INTRODUCTION
Cardiovascular pathologies often complicate diabetes mellitus (DM). 1 Specifically, DM increases risk of ventricular arrhythmias and sudden cardiac death in patients with coronary artery disease as well as those with no signs of heart problems. 2-4 However, experimental studies often yield inconsistent results concerning arrhythmic outcomes in DM. Susceptibility to arrhythmias in the diabetic hearts has been reported to be either increased 5-7 or decreased. 8-13
These conflicting data obtained in clinical and experimental studies present a significant problem and warrant some unifying explanation for the changes of the arrhythmic risk in the diabetic heart. The differences concerning arrhythmia susceptibility in the above-mentioned observations may be related to concomitant pathologies, effects of therapy in clinical investigations, characteristics of the models used in the experimental studies (different species, in vivo vs in vitro preparations), etc. Among other causes, duration of exposure to diabetic conditions can influence arrhythmic outcomes of experimental DM. The duration of diabetic conditions is obviously shorter in experimental as compared to clinical studies. There are data showing that prolongation of the experimental DM duration promotes proarrhythmic changes in the myocardium. 14-16 Similarly, the level of hyperglycemia affects vulnerability of myocardium to ischemia/reperfusion injury, 17 and its effect on susceptibility to ischemia/reperfusion arrhythmias cannot be excluded. However, the electrophysiological mechanisms of these changes are not clear.
We hypothesized that DM-related electrical remodeling develops gradually and does not immediately become arrhythmogenic. The aim of this work was to evaluate the role of the DM duration and level of hyperglycemia in the development of ventricular electrophysiological changes and the risk of ischemic and reperfusion arrhythmias in an experimental type 1 DM model.