Are reentrant atrial tachycardias sensitive to adenosine administration?

Abstract

Abstract Funding Acknowledgements Type of funding sources: None. Background Adenosine (ADN) infusion may terminate focal atrial tachycardia (AT). However, the effect of ADN on reentrant atrial tachycardia (RAT) is unclear and based on case reports and small series. These latter included mostly patients with cavotricuspid isthmus-dependent atrial flutter and provided conflicting results, with RAT termination found when it involved the septal or the tricuspid/mitral valve regions. Purpose The aim of this study was to test the response (termination, transient suppression or no effect) to ADN infusion on RATs and to evaluate differences according to the AT location. Methods The effect of ADN was prospectively studied at the time of catheter ablation in consecutive patients with AT. Only patients with RAT were included. This latter mechanism was established by activation and entrainment mapping and confirmed by catheter ablation. A 10 mg adenosine 5'-triphosphate (ATP) bolus was administered in all to evaluate the effects on AT cycle length and termination. Additional ATP bolus of 20 or 30 mg was administered if no AV block for at least 2 secs was obtained with the former ones. Results 58 patients (67, ±13 years old; 11 female) with 79 RAT were included. 38 RATs were right sided (34 cavotricuspid isthmus-depend atrial flutters, 1 lateral right atrium reentry, 1 upper loop reentry, 1 superior vena cava reentry, and 1 septal reentry around the coronary sinus) and 41 were left sided (21 perimitral reentry, 16 peripulmonary vein reentry and 4 with a small free wall reentry). No RAT was terminated or had a >20 ms cycle length prolongation following ADN administration. There was no transformation of the RAT into other mechanisms of AT or atrial fibrillation by ADN in any case. There were no complications. Conclusion RATs are insensitive to ADN infusion, with neither termination nor cycle length prolongation.