This case study (n=1) documents the cardiotoxicity of the highest survived dose of ibogaine (4.55‐4.9g/70kg) ingested by a 61-year-old man in the context of seeking alternative treatment to overcome a long-standing opioid dependency related to chronic pain. Ibogaine increased heart rate and prolonged the time to recharge heart muscles between beats, and it took 7 days for the patient’s heart rhythm to normalize due to the long plasma half-life of the substance. Ibogaine intoxication is therefore a potentially life-threatening scenario due to the cardiotoxic risk of ventricular arrhythmia and requires prolonged cardiac monitoring within a critical care unit.

Abstract

“Introduction: Ibogaine is a psychoactive herbal medication with alleged antiaddiction properties.

Method: We report a case of ibogaine intoxication mimicking Long‐QT syndrome resulting in ventricular flutter and nearby cardiac arrest.

Result: A 61‐year‐old man experienced massive QT prolongation and ventricular flutter at a rate of 270 beats per minute requiring defibrillation after ingestion of a large dose of Ibogaine. The ingested dose of 65‐70 mg/kg represents the highest survived ibogaine dose reported to date. As a result of the long plasma half‐life of ibogaine, it took 7 days for the patient’s QT interval to normalize.”

Authors: Christian Steinberg & Marc W. Deyell

Summary

A 61-year-old man suffered massive QT prolongation and ventricular flutter after ingesting 6570 mg/kg of ibogaine. He required defibrillation.

1 | INTRODUCTION

A 61-year-old male presented to a holistic, naturopathic clinic with a long-standing opioid dependency and chronic pain. He had no history of cardiovascular disease or inherited arrhythmia.

A patient was provided with ibogaine capsules (first-time use) and ingested an approximate single dose of 5.6 g of ibogaine. He developed severe gastrointestinal symptoms and was transferred to the ER of the nearest hospital.

On arrival at the emergency room, the patient was pale, diaphoretic, barely arousable, and had a monomorphic wide QRS complex tachycardia with a rate of 270 beats per minute. He was converted to sinus rhythm with emergency defibrillation, and his hypokalemia was aggressively treated.

A patient was admitted with ibogaine-induced QT prolongation (cotriggered by secondary hypokalemia) triggering ventricular tachycardia. His QTc corrected after 7 days and no further ventricular arrhythmia occurred.

3 | DISCUSSION

Ibogaine, a substance that is not approved in many Western countries, has been used by independent addiction clinics over the last decade.

Ibogaine causes sinus bradycardia and marked QT prolongation, which mimic the hereditary Long-QT syndrome type 2 that is caused by a genetic loss-of-function of the IKr channel (encoded by the KCNH2 gene). Ibogaine can also cause life-threatening ventricular arrhythmia and sudden death.

A patient with severe cardiotoxicity after ibogaine use presented with significant hypokalemia, heavy gastrointestinal symptoms, and a massive QT prolongation up to 714 ms. The estimated ingested dose of 65-70 mg/kg would represent the highest survived ibogaine dose reported to date.

The long half-life of noribogaine is illustrated by the delayed QT recovery of our patient. This emphasizes the need for prolonged cardiac monitoring in those patients.

Ibogaine intoxication is a potentially life-threatening scenario due to the high cardiotoxicity of this substance. Prolonged cardiac monitoring is recommended until entire QT normalization.