Effects Of Mid-myocardial Pacing On Transmural Dispersion Of Repolarization In Heart Failure Canine

Objective:The Purpose of this study was to investigate the effcts of pacing at left ventricular（LV） mid-myocardium on Transmural Dispersion of Repolarization（TDR） in normaland heart failure canines. This study would provide experimental evidence for preventionand treatment of arrhythmias which were related with amplification of TDR.Methods:Adult mongrel canines weighing15~25kg (n=16) were randomized into two groups：Control group (n=8) was the sham operation．Canines in HF (heart failure) group (n=8)were the HF models induced by rapid right ventricular pacing (260bpm for4weeks).Arterially perfused canine LV (left ventricule) wedge preparations were produced fromcontrol and HF canines. A transmural ECG and transmembrane action potentials weresimultaneously recorded from epicardial, M, and endocardial cells of arterially perfusedcanine LV wedge preparations, paced at epicardial, M, and endocardial layer respectively.Action potential duration (APD) and the TDR were observed. Statistical analysis was doneusing SPSS17.0software. Data of electrophysiological parameters were presented asMean and standard deviations (SD). To evaluate difference of electrophysiologicalparameters among Endo pacing, M pacing and Epi pacing, one-way analysis of variance(ANOVA) was performed. The Student–Newman–Keuls (SNK test) was used as a posthoc test in the subsequent multiple comparative analysis. The T test was applied incomparison of electrophysiological parameters between control and HF group. Criterionfor statistical significance was P<0.05.Results:1. APD90in all three layers showed no significant difference under Epi, M and Endopacing (P>0.05) in either control or HF group.2. TDR varied when the preparations were paced at each layer respectively (Endopacing,35.6±6.6ms; M pacing,34.9±7.3ms; Epi pacing,72.4±4.9ms; P<0.001). Asignificant difference was noted in TDR between M pacing and Epi pacing (P<0.001), butnot between M pacing and Endo pacing (P=0.831).3. The above results was reproducible in the presence of HF experiments (n=8). TDRwas amplified as compared with control group and differed when preparations were pacedat each layer (Endo pacing,62.8±13.8ms; M pacing,63.3±13.3ms; Epi pacing, 111.1±17.7ms; P<0.001). There was again no significant difference between Endo pacingand M pacing (P=0.701). However, as pacing was shifted from M to Epi, there was asignificant increase in TDR (P<0.001).4. Ventricular arrhythmias were induced in3of8Heart Failure preparations duringEpi pacing, but did not occur in either M or Endo pacing.Conclusion:M pacing can significantly decrease the TDR and prevent the occurrence ofventricular arrhythmias as compared with Epi pacing.