Abstract

The ventricular distributions of activation‐repolarization intervals (ARIs) were determined in control and diabetic (DM) rabbits (alloxan model, 1 and 2 months). In DM (1 month), the epicardial ARIs were prolonged heterogeneously, being longer on the right than on the left ventricle (LV) and on the LV apex than on the LV base. In DM (2 months), the ARIs lengthened ubiquitously. Coronary occlusion led to the repolarization shortening and repolarization dispersion increase in the control and DM (2 months) groups. However, the repolarization dispersion did not increase in the DM (1 month) rabbits since the ARIs shortened predominantly in the areas where they were prolonged in the preischemic conditions. The ventricular tachyarrhythmias were induced more frequently in the DM (2 months) group as compared to the DM (1 month), whereas the latter did not differ from the controls. The DM‐related precordial T wave flattening was associated with the apicobasal repolarization gradient changes. Thus, the enhanced arrhythmogenicity in DM was associated with the pattern of the overall prolongation of repolarization observed at the 2 months but not 1 month follow‐up, which predisposed to the increase of repolarization dispersion under myocardial ischemia. Grants ‐ Ural Branch of RAS (12‐I‐4‐2059, 13‐4‐032‐KSC) and RFBR (14‐04‐31070 young_a).

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