• K L Lee, H M Chun, L B Liem, and R J Sung.
• University Department of Medicine, Queen Mary Hospital, Hong Kong, PR China. klflee@khucc.hku.hk
• Pacing Clin Electrophysiol. 1999 Jun 1; 22 (6 Pt 1): 866-70.

AbstractAccelerated AV junctional rhythm is postulated to be due to enhanced automaticity of a high AV junctional focus. The adenosine response of this rhythm was tested in 17 patients (7 males, 12-83 years). The indications of electrophysiology study were nonspecific palpitation (n = 5), unexplained syncope (n = 6), postablation of accessory pathways (n = 4), and postmodification of AV nodal reentry tachycardia (n = 2). The sinus node and AV nodal functions were normal. Pacing and programmed electrical stimulation failed to induce any arrhythmia at baseline. The accelerated junctional rhythm (cycle length = 553 +/- 134 ms) was initiated spontaneously in all patients after isoproterenol infusion (1-2 micrograms/min). It was not suppressible by overdrive pacing. Cessation of isoproterenol infusion terminated the rhythm in all patients. Adenosine (6 mg) reproducibly terminated the accelerated junctional rhythm in all patients. In six patients, adenosine suppressed the junctional rhythm without producing AV nodal block. In the other 11 patients, the junctional rhythm was terminated prior to the occurrence of AV nodal block. Verapamil was tested in ten patients and 5 mg of intravenous verapamil terminated the junctional rhythm in all patients. In conclusion, the mechanism of catecholamine-induced accelerated AV junctional rhythm is most likely enhanced automaticity, and catecholamine-induced accelerated AV junctional automaticity is sensitive to adenosine and verapamil. Adenosine appears to have differential effects on catecholamine-enhanced AV junctional automaticity and AV nodal conduction. This suggests that, under catecholamine stimulation, adenosine may have different mechanisms of action on AV nodal conduction and automaticity.

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