AIMS: Intravenous administration of adenosine after a pulmonary vein (PV) isolation procedure can unmask residual, so-called 'dormant', conduction that would otherwise remain unnoticed. Elimination of these dormant potentials is challenging because of the transient effect of adenosine, often requiring repeated injections. We tested the hypothesis that dipyridamole, a drug which inhibits adenosine deamination, can provoke longer-lasting unmasking of dormant conduction. METHODS AND RESULTS: In 191 patients with drug refractory paroxysmal atrial fibrillation, a bolus of 12-24 mg of adenosine was administered after all 764 PVs were isolated. In the case of transient dormant conduction, a short infusion of dipyridamole 50 mg was given and a bolus of adenosine was repeated. In all cases, re-isolation was attempted guided by the activation pattern in the PV on a circular mapping catheter. Duration of adenosine-induced dormant conduction before and after dipyridamole was recorded as the time between administration of adenosine and cessation of dormant conduction either spontaneously or by catheter ablation. Transient dormant conduction was re-established by a single bolus of adenosine in 24 of 191 patients (12.6%). Mean duration of adenosine-induced dormant conduction before dipyridamole was 13.1 ± 6.4 s, whereas it was significantly longer at 218.9 ± 165.6 s after dipyridamole (P < 0.0001). Eighteen of the 24 PVs were re-isolated by catheter ablation before spontaneous cessation of dormant conduction, and in 6 cases dormant conduction disappeared spontaneously before PV re-isolation was achieved. CONCLUSION: Dipyridamole significantly prolongs the effect of adenosine to unmask dormant conduction after PV isolation and may thus facilitate its elimination by catheter ablation.
AIMS: Intravenous administration of adenosine after a pulmonary vein (PV) isolation procedure can unmask residual, so-called 'dormant', conduction that would otherwise remain unnoticed. Elimination of these dormant potentials is challenging because of the transient effect of adenosine, often requiring repeated injections. We tested the hypothesis that dipyridamole, a drug which inhibits adenosine deamination, can provoke longer-lasting unmasking of dormant conduction. METHODS AND RESULTS: In 191 patients with drug refractory paroxysmal atrial fibrillation, a bolus of 12-24 mg of adenosine was administered after all 764 PVs were isolated. In the case of transient dormant conduction, a short infusion of dipyridamole 50 mg was given and a bolus of adenosine was repeated. In all cases, re-isolation was attempted guided by the activation pattern in the PV on a circular mapping catheter. Duration of adenosine-induced dormant conduction before and after dipyridamole was recorded as the time between administration of adenosine and cessation of dormant conduction either spontaneously or by catheter ablation. Transient dormant conduction was re-established by a single bolus of adenosine in 24 of 191 patients (12.6%). Mean duration of adenosine-induced dormant conduction before dipyridamole was 13.1 ± 6.4 s, whereas it was significantly longer at 218.9 ± 165.6 s after dipyridamole (P < 0.0001). Eighteen of the 24 PVs were re-isolated by catheter ablation before spontaneous cessation of dormant conduction, and in 6 cases dormant conduction disappeared spontaneously before PV re-isolation was achieved. CONCLUSION:Dipyridamole significantly prolongs the effect of adenosine to unmask dormant conduction after PV isolation and may thus facilitate its elimination by catheter ablation.