Polymorphic reentrant ventricular tachycardia in the isolated rabbit heart studied by high-density mapping.

Abstract

The role of dispersion of refractoriness and reentry for the genesis of polymorphic ventricular tachycardia (VT) has recently become emphasized. We investigated the mechanisms of polymorphic arrhythmias in a 2D preparation confining an area of prolonged refractoriness. In 16 Langendorff-perfused rabbit hearts, a sheet of left ventricular epicardium was obtained by a cryoprocedure. Enhanced spatial heterogeneity in a refractory period was created by cooling a central region (diameter=12 mm). This markedly prolonged the refractory period (by 36+/-14 ms) inside but only slightly prolonged it (by 5+/-11 ms) outside the cooled area (n=6). During a control procedure, programmed stimulation with up to 3 premature stimuli induced an episode of monomorphic VT in only 1 of 10 hearts. During regional cooling, episodes of polymorphic VT with a maximum duration of 35 seconds could be induced in all hearts. High-resolution mapping (229 electrodes) of epicardial activation revealed that polymorphic VT was caused by a functional reentrant circuit located partially within the region of prolonged refractoriness. The reentrant wavefront was continuously shifting along the border of the cooled region, resulting in beat-to-beat changes in the excitation pattern. Spontaneous termination of polymorphic VT occurred either by a shift of the reentrant circuit outside the cooled region or by a block in the central common pathway during figure-of-8 reentry in the region of prolonged refractoriness. A shifting functional reentrant circuit was the underlying mechanism of polymorphic VT in a substrate of enhanced spatial heterogeneity of refractoriness.