Beta-Receptor Blockade Reproduces Electrophysiological Effects of Early Diabetes Mellitus in Ventricular Myocardium

Diabetes mellitus (DM) increases the risk of sudden cardiac death, which suggests the involvement of arrhythmogenic mechanisms. Among other changes, DM causes cardiac autonomic neuropathy (CAN), but its role in electrophysiological myocardial remodeling is unclear. The objective of the present study was to test the effects of β-adrenergic blockade regarding ventricular spatiotemporal electrophysiological properties in an experimental DM model. Epicardial mapping (64-lead sock electrode array) was done in 13 control and 11 alloxan-induced DM rabbits. Activation times (AT), end of repolarization times (RT), and activation-repolarization intervals (ARI) were determined as dV/dt min during QRS, dV/dt max during T-wave, and RT-AT difference, respectively. The β-adrenergic blockade was produced by esmolol infusion (0.5 mg/kg, i.v.). It was found that the early-stage DM in rabbits was characterized by relatively mild changes in ventricular myocardium, which did not involve ventricular activation and the average duration of repolarization. The signature of this stage was the local prolongation of repolarization, which pertained to the RV apical region. The blockade of β-adrenergic receptors in healthy animals produced a ventricular spatiotemporal repolarization pattern similar to that observed in diabetic rabbits with the local apical prolongation of repolarization. On the other hand, the blockade of β-adrenergic receptors in diabetics prolonged the relatively short basal repolarization. It can be concluded that β-adrenergic blockade in healthy animals reproduced the early-stage DM effects on the spatiotemporal electrophysiological properties of the ventricular myocardium. This demonstrated the role which CAN could play in the electrical remodeling of ventricular myocardium in early-stage DM.