The mechanism by which magnesium therapy suppresses some ventricular tachyarrhythmias characterized by a prolonged QT interval (e.g., torsades de pointes) is unknown. Since early afterdepolarizations have been proposed as a cause of the long QT syndrome and the related ventricular tachyarrhythmias, we hypothesized that magnesium therapy would suppress both the early afterdepolarizations and the ventricular arrhythmias. The present study was performed to test that hypothesis. Using monophasic action potentials (MAP) recorded with a contact electrode from the right ventricular endocardium to demonstrate early afterdepolarizations, cesium chloride (168 mg/kg iv) was administered before, during, and 1 to 2 hr after discontinuation of a magnesium infusion (1 to 2 mg/kg/min for 20 to 30 min). Before magnesium infusion, cesium induced early afterdepolarizations that were 49.7 + 1.6% (mean + SE) of the amplitude of the corresponding monophasic action potential. The amplitude of the early afterdepolarization decreased to 31.2 ± 3.8% of the MAP amplitude during magnesium infusion (p<.003) and increased to 48.0 ± 4.0% 1 to 2 hr after termination of the magnesium infusion (p<.003). Cesium induced sustained monomorphic ventricular tachycardia, torsades de pointes, or ventricular fibrillation in 12 of 13 dogs before magnesium infusion, and in eight of 11 dogs 1 to 2 hr after stopping infusion, but in only three of 13 dogs during magnesium infusion. Cesium prolonged the corrected QT interval from 338 ± 16 msec (control) to 387 ± 14 msec before (p<.003), 356 ± 12 msec during (p<.003), and 406 ± 16 msec after stopping the magnesium infusion (p< .003). Magnesium also suppressed early afterdepolarizations induced with cesium in isolated canine Purkinje fibers. These data support the conclusion that magnesium's mechanism of action is to suppress early afterdepolarizations, prolonged QT interval, and ventricular tachyarrhythmias induced by cesium. Successful responses in patients may occur by a similar mechanism of early afterdepolarization suppression. Circulation 77, No. 6, 139577, No. 6, -140277, No. 6, , 1988 INITIALLY described by Dessertenne, torsades de pointes is characterized by a prolonged QT interval and paroxysms of ventricular tachycardia with polymorphic QRS complexes revolving around an isoelectric baseline.2' 3 The mechanism responsible for torsades de pointes is not clear; it may result from triggered activity induced by early afterdepolarizations (EADs).4-9 While recommended therapy for torsades de pointes is a rate increase induced with isoproter-

Early afterdepolarizations (EADs) are depolarizing potentials that occur before complete repolarization. They may be important in the acquired and possibly the idiopathic long QT syndrome and associated ventricular tachycardia (VT). (Circulation 1988;78:1241-1250 Under certain conditions, the sympathetic nervous system can profoundly influence the electrophysiological properties of the heart and thereby the genesis of ventricular tachy-

Amiodarone instilled into the pericardial sac migrates transmurally to produce significant electrophysiologic effects at superficial sites and appears to suppress electrically induced atrial fibrillation.

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