Key result
Intravenous magnesium rapidly eliminated polymorphic ventricular tachyarrhythmia and transiently decreased mean transmural activation-recovery interval dispersion from 80 to 45 ms within 30 seconds.
Why the study?
Does intravenous magnesium sulfate improve transmural ventricular repolarization and suppress arrhythmias in a canine model of prolonged QT interval?
Does intravenous magnesium sulfate improve transmural ventricular repolarization and suppress arrhythmias in a canine model of prolonged QT interval?
Absolute Event Rate: 45% vs 80%
Intravenous magnesium transiently homogenizes transmural ventricular repolarization and suppresses polymorphic ventricular tachyarrhythmia in a prolonged QT canine model, suggesting continuous infusion is needed to prevent recurrence.
Transient magnesium effect in canine long QT supports acute suppression; leaves open continuous infusion needs and human translation.
BACKGROUND: This study was performed to clarify the antiarrhythmic effects of magnesium sulfate (Mg(++)) in a prolonged QT interval canine model of polymorphic ventricular tachyarrhythmia (VTA). METHODS: In six experiments in a canine model of prolonged QT by anthopleurin-A, Mg(++) was administered in boluses of 0.2 mL/kg during repetitive episodes of self-terminating polymorphic VTA or frequent premature ventricular complexes (PVCs). The distribution of ventricular repolarization across the left ventricular(LV) wall and dispersion of transmural repolarization were analyzed before, and 30 and 120 seconds after Mg(++) administration, during ventricular pacing at 100 bpm. Transmural unipolar electrograms were recorded from multipolar needle electrodes, and local activation-recovery intervals (ARI) were measured. RESULTS: Mg(++) rapidly eliminated self-terminating polymorphic VTA and all isolated PVCs. During ventricular pacing at 100 bpm, Mg(++) caused modest shortening of ARI at all recording sites. Since the magnitude of ARI shortening was greater at mid-myocardial sites than at other ventricular sites, mean transmural ARI dispersion decreased from 80 +/- 22 to 45 +/- 18 ms within 30 seconds after Mg(++) injection. However, this effect was transient, and, at 120 seconds after Mg(++) administration, ARI had increased all sites and transmural ARI dispersion lengthened to 65 +/- 18 ms. Besides suppression of triggered premature activity, homogenization of transmural ventricular repolarization was associated with the antiarrhythmic effects of intravenous Mg(++) in this model. CONCLUSION: Since these effects were transient, a continuous intravenous infusion of Mg(++) is preferred to prevent recurrences of VTA.
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Chinushi et al. (2005) studied Prolonged QT interval model of polymorphic ventricular tachyarrhythmia (n=6). Intravenous magnesium sulfate vs. Baseline (before administration) was evaluated on Mean transmural activation-recovery interval (ARI) dispersion. Intravenous magnesium rapidly eliminated polymorphic ventricular tachyarrhythmia and transiently decreased mean transmural activation-recovery interval dispersion from 80 to 45 ms within 30 seconds.
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