In vivo effects of mid-myocardial pacing on transmural dispersion of repolarization and conduction in canines

Abstract

In our previous in vitro study mid-myocardial relative to epicardial pacing decreased transmural dispersion of depolarization (TDR) and prevented ventricular arrhythmia. We therefore hypothesized that in vivo mid-myocardial pacing in canines has a similar effect. Using custom-made electrodes, monophasic action potentials were simultaneously recorded in vivo from left ventricular epicardial (Epi), mid-myocardial (Mid) and endocardial (Endo) layers of canines (n = 12). TDR was significantly increased at Epi (44.6 ± 6. 4 ms, 14.2 ± 5.1 ms, and 13.8 ± 5.4 ms for Epi, Mid and Endo pacing, respectively, P < 0.001), and similarly at Mid and Endo pacing (P = 0.855). This result was reproducible after ibutilide administration (n = 12). TDR was augmented at each layer pacing and significantly increased at Epi (78.1 ± 15.9 ms, 46.8 ± 16.0 ms, and 46.5 ± 15.2 ms for Epi, Mid, and Endo pacing, respectively, P < 0.001), but was similar at Endo and Mid pacing (P = 0.965). TDR at 3 cm from left ventricular apex pacing site was similar between Mid and Endo pacing, and still significantly increased at Epi pacing. At 3 cm distance, the first activation myocardium was still the epicardium at Epi, while sequence transformed from mid-myocardium to endocardium at Mid pacing. Mid as compared to Epi pacing significantly decreases TDR and remains this advantage on the distant myocardium away from the pacing site