Idiopathic right ventricular outflow tract-ventricular tachycardia (RVOT-VT) generally occurs when sympathetic nervous system activity is increased, though, in a few patients, it develops when parasympathetic nervous activity (PNA) is increased. Among 101 consecutive patients with RVOT-VT confirmed by endocardial catheter mapping, 5 (4.9%) presented with nocturnal RVOT-VT. Autonomic nervous balance was studied by heart rate variability (HRV) analysis from 24-hour ambulatory electrocardiogram (ECG). Standard programmed ventricular stimulation (PVS), ventricular burst pacing, and drug provocation were performed to induce RVOT-VT. In the studied five patients, the average number of mostly nocturnal ventricular premature contractions (VPCs) was 6649 +/- 4472/day. Two patients had nocturnal nonsustained RVOT-VT on 24-hour ambulatory ECG recordings. The HRV analysis revealed that a progressive increase in high-frequency power coincided with an increase in VPCs or development of RVOT-VT at night, whereas low/high frequency ratio did not change significantly during the 24-hour period. RVOT-VT could not be induced by PVS, ventricular burst pacing, or isoproterenol or adenosine triphosphate i.v. However, RVOT-VT could only be induced by edrophonium, 5 mg i.v., in all patients. An increase in PNA was observed in a few patients before the development of RVOT-VT. Edrophonium facilitated induction of RVOT-VT in such patients.