Effects of Digoxin on Ventricular Vulnerability During Atrial Defibrillation via Implanted Transvenous Catheter Electrodes in the Sterile Pericarditis Model

Abstract

Because digoxin is often used in patients with atrial fibrillation, we evaluated its effects on the relative risk of inducing ventricular tachyarrhythmia (VT/NF) during synchronized atrial defibrillation shocks delivered through implanted transvenous catheter electrodes. Sterile pericarditis was created in 10 mongrel dogs. Two catheter electrodes with a 6 cm coil tip were inserted through the right external jugular vein and placed in the distal coronary sinus and in the right atrial appendage. To systematically achieve variable preceding ventricular coupling intervals (VCls). the ventricles were paced during sinus rhythm before delivery of the atrial shock in two protocols: 1) rapid pacing (8 stimuli, S 1 S 1 protocol); and 21 double extra stimuli (long-short intervalsl following 8 basic stimuli (S 1 S 2 S 3 protocol). The VCI (S 1 S 1 or S 2 S 3 )was shortened by 10 ms until the ventricular effective refractory period was achieved. After sensing the last paced ventricular beat. an atrial shock was delivered with a 2 ms delay at a shock intensity of 300 V (3.2–3.6 J), i.e., maximum shock intensity ofthe device. Atrial shocks were delivered 4 times at each VCI in each protocol. VCI was normalized by subtracting the OT interval in the surface ECG from the actual VCI. The relationship between the VCI and induction of VT/NF was evaluated in the drug free state and after administration of a therapeutic (50 μ g/kg. 5 dogs) or toxic (to obtain toxic arrhythmia. 5 dogs) dose of digoxin. Data are shown in mean ± SD, for each protocol (S 1 S 1 or S 1 S 2 S 3 ). To calculate a 99% probability of sinus rhythm (SR) after an atrial shock.logistic regression was used. No significant difference was observed before and after digoxin administration. The longest VCI that preceded VTNF induction was QT + 50 ms (290 ms) before digoxin and QT + 50 ms (310 ms) after digoxin. digoxin QT (ms) VTNF induction 99% probability of SR (ms) control 226 ± 22 6/377 (S 1 S 1 ) 27/303 (S 1 S 2 S 3 ) QT – 4 (S 1 S 1 ) QT + 71 (S 1 S 2 S 3 ) therap 237 ± 44 8/178 (S 1 S 1 ) 16/151 (S 1 S 2 S 3 ) QT + 1 (S 1 S 1 ) QT + 73 (S 1 S 2 S 3 ) toxic 220 ± 8 8/177 (S 1 S 1 ) 15/142 (S,S 2 S 3 ) QT + 1 (S 1 S 1 ) OT + 63 (S 1 S 2 S 3 ) Digoxin did not significantly change the risk of VT/NF induction during atrial defibrillation shocks delivered through transvenous catheter electrodes at maximum shock intensity. Shocks delivered at VCls longer than 310 ms resulted in no VT/NF induction.