Effects of nicorandil, a potassium channel opener, on idiopathic ventricular tachycardia
Youichi Kobayashi, MDa,
Akira Miyata, MDa,
Kaoru Tanno, MDa,
Shuji Kikushima, MDa,
Takao Baba, MDa and
Takashi Katagiri, MDa
a Third Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan
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Figure 1 Termination of sustained VT by nicorandil. Ventricular tachycardia with an LBBB pattern and a left inferior axis was induced by RV stimulation under isoproterenol provocation. Ventricular tachycardia was gradually slowed and terminated by injection of 5.2 mg nicorandil.
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Figure 2 Efficacy of ATP, nicorandil and verapamil on nonsustained VTs in a representative case. The VT revealed an LBBB pattern and an inferior axis. (A) Nonsustained VTs that were observed 45 times in a 3-min period (150 per 10 min) in the control state. An ATP bolus injection was performed between calibrations in line 8. Nicorandil injection started at calibration in line 11. The nonsustained VT was suppressed from six times in 30 s before ATP administration to once in 30 s after ATP administration. Couplets and nonsustained VTs were suppressed from 13 times in 30 s before ATP administration to five times in 30 s after ATP administration (reduction rate 83% and 62%, respectively, C). The nonsustained VTs were suppressed after nicorandil administration, from 45 times in 3 min before administration to 17 times in the same period after administration (before administration 150 times in 10 min; after administration 60 times in 10 min; reduction rate 60%; C). (B) Forty minutes later nonsustained VT returned to the control level, and the VTs were suppressed from 83 times to 6 times in a 5-min period after verapamil administration (before administration 166 in 10 min; after administration 12 times in 10 min; reduction rate 93%; C).
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Figure 3 The efficacy of nicorandil and verapamil on nonsustained VTs. (Top) Time course of couplets and nonsustained VTs in five patients who had nicorandil-sensitive nonsustained VT. The arrhythmias were reduced significantly by nicorandil (before nicorandil: 141 ± 99 in 10 min; after nicorandil: 34 ± 40 in 10 min; p < 0.05), and then reappeared 30 min later (68 ± 62 in 10 min). The arrhythmias were reduced again after verapamil (4 ± 4 in 10 min). (Bottom) Percentage of inhibition of the arrhythmias by drugs. Verapamil suppressed >50% of the arrhythmias in four of four patients with nicorandil-sensitive nonsustained VT who were tested. One VT (patient H.T.) was not suppressed by nicorandil and verapamil, although ATP suppressed it.
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Figure 4 Effect of nicorandil on QT intervals. (Open circles) Eight patients with nicorandil-sensitive VT. (Crosses) Four patients with nicorandil-insensitive VT. In all 12 patients the RR intervals did not change after nicorandil (p = NS), although both the QT and QTc intervals were significantly reduced. A similar trend was also seen in the patients in whom nicorandil was effective (control vs. nicorandil: RR—515 ± 73 vs. 511 ± 67 ms, p = NS; QT—359 ± 50 vs. 339 ± 50 ms, p < 0.05; QTc—500 ± 46 vs. 474 ± 51, p < 0.05). However, no significant difference was seen in the three indexes in patients in whom nicorandil was not effective (control vs. nicorandil: RR—511 ± 76 vs. 545 ± 125 ms, p = NS; QT—328 ± 27 vs. 320 ± 52 ms, p = NS; QTc—460 ± 15 vs. 434 ± 38, p = NS).
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