Watanabe Hiroshi, Chinushi Masaomi, Washizuka Takashi, Sugiura Hirotaka, Hirono Takashi, Komura Satoru, Hosaka Yukio, Yamaura Masayuki, Tanabe Yasutaka, Furushima Hiroshi, Fujita Satoru, Aizawa Yoshifusa
Division of Cardiology, Niigata University Graduate School of Medical and Dental Science, Asahimachidori, Niigata, Japan.
Pacing Clin Electrophysiol. 2005 May;28(5):372-7. doi: 10.1111/j.1540-8159.2005.09494.x.
Quinidine, a class I antiarrhythmic agent with blocking property of transient outward current, is a possible candidate for the suppression of ventricular fibrillation in patients with Brugada syndrome; although there is a concern that its ability to these effects may be proarrhythmic. Therefore, we evaluated the effect of quinidine sulfate on ST-segment elevation in Brugada syndrome. In 8 patients with Brugada syndrome, the magnitude of ST-elevation at the J-point (ST(J)), and the ST-segment configuration in leads V1-V3, were compared before and on day 2 after the initiation of quinidine administration. In 3 patients, quinidine attenuated ST(J) by > or = 0.1 mV. Of these 3 patients, ST-segment elevation was normalized in 2 patients, while the ST-segment configuration was unchanged in another. In another 3 patients, quinidine augmented ST(J) by > or = 0.1 mV without any change of ST-segment configuration, and the augmentation was returned to baseline after the discontinuation of quinidine. Quinidine exhibited no effect on the ST-segment in the remaining 2 patients. The favorable effects of quinidine on the ST-segment tended to be more pronounced in patients with prominent ST-elevation at baseline. In 1 patient, quinidine was effective in eliminating both ST-segment elevation and repetitive tachyarrhythmia episodes. In conclusion, the effects of quinidine on ST-segment elevation were variable. Quinidine may potentially augment the ST-segment elevation in some patients with Brugada syndrome.
