ST-segment elevation and ventricular fibrillation without coronary spasm by intracoronary injection of acetylcholine and/or ergonovine maleate in patients with Brugada syndrome
Takashi Noda, MD*,
Wataru Shimizu, MD, PhD*,*,
Atsushi Taguchi, MD*,
Kazuhiro Satomi, MD*,
Kazuhiro Suyama, MD, PhD*,
Takashi Kurita, MD, PhD*,
Naohiko Aihara, MD* and
Shiro Kamakura, MD, PhD*
* Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, Suita, Japan

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Figure 1 Twelve-lead electrocardiogram (ECG) in the baseline condition (A), after injection of 50 µg acetylcholine (ACh) into the right coronary artery (B), and after ventricular fibrillation (VF) induction by ACh (C) in a patient with Brugada syndrome. The baseline ECG shows coved or saddle-back type ST-segment elevation in leads V1 and V2. Injection of ACh augmented the ST-segment elevation in leads V1 and V2 (B, arrows), without any induction of coronary spasm, resulting in spontaneously induced VF.
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Figure 2 Twelve-lead electrocardiogram in the baseline condition (A) and after injection of 40 µg ergonovine maleate (EM) into the right coronary artery (B) in a control subject. Injection of EM produced right coronary spasm (segment no. 2, 75%; segment no. 4, 100%), associated with ST-segment elevation in leads II, III, and aVF (B, arrows). However, no ST-segment elevation was observed in leads V1 to V3, like that in patients with Brugada syndrome (B, arrows).
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Figure 3 Twelve-lead electrocardiogram in the baseline condition (A), after injection of 50 µg acetylcholine (ACh) into the right coronary artery (B), and after injection of 40 µg ergonovine maleate (EM) into the right coronary artery (C) in a patient with Brugada syndrome. Injection of ACh augmented the ST-segment elevation in leads V1 and V2, without any induction of coronary spasm (B, arrows), whereas injection of EM did not change the ST-segment elevation.
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