Key Points
- To examine the effects of predisposing factors for torsade de pointes on epicardial dispersion of repolarization and arrhythmogenesis in a porcine model lacking midmyocardial M cells.
- Conducted computerized epicardial mapping of activation and repolarization via 128 unipolar electrograms in 29 Langendorff-perfused hearts of eight-week-old pigs.
- Measured activation-recovery intervals during interventions including altered pacing rates, low extracellular potassium, low extracellular magnesium, DL-sotalol (0.1 mmol/l), and phenylephrine (1 µmol/l).
- Baseline iso-interval maps were dipolar in 41% and multipolar in 59% of hearts, with repolarization dispersion exhibiting reverse frequency dependence but no sensitivity to reduced extracellular potassium.
- DL-sotalol amplified local repolarization gradients and heightened epicardial dispersion without midmyocardial predominance, an effect further augmented by phenylephrine.
- Lowering extracellular magnesium alongside DL-sotalol provoked spontaneous polymorphic ventricular tachycardia in 7 out of 9 experiments, with functional dissociation lines near steep repolarization gradients in 2 out of 9 tachycardias.
Structured PICO
PPopulation29 Langendorff-perfused hearts of eight-week-old pigs
IInterventionDL-Sotalol (0.1 mmol/l), Phenylephrine (1 mumol/l), lowering [K+]o, lowering [Mg++]o
CComparatorBaseline conditions
OOutcomeEpicardial dispersion of repolarization and occurrence of polymorphic ventricular tachycardiasurrogate
In an isolated porcine heart model, epicardial dispersion of repolarization is increased by slow rates, DL-sotalol, and phenylephrine, contributing to the continuation of polymorphic ventricular tachycardia.