RESULTS
As expected, the rabbits from DM group had a higher median venous plasma
glucose level [25.6 (IQR 18.4-30.5) vs 6.0 (IQR 5.6-6.5) mmol/l,
p<0.001]. In the DM group, glucose concentration and DM
duration had weak significant correlation with each other (r = 0.308,
p = 0.025).
First, we tested, if DM duration and/or plasma glucose level had any
associations with arrhythmia inducibility. Diabetic conditions were
associated with arrhythmogenesis during reperfusion but not ischemia.
Table 1 shows that the diabetic animals did not differ from the controls
concerning ischemic arrhythmias, but the number of arrhythmias induced
at reperfusion was higher in the DM group. This increase in reperfusion
arrhythmogenicity developed only in the prolonged DM group (Table 1). In
the diabetic animals, both DM duration and glucose concentration were
associated with reperfusion VT/VF 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). In multivariate
logistic regression analysis, only DM duration remained an independent
predictor of reperfusion VT/VF (OR 1.060; 95% CI 1.006‑1.117; p =
0.029). No associations were found between ischemic VT/VF on one hand
and neither DM duration, nor glucose concentration on the other hand.
Then, to find out which electrophysiological parameters were affected by
DM duration, we compared electrophysiological parameters in the control
group, and groups with short and prolonged DM (Fig. 1). The groups did
not differ in DOR, time of epicardial breakthrough, duration of
epicardial and total ventricular activation. Among the studied
electrophysiological variables obtained by ventricular epicardial
contact potential mapping, only duration of ARIs differed between the
groups being increased in the prolonged DM group.
Within the diabetic group (any DM duration), we tested which
electrophysiological mapping parameters were associated with DM duration
and/or glucose concentration in multivariate linear regression analysis
(Table 2). Duration of epicardial activation was associated with glucose
concentration, whereas total ventricular activation and ARI duration
were associated with DM duration. Epicardial isochronal maps show
prolongation of ARIs particularly in the apical areas of ventricular
epicardium in the animals with DM, especially at the long follow-up
(Fig. 2). DOR demonstrated no associations with neither DM duration, nor
glucose concentration.
We established electrophysiological determinants of ischemic and
reperfusion VT/VF development. Table 3 shows results of univariate
logistic regression analysis of arrhythmia predictors. It demonstrates
association of VT/VF development during ischemia with activation time of
epicardial breakthrough, DOR and average ARI duration. On the other
hand, reperfusion VT/VFs were associated with only average ARI duration.
ROC curve analysis demonstrated significant association of prolonged ARI
with reperfusion VT/VF inducibility (AUC 0.781, p = 0.001). The optimal
cut-off for the ARI ≥ 120 ms predicted reperfusion VT/VF with
sensitivity 0.80 and specificity 0.75 (OR 8.119 95%CI 2.334-28.247,
p = 0.001 in logistic regression analysis).