abstract


presented


at the 1997 NASPE

New Orleans, Louisiana


May 7-10, 1997


Mechanism of Initiation of Ventricular Fibrillation During T Wave Alternans

PACE 1997;20:II-584

Joseph M. Pastore, Steven D. Girouard, David S. Rosenbaum, Case Western Reserve University, Cleveland, OH

Although T wave alternans (TWA) of the surface ECG has been closely associated with vulnerability to ventricular arrhythmias, an explanation for this relationship is unknown. To determine if TWA plays a role in the initiation of ventricular fibrillation (VF), TWA was induced by steady-state pacing in 4 Langendorff perfused (27°C) guinea pig hearts. Action potentials were recorded simultaneously from 128 left ventricular sites (1 cm2 area) using high resolution optical mapping with the voltage-sensitive dye di-4-ANEPPS (15 µM). Above a threshold heart rate (213±51 bpm), alternations of the plateau and late repolarization of the action potential were elicited from all ventricular recording sites such that action potential duration (APD) oscillated from beat to beat with identical phase at each recording site (i.e. concordant alternans). However, at faster heart rates (> 300 bpm), APDs prolonged in some regions while shortening in others during the same beat (i.e. discordant alternans). Discordant alternans produced a marked increase in the spatial dispersion of repolarization (DOR) as measured form the variance of repolarization times across the ventricle (Figure).

The DOR was characterized by large gradients of repolarization whose orientation changed by 180° on consecutive beats. This, in turn, caused regional conduction slowing (14±7 cm/s @ 315 bpm) compared to control (36±16 cm/s @120 bpm) into areas of delayed repolarization. Moreover, during discordant alternans, a small (3 bpm) increase in heart rate produced conduction block into areas of delayed repolarization, followed by reentry and VF.

Conclusions: Discordant alternans causes increased spatial inhomogeneity of repolarization which leads to conduction block, reentry, and VF. These data suggest that there is indeed a mechanistic relationship between TWA and initiation of VF.


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