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The relationship between early afterdepolarization (EAD) and the occurrence of torsades de pointes (TdP) was studied in a canine model. Twelve dogs of both sexes, weighing 9.9-16 Kg, were studied. After reducing the concentration of serum potassium to 3.0-4.0 mEq/l, by administration of calcium polystyrene sulfonate at 15-20 g/day for 1 or 2 weeks, a 6F electrode catheter was introduced via the femoral vein and positioned at the atrioventricular (AV) junction. Complete AV block was produced by catheter ablation using a high frequency current. A Franz 6F catheter was introduced into the right ventricle to record monophasic action potentials (MAPs) using the contact electrode technique. After a stable recording of the MAPs was achieved, cesium chloride (CsCl; 1 mM/Kg) was administered as an intravenous bolus over 15 sec. The MAPs and electrocardiogram (ECG) changes were simultaneously recorded for 30 min after the administration of CsCl. The administration was repeated several times at intervals 30 min. Sustained or non-sustained ventricular tachycardia was produced in all dogs. EAD appeared in 8 of 12 dogs. When EAD developed sufficiently high amplitude, ventricular premature beats occurred near the peak of EAD and TdP was induced in 3 of 8 EAD-positive dogs. TdP was not induced in EAD-negative dogs. Although TdP was comparatively difficult to induce, EAD-triggered activity was suggested to be one of the necessary conditions for TdP, because TdP occurred only when EAD reached a sufficiently high amplitude to produce ventricular premature beats.

The relationship between early afterdepolarization and the occurrence of torsades de pointes. An in vivo canine model study.