Objective 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. Methods and results 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. 4ms; 14.2±5.1ms; and 13.8±5.4ms 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±15.9ms; 46.8±16.0ms; and 46.5±15.2ms for Epi, Mid, and Endo pacing, respectively; P <0.001), but was similar at Endo and Mid pacing ( P =0.965). TDR at 3cm from left ventricular apex pacing site was similar between Mid and Endo pacing, and still significantly increased at Epi pacing. At 3cm distance, the first activation myocardium was still the epicardium at Epi, while sequence transformed from mid-myocardium to endocardium at Mid pacing. Conclusion Mid as compared to Epi pacing significantly decreases TDR and remains this advantage on the distant myocardium away from the pacing site. Highlights ? We studied the effect of in vivo mid-myocardial pacing in canines on TDR, based on our previous in vitro study. ? Under epicardial pacing, epicardium repolarizes first; longest T Mid–Epi results in the longest TDR. ? In vivo TDR under mid-myocardial pacing remains the same level as that under endocardial pacing and keeps this advantage on the distant myocardium. ? Mid-myocardial pacing as compared to epicardial pacing significantly decreases TDR and remains this advantage on the distant myocardium.
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