This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kobayashi, Y. Articles by Katagiri, T. Search for Related Content PubMed PubMed Citation Articles by Kobayashi, Y. Articles by Katagiri, T.

CLINICAL STUDIES

Effects of nicorandil, a potassium channel opener, on idiopathic ventricular tachycardia

^a Third Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan

Manuscript received October 20, 1997; revised manuscript received June 15, 1998, accepted July 2, 1998.

Address for correspondence: Dr. Youichi Kobayashi, Third Department of Internal Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, Japan 142-8666

Objectives. We assessed the effects of the adenosine triphosphate (ATP)–sensitive potassium channel opener, nicorandil, on ATP- and verapamil-responsive ventricular tachycardias (VTs).

Background. Adenosine- or ATP-sensitive VTs are thought to be due to a nonreentrant mechanism, presumably delayed afterdepolarization. We suggest that this potassium channel opener may suppress ATP- and verapamil-sensitive VTs.

Methods. The subjects included 13 patients with idiopathic VTs, 7 of whom had sustained VT and 6 of whom had nonsustained VT. We evaluated the effects of ATP, nicorandil and verapamil on VTs.

Results. Sustained VT: Verapamil had preventive effects on seven VTs. Four VTs were terminated by ATP, and of these, nicorandil terminated two and prevented exercise-induced VT in the two others. Three ATP-insensitive VTs, which were determined to be due to a reentry by an electrophysiologic study, were not terminated by nicorandil. Nonsustained VT: All six VTs were inhibited by ATP, and five of these were suppressed by nicorandil. Verapamil inhibited four of the five VTs. QT intervals and the corrected QT intervals were significantly shortened by nicorandil.

Conclusions. Nicorandil suppresses ATP- and verapamil-responsive VTs. One of the mechanisms of suppression by nicorandil might be related to a reduction of calcium in the myocardium, because it reduces the action potential duration.

Abbreviations and Acronyms   APD = action potential duration   ATP = adenosine triphosphate   LBBB = left bundle branch block   LV = left ventricular   QTc = corrected QT interval   RBBB = right bundle branch block   RV = right ventricular   VPC = ventricular premature contraction   VT = ventricular tachycardia

This article has been cited by other articles:

				H. Ueda, T. Hayashi, K. Tsumura, K. Yoshimaru, Y. Nakayama, and J. Yoshikawa Intravenous Nicorandil Can Reduce QT Dispersion and Prevent Bradyarrhythmia During Percutaneous Transluminal Coronary Angioplasty of the Right Coronary Artery Journal of Cardiovascular Pharmacology and Therapeutics, July 1, 2004; 9(3): 179 - 184. [Abstract] [PDF]

				J P Greenwood, I Malik, P Jennings, and R N Stevenson Haemodynamic and electrocardiographic consequences of severe nicorandil toxicity Emerg. Med. J., January 1, 2003; 20(1): 98 - 100. [Abstract] [Full Text] [PDF]