Response to Pharmacological Challenge of Dissociated Pulmonary Vein Rhythm

UNLABELLED: Dissociated pulmonary vein rhythm. INTRODUCTION: Characterization of the electrophysiologic behavior of the pulmonary vein (PV) triggers initiating atrial fibrillation (AF) is still lacking. We conducted the current study to evaluate the behavior of the dissociated PV rhythm (PVD) observed after electrical disconnection from the left atrium of the PV responsible for initiation of AF. METHODS AND RESULTS: Four hundred and seven consecutive patients (102 women; mean age 55+/-11 years) presented for ablation of symptomatic AF to our laboratory. After isolation, sustained dissociated rhythm (>10 minutes) was documented in 2.1% (34 of 1,568 PVs) of the PVs (initiating AF prior to isolation). Adenosine (18 mg IV bolus), verapamil (10 mg IV bolus), phenylephrine (200 mcg bolus followed by infusion at 100 mcg/hour), and isoproterenol (infusion rate of 15 mcg/hour) were administered in these patients. The cycle length of the PV rhythm before and after the administration of drugs was measured. Adenosine prolonged the sinus node (SN) cycle length (from 750+/-105 to 1,900+/-200 ms; P<0.05) and suppressed the PVD. Isoproterenol shortened both the SN (from 750+/-105 to 420+/-150 ms; P<0.05) and the PVD (from 2,225+/-300 to 800+/-190 ms; P<0.05) cycle length. A similar response to adenosine and isoproterenol of the PV firing was observed prior to isolating the arrhythmogenic PV. Phenylephrine prolonged the cycle length of both the SN (from 740+/-115 to 960+/-90 ms; P<0.05) and the PV rhythm (from 2,200+/-300 to 2,355+/-280 ms; P=0.87). Verapamil did not cause a significant change either in the SN or in the PVD cycle length. CONCLUSION: Our data suggest that the PVD within isolated PV responsible for initiating AF exhibits a response to pharmacologic agents similar to the SN cells.