Volume 28, Issue s1 pp. S158-S162

Edrophonium-Induced Right Ventricular Outflow Tract Tachycardia

HITOSHI HACHIYA

HITOSHI HACHIYA

Cardiology Department, Yokosuka Kyosai General Hospital, Kanagawa

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KAZUTAKA AONUMA

KAZUTAKA AONUMA

Division of Cardiology, University of Tsukuba Graduate School of Comprehensive Human Sciences

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YASUTERU YAMAUCHI

YASUTERU YAMAUCHI

Cardiology Department, Yokosuka Kyosai General Hospital, Kanagawa

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YUKIO SEKIGUCHI

YUKIO SEKIGUCHI

Cardiology Department, Yokosuka Kyosai General Hospital, Kanagawa

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YOSHITO IESAKA

YOSHITO IESAKA

Cardiology Department, Tsuchiura Kyodo Hospital, Ibaraki, Japan

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First published: 31 January 2005
Citations: 8
Address for reprints: Kazutaka Aonuma, M.D., Division of Cardiology, University of Tsukuba Graduate School of Comprehensive Human Sciences, 1–1-1 Tennoudai, Tsukuba-shi, Ibaraki-ken 305-8575, Japan. Fax: (29)-853-3143; e-mail: [email protected]

Abstract

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.

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