Key result
Artemisinin completely suppresses VT in canine Brugada syndrome models, reducing J-wave area and AP notch.
Why the study?
Certain natural flavones show promise as Ito current inhibitors in BrS models, prompting investigation of the antiarrhythmic effects of acacetin and artemisinin in an experimental canine BrS model.
Do the flavones artemisinin and acacetin suppress ventricular tachyarrhythmia in an experimental canine model of Brugada syndrome?
Do the flavones artemisinin and acacetin suppress ventricular tachyarrhythmia in an experimental canine model of Brugada syndrome?
Artemisinin and acacetin demonstrate antiarrhythmic potential in an experimental Brugada syndrome model, with artemisinin showing more effective suppression of electrophysiological abnormalities.
Answers are grounded in this paper and cite their sources.
Artemisinin shows antiarrhythmic effects in canine Brugada model; hypothesis-generating and leaves open human translation.
Background and Objectives Certain natural flavones, such as acacetin (AC) and artemisinin (AR), have shown promise as inhibitors of Ito currents in Brugada syndrome (BrS) models. This study aimed to investigate the antiarrhythmic effects of these flavones in an experimental canine model of BrS. Subjects and Methods Ventricular transmembrane action potentials (APs) and transmural pseudo-electrograms were simultaneously recorded from coronary-perfused left ventricular wedge preparations in pharmacologically induced canine BrS phenotypes (using acetylcholine, verapamil, and an Ito agonist). Electrophysiological and antiarrhythmic effects were evaluated following perfusion with AR and AC. Results The provocative agents successfully induced BrS. Heterogeneous loss of the AP dome resulted in significant repolarization dispersion, leading to phase 2 reentry and the subsequent development of ventricular tachyarrhythmia (VT). AR (100 µM) effectively suppressed VT in 9/9 preparations. It significantly reduced transmural dispersion of repolarization (TDR), AP notch magnitude, and J-wave area (TDR: 24.64 ± 4.34 ms to 14.66 ± 2.63 ms, p = 0.06; AP notch magnitude: 25.84 ± 2.81% to 10.62 ± 1.62%, p < 0.001; J-wave area: 22.81 ± 3.70 mV·ms to 6.25 ± 1.54 mV·ms, p < 0.001). AC (4 µM) suppressed VT in 4/4 preparations but failed to restore TDR, AP notch magnitude, or J-wave area. The percentage reduction in TDR and decrease in AP notch magnitude showed no significant difference between AR and AC (TDR reduction: 40.53 ± 20.79% vs. 51.52 ± 49.55%, p = 0.102; AP notch magnitude decrease: 58.91 ± 12.11% vs. 24.28 ± 19.07%, p = 0.138). Conclusions Both AR and AC demonstrated antiarrhythmic potential in an experimental BrS model. However, AR (100 µM) more effectively suppressed VT. Further studies on dose titration are warranted.
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Yoon et al. (2025) studied Brugada syndrome (experimental canine model) (n=13). Artemisinin and Acacetin vs. Baseline (pharmacologically induced BrS) was evaluated on Suppression of ventricular tachyarrhythmia (VT). Artemisinin (100 µM) and acacetin (4 µM) suppressed ventricular tachyarrhythmia in a canine Brugada syndrome model, with artemisinin significantly reducing AP notch magnitude (p<0.001).
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