Dispersion of ventricular repolarization, assessed as QT dispersion in
the ECG or by multiple monophasic action potential (MAP) recordings,
is defined as the difference between the earliest and latest repolariz
ation. It is thus measured in the time domain. However, myocardial ref
ractoriness is primarily a function of the membrane potential during p
hase 3 repolarization, The purpose of this study, therefore, was to me
asure dispersion of ventricular repolarization in the voltage domain a
nd to study its relation to SIF inducibility. To further validate this
concept, the effects of chronic amiodarone treatment on the voltage d
ispersion were assessed. MAPs were recorded simultaneously at 10 epica
rdial and endocardial sites in isolated rabbit hearts, both under base
line conditions (n = 8) and after chronic amiodarone treatment (n = 8)
. Repolarization dispersion in the voltage domain n as calculated as t
he difference between the highest and lowest repolarization level of a
ll 10 MAPs at 10-ms steps, starting from the MAP plateau level to comp
lete repolarization. Plotting these voltage differences along the time
axis resulted in a dispersion curve, which rose during early repolari
zation, reached a peak during phase 3 repolarization, and thereafter d
eclined toward zero. There was a close correlation between VF vulnerab
ility in response to electrical field stimuli and the time during whic
h voltage dispersion was maximal (r = 0.828, P < 0.0001). Amiodarone c
aused a rightward shift of both the dispersion curve (P = 0.007) and V
F vulnerability (P = 0.025), but did not change the magnitude nor the
shape of the voltage dispersion curve and its relation to VF vulnerabi
lity. Repolarization dispersion in the voltage domain describes an alt
ernate approach for evaluating the heterogeneity of ventricular repola
rization and may help to characterize arrhythmia susceptibility under
experimental conditions.