Abstract.
Introduction. Diabetes mellitus (DM) is associated with
increased risk of sudden cardiac death, but its role in arrhythmogenesis
is not clear. We evaluated contributions of DM duration and
hyperglycemia level to development of proarrhythmic electrophysiological
changes in the experimental ischemia/reperfusion model.
Methods and Results : Ventricular epicardial 64-lead mapping and
arrhythmia susceptibility burst-pacing testing were performed in 43
healthy and 55 diabetic (alloxan model) anesthetized rabbits undergoing
15-min left anterior descending coronary artery occlusion, followed by
15-min reperfusion. During ischemia, arrhythmia inducibility did not
differ between the groups, but the number of reperfusion ventricular
tachycardias and/or fibrillations (VT/VFs) was higher in the DM group
(14 out of 55) as compared to control (3 out of 43, p=0.017). In the
diabetic animals, both DM duration and glucose concentration were
associated with reperfusion VT/VF development in univariate logistic
regression analysis (OR 1.058; 95% CI 1.025-1.092; p < 0.001;
and OR 1,119; 95% CI 1,045-1,198; p = 0.001; respectively). However,
only the DM duration remained an independent predictor of reperfusion
VT/VF in multivariate logistic regression analysis (OR 1.060; 95% CI
1.006‑1.117; p = 0.029). Among mapping parameters, DM duration was
associated with the prolongation of total ventricular activation
duration (B 0.152; 95% CI 0.049-0.255; p=0.005) and
activation-repolarization intervals (ARIs) (B 0.900; 95% CI
0.315-1.484; p=0.003). The prolonged ARI was the only mapping
characteristic predicting reperfusion VT/VF development (OR 1.028; 95%
CI 1.009-1.048; p = 0.004).
Conclusions : The DM duration-dependent prolongation of
ventricular repolarization presents a link between DM development and
reperfusion VT/VF inducibility.