Sc. Verduyn et al., ROLE OF INTERVENTRICULAR DISPERSION OF REPOLARIZATION IN ACQUIRED TORSADE-DE-POINTES ARRHYTHMIAS - REVERSAL BY MAGNESIUM, Cardiovascular Research, 34(3), 1997, pp. 453-463
Objective: The mechanism of acquired torsade-de-pointes arrhythmias (T
dP) is not clear but is suggested to be based on several parameters in
cluding early afterdepolarizations (EADs) and/or dispersion of repolar
ization (Delta APD). In our animal model of TdP (anaesthetized dogs wi
th chronic AV block), we assessed the relevance of interventricular di
spersion for the initiation of TdP. Methods: In 24 experiments, multip
le endocardial monophasic action potential (MAP) recordings were made
at baseline, after d-sotalol (2 mg/kg), and after MgSO4 (100 mg/kg, n
= 11) to measure regional differences in action potential duration (AP
D). Rate-dependent behavior of the interventricular Delta APD (APD of
left minus right ventricle) and intraventricular dispersion was studie
d under the different circumstances. Results: Dogs with induction of T
dP by d-sotalol and pacing (11/20 = 55%) had longer cycle lengths of i
dioventricular rhythm, longer QT-durations, increased presence of EADs
(14/22 vs 5/18 MAPs, P < 0.05) and increased interventricular Delta A
PD (135 +/- 55 vs 60 +/- 40 ms, P < 0.05) compared with non-inducible
dogs. There were no differences in intraventricular dispersion. MgSO4
diminished Delta APD (110 +/- 45 to 55 +/- 60 ms, P < 0.05) and preven
ted TdP (4/4). In contrast to intraventricular dispersion, interventri
cular Delta APD is clearly bradycardia-dependent. Conclusions: Next to
bradycardia, prolonged repolarization, and EADs, we propose that Delt
a APD should be added to the relevant factors for the initiation of Td
P. Interventricular dispersion is much larger than intraventricular di
spersion and demonstrates a very strong bradycardia dependence.