (FW). Pt 2 (8 y/o male, 33kg) had abnormal RV Bi and Uni ENDO RV voltage map with fractionated EGMs on the RV FW and RVOT. LV voltage map was performed and was normal. PES induced 2 sustained MMVTs (VT1: 200ms, left bundle-inferior, VT2: 210ms, right bundle-inferior). The VTs were only briefly hemodynamically tolerated, with 1 VT terminating during ablation at the RCC. Progressive fusion was demonstrated for VT-1.
Conclusion: Boxer’s with VT can have RV ENDO substrate abnormalities with inducible reentrant MMVT similar to humans with ARVC. Future electrophysiologic studies characterizing the pathogenesis of ARVC in Boxer dogs can be helpful in determining the utility of developing a large-animal model of ARVC and VT. Enrollment of additional subjects is on-going.