Electrophysiological recordings obtained from a single anesthetized dog in sinus rhythm (t = –2 weeks) (A), in atrially triggered high-septal pacing (VDD) directly after atrioventricular (AV)-nodal ablation (t = –2 weeks) (B), and in continued VDD pacing, 2 weeks after pacemaker implantation (t = 0 weeks) (C). In each panel, electrocardiographic (ECG) leads II and AVR and left (LV) and right ventricular (RV) monophasic action potential (LV and RV monophasic action potential [MAP], respectively) recordings are shown. From top to bottom are indicated: RT, QRS, RR, duration of LV and RV MAP, and activation time (all ms). Horizontal and vertical calibrations represent 1 s (paper speed 25 mm/s) and 1 mV for ECG recordings and 20 mV for monophasic action potential (MAP) signals. Altering origin of ventricular activation from AV nodal to high septal preserves QRS axis but increases QRS duration and alters activation time to negative values. In contrast, VDD pacing does not alter ventricular repolarization parameters.

Representative electrophysiological recordings obtained from an anesthetized chronic AV block (CAVB) dog before and after 4 weeks of electrical remodeling. (A) idioventricular rhythm at 0 and 4 weeks. (B) Torsades de pointes (TdP) arrhythmia after proarrhythmic challenge with dofetilide at 4 weeks. In all tracings, ECG leads II and AVR and left and right ventricular monophasic action potential (LV and RV MAP, respectively) recordings are shown. From top to bottom, RT, RR, QRS, duration of LV and RV MAP, and activation time (all ms) are indicated. Horizontal and vertical calibrations represent 1 s (paper speed 10 mm/s) and 1 mV for ECG recordings and 20 mV for MAP signals. Four weeks of AV block caused prolongation of RT and LV and RV MAP durations (A, right side). Dofetilide reproducibly induced TdP in this (B) and 6 other CAVB dogs. Abbreviations as in Figure 1.

In panel A, recordings of ECG leads II and AVR, and left and right ventricular monophasic action potential (LV and RV MAP, respectively) are shown during high-septal pacing (HSP) with a cycle length of 1,000 ms at 0 weeks (left side) and 4 weeks (right side). From top to bottom, RT, QRS, RR, duration of LV and RV MAP, and activation time (all ms) are indicated. Horizontal and vertical calibrations represent 1 s (paper speed 25 mm/s) and 1 mV for ECG recordings and 20 mV for monophasic action potential signals. Graphs in panel B show RT time in CAVB (left side) and HSP dogs (right side) during pacing at cycle lengths between 600 and 1,000 ms. Note that controlling activation with HSP reduces electrical remodeling after AVB. Dashed lines = 0 weeks; solid lines = 4 weeks. For differences in RT between 0 and 4 weeks at the same pacing cycle length within the CAVB and HSP groups, paired Student t tests were used. *p < 0.05 versus 0 weeks. For differences between CAVB and HSP at 600 and 1,000 ms pacing cycle length, 2-way analysis of variance followed by Bonferroni post-hoc test was used. p < 0.05 versus CAVB. Panel C shows values of RT interval (left side) and LV MAPD (right side) in 5 CAVB dogs with consecutive RV apex pacing (solid lines) or HSP (dashed lines). Paired Student t tests were used to analyze differences between RV pacing and HSP at the same pacing cycle length (all p > 0.7). Abbreviations as in Figures 1 and 2.

Arrhythmogenic outcome is depicted for CAVB and high-septal pacing (HSP) dogs. (A) Number of dogs with reproducible TdP relative to group size. Actual numbers indicated in bars (p = NS, Fisher exact test). (B) Mean number of TdP per inducible dog in each group. (C) Mean cumulative durations of TdP within inducible dogs. (D) Mean number of defibrillations necessary to terminate arrhythmias. Mann-Whitney U tests were used for statistical testing in B, C, and D. *p < 0.05 versus CAVB. Note that HSP dogs show less proarrhythmia than CAVB dogs. Abbreviations as in Figures 1 and 2.