Effect of adenosine or adenosine triphosphate on antidromic tachycardia

Objectives. This study was designed to determine the effect of adenosine or adenosine triphosphate (ATP) on antidromic tachycardia. Background. Adenosine and adenosine triphosphate are useful for differential diagnosis of wide QRS tachycardia. It has been believed that tachycardia termination caused by these agents is due to the preferential depressive effect on the atrioventricular (AV) node, whereas their effect on accessory pathways is minimal. Methods. We studied the effect of adenosine or ATP on the termination pattern of antidromic tachycardia in 17 patients (10 men, 7 women; mean age [±SD] 32 ± 11 years) with one or more accessory pathways. Adenosine (6 to 12 mg [n = 10]) or ATP (8 to 20 mg [n = 7]) was injected rapidly through a central venous line and followed by 10 ml of saline flush after induction of sustained antidromic tachycardia. Results. Tachycardia was terminated in < 2 min in 14 patients (82%) after the injection and remained unchanged in 3 (18%). Tachycardia termination was due to conduction block in the accessory pathway (anterograde limb) in seven patients (50%) and in the AV node (retrograde limb) in another seven. Adenosine or ATP caused accessory pathway block in seven (88%) of the eight patients lacking retrograde accessory pathway conduction and in none of the nine patients having retrograde accessory pathway conduction (p < 0.01). All five ptients with an atriofascicular accessory pathway and unidirectional anterograde conduction had tachycardia termination due to anterograde accessory pathway block after injection of adenosine or ATP. Conclusions. 1) Adenosine or ATP effectively terminates antidromic tachycardia; 2) the termination is related to block in either the accessory pathway or the AV node; 3) accessory pathway block occurs in patients with a unidirectional, anterogradely conducting accessory pathway, especially an atriofascicular accessory pathway.