Prolongation of experimental diabetes mellitus increased susceptibility to reperfusion ventricular tachyarrhythmias

Abstract

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. 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) were higher in the DM group (14 out of 55) as compared with 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 (odds ratio (OR) 1.058, 95% confidence interval (CI) 1.025–1.092, p < 0.001; and OR 1.119, 95% CI 1.045–1.198, p = 0.001, respectively). Only the DM duration, however, 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 (regression coefficient 0.152, 95% CI 0.049–0.255, p = 0.005) and activation-repolarization intervals (ARIs) (regression coefficient 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). The DM duration-dependent prolongation of ventricular repolarization presents a link between DM development and reperfusion VT/VF inducibility.