Shift and Termination of Functional Reentry in Isolated Ventricular Preparations with Quinidine‐Induced Inhomogeneity in Refractory Period

Mechanism of Reentry's Instability. Introduction: The purpose of this investigation was to study the mechanisms responsible for instability and termination of functionally determined reentry. Methods and Results: The activation sequence was recorded using multielectrode mapping technique in preparations isolated from rabbit right ventricle. In nine preparations, functional inhomogeneity was created on the epicardial surface. For this purpose, two parts of a preparation divided by a thin rubber barrier were superfused by different solutions: normal Tyrode's solution and Tyrode's solution containing quinidine (5–10 mg/L). As a result, there was a difference of refractory period of 45 ± 12 msec (n = 6). Premature stimulation of sites situated in the normally superfused region led to the appearance of unstable reentrant circuits at the border of inhomogeneity (32 cases) in seven of the nine preparations. In most cases (24 of 32) reentrant circuits shifted along the border of inhomogeneity. Reentrant circuits with clockwise and counterclockwise rotations had opposite directions of shift. Because of the shift, reentrant circuits moved to the border of the preparation where they were extinguished. Conclusion: Our results suggest that inhomogeneity in refractoriness that gives rise to initiation of reentrant circuits also causes their termination. ( J Cardiovasc Electrophysiol, Vol. 3, pp. 255–265, June 1992 )