Abstract

Rotating waves of electrical activity may be observed in small (20 × 20 × < 1 mm) pieces of normal ventricular epicardial muscle from the sheep heart. Application of an appropriately timed voltage gradient perpendicular to the wake of a quasiplanar wavefront gives rise to sustained vortex-like reentry which may last indefinitely, unless another stimulus of appropriate characteristics and timing is applied to terminate the arrhythmia. Once established, the vortex pivots at a frequency of 5 to 7 Hz around a small elongated core (≈ 2 by 4 mm) which only develops small electrotonically mediated depolarizations. Imaging of the entire course of local activation and recovery may be accomplished with high temporal and spatial resolution using the voltage-sensitive dye di-4-ANEPPS and a 10 x 10 photodiode array system focused onto the preparation. Two- and three-dimensional reconstructions of the optical images generated by the local fluorescence response to the circulating waves provide accurate maps of the distribution of voltage across most of the surface of the tissue and gives insight into the dynamics and mechanisms of initiation, maintenance and termination of the arrhythmia. The overall results suggest that neither dispersion of action potential duration (APD) nor tissue anisotropy are essential for the induction or maintenance of reentry. A transient nonuniformity in refractoriness created by the appropriately timed voltage gradient is sufficient to establish the circulating activity. Anisotropy and dispersion of APD serve only to produce a nonuniform topographical distribution of conduction velocity and excitable gap (i.e., that interval during which part of the circuit is excitable). Annihilation of the reentry by an appropriately timed stimulus is the result of collision of the reentrant wavefront with the stimulus-induced excitation wave propagating in the opposite direction. These results may be useful in the understanding of the mechanisms of ventricular tachycardia and may have important implications in the development of new and more specific antiarrhythmic therapies.

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