Fig. 1
Ibogaine and noribogaine impair the electrophysiology of the human heart.
a Action potential (AP) recordings from human cardiomyocytes under control conditions and after superfusion with bath solution containing 3 µM ibogaine (ibo,
top) or noribogaine (noribo,
bottom).
b Analysis of the retardation of AP repolarization by ibogaine and noribogaine. APD90 (mean ± SD,
n = 6–16), AP duration at 90 % repolarization. **(
p < 0.01) and ***(
p < 0.001), significantly different from control (paired Student’s
t test performed on raw data prior to normalization). The absolute APD90 values (in ms) were 282 ± 147 for control and 322 ± 165 for 3 µM ibogaine, as well as 264 ± 137 for control and 305 ± 155 for 3 µM noribogaine. APD50, AP duration at 50 % repolarization, was neither altered by 3 µM ibogaine (
p = 0.64) nor noribogaine (
p = 0.39).
c Proposed mechanism of cardiac arrhythmia generation after ibogaine intake. The cartoon summarizes the causal sequence of drug effects at the ion channel, cellular, and organ level: both ibogaine and noribogaine, the latter generated from ibogaine by CYP2D6 enzymes in the liver [
21,
22], block hERG potassium channels and thereby retard the repolarization phase of the ventricular AP. As a consequence, the QT interval in the ECG gets prolonged, and finally, cardiac arrhythmias emerge