Objectives: The goal of this study was to establish the role of ventricular filling on the 1b phase of ischemia-induced arrhythmias.
Background: Ischemia-induced ventricular arrhythmias occur in two phases. The mechanism of the initiation of delayed (1b) arrhythmias is unknown. The 1b arrhythmias (15 to 60 min of ischemia) are abundant in in situ hearts but scarce in isolated perfused hearts (with drained ventricles).
Methods: Left ventricular (LV) epicardial mapping (11 x 11 matrix, 5 mm interelectrode distance) of the initiation of delayed arrhythmias was performed in open-chested pigs (group A, n = 7) and isolated pig hearts without (group B, n = 8) and with a filled intraventricular balloon (group C, n = 5).
Results: There were no differences in ischemic zone size between groups. The ischemia-induced rise in tissue impedance was similar in groups A and B. Arrhythmias were less frequent and less severe in group B than in groups A or C, with no differences between groups A and C. An epicardial focal origin was detected in 26% of all first beats, significantly more from the ischemic border than from elsewhere. During a pacing protocol with a long pause (a separate group of four isolated hearts with a balloon), more premature beats occurred in the first postpause interval than in any other interval.
Conclusions: In isolated hearts 1b arrhythmias were less frequent and less severe than in working preparations. Focal activity was documented in 26% of arrhythmias and emerged from the ischemic border. Postpause contractile potentiation was associated with more arrhythmias. Our study suggests that the initiation of ischemia-induced 1b arrhythmias is related to LV wall stress.