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.