Cesium‐Induced Atrial Tachycardia Degenerating into Atrial Fibrillation in Dogs: Atrial Torsades de Pointes?

INTRODUCTION: In this study, we investigated whether the potassium channel blocker, cesium chloride (CsCl), which is capable of producing early after-depolarizations (EADs) and polymorphic ventricular tachyarrhythmias resembling torsades de pointes, might exert similar effects in the atria. METHODS AND RESULTS: In nine anesthetized open chest dogs, 5 mL of CsCl in incremental doses (0.05, 0.1, 0.15, 0.2, 0.25 mM/mL) was injected into the sinus node artery to induce atrial arrhythmias. A polymorphic atrial tachycardia (P-AT) apparently triggered by an EAD and degenerating into atrial fibrillation resulted after CsCl administration in six dogs, but not in the remaining three dogs at any dose of CsCl. The P-AT developed during a normal atrial rate (110+/-13.5 beats/min) on six occasions and during atrial bradycardia (58.6+/-17.9 beat/min) five times. P-AT that occurred during a normal atrial rate had the last normal P wave temporally closely related to ventricular activation, with a VA interval of almost zero (1.3+/-3.3 msec), whereas P-AT induced from an atrial bradycardia had no relation to ventricular activation. The %EAD in the atrial bradycardia group (13.9+/-2.5) exceeded that in the normal atrial rate group (10.9+/-1.8) (P < 0.05). CONCLUSION: CsCl induces atrial EADs that provoke P-AT that degenerates into atrial fibrillation. P-AT has some characteristics similar to ventricular torsades de pointes.