Cardiac arrest after ibogaine intoxication

Drug-induced prolongation of the QT interval on the electrocardiogram can precipitate life‑threatening ventricular arrhythmias and is an important consideration when evaluating unexplained torsades de pointes or ventricular fibrillation. The introduction frames ibogaine, a psychoactive plant alkaloid used informally for its alleged antiaddiction effects, as a potential cause of such cardiotoxicity. Steinberg and colleagues present a single case that illustrates severe QT prolongation after ibogaine ingestion leading to malignant ventricular arrhythmia and near cardiac arrest. The report aims to document the clinical course, emphasise the delayed recovery of QT interval related to the drug's pharmacology, and highlight safety concerns around unsupervised use.

This paper is a single‑patient case report. The extracted text describes a 61‑year‑old man with chronic pain–related opioid dependence who self‑presented to a naturopathic clinic for alternative therapy. Relevant medical history included prior spinal surgeries, chronic cervicolumbar pain, depression, mild hypertension and dyslipidaemia. There was no personal or family history of cardiovascular disease, unexplained syncope, or inherited arrhythmia reported in the extraction. The patient ingested an estimated single oral dose of approximately 5.6 g of ibogaine, which the authors convert to roughly 65–70 mg/kg based on body weight; ibogaine was administered without medical prescription or supervision. Clinical monitoring and investigations after deterioration included serial 12‑lead ECGs, serum electrolytes (potassium, magnesium, calcium), laboratory screening for co‑intoxication, and supportive care in an emergency department setting with subsequent transfer to intensive care. The ECG QT interval was measured using a maximal slope technique and corrected for heart rate using Bazett's formula (QTc). The authors did not report measurement of serum ibogaine or noribogaine concentrations.

Six to twelve hours after ingestion the patient developed severe gastrointestinal symptoms (heavy vomiting and diarrhoea), followed by altered level of consciousness and collapse. On arrival to the emergency department he was pale, diaphoretic, barely arousable, and had no palpable radial pulse or measurable blood pressure. The presenting 12‑lead ECG showed a monomorphic wide QRS complex tachycardia at about 270 beats per minute, described as near‑ventricular flutter. Emergent defibrillation restored sinus rhythm. Post‑defibrillation ECGs demonstrated marked QT prolongation with ventricular bigeminy. The absolute QT interval in this patient reached up to 714 ms, among the largest values reported in the literature according to the authors. Initial laboratory tests showed pronounced hypokalaemia (serum K+ 2.4 mmol/L) with normal magnesium and calcium concentrations. Hypokalaemia was aggressively corrected within 12 hours and the patient's haemodynamics improved with supportive care. Screening for additional toxic substances was negative. Serial ECG monitoring documented delayed QTc recovery, with complete normalisation of the QTc interval occurring after 7 days despite normal electrolytes and absence of other QT‑prolonging medications. The extracted text notes that the estimated ingested dose (65–70 mg/kg) would represent the highest survived ibogaine dose reported to date, but the authors caution that dosing estimates are uncertain because preparations are nonstandardised and no serum ibogaine measurement was performed.

Steinberg interprets this case as an example of pronounced ibogaine cardiotoxicity. Ibogaine is a psychoactive indole alkaloid derived from Tabernanthe iboga and has been used traditionally in West‑Central African spiritual contexts; it attracted medical interest for alleged antiaddiction effects but is not approved in many Western countries because of safety concerns. The authors emphasise that nonmedical clinics have increasingly offered ibogaine treatment in recent years, often operating without cardiac monitoring. Pharmacologically, ibogaine is metabolised to the active compound noribogaine, which has a long plasma half‑life (reported here as 28–40 hours) and detectable levels in serum and urine. Cardiac effects include sinus bradycardia and marked QT prolongation resulting from interactions with multiple cardiac ion channels; the electrophysiological profile mimics congenital Long‑QT syndrome type 2, which is caused by loss‑of‑function in the IKr channel (encoded by KCNH2). The authors propose that arrhythmia in this case was initiated by late‑coupled ventricular ectopy (triggered activity) on the background of massive QT prolongation, with hypokalaemia serving as a proarrhythmic co‑trigger related to the patient's vomiting and diarrhoea. They note reported onset of cardiotoxic symptoms in the literature ranges from about 1.5 to 76 hours after ingestion. Key limitations acknowledged in the report are uncertainty about the actual ingested dose because of nonstandardised capsule preparations (ibogaine content may vary substantially, cited as roughly 15%–50% depending on preparation) and the absence of direct serum measurements of ibogaine or noribogaine. The prolonged QTc normalisation over 7 days is attributed to the long half‑life of noribogaine, and the authors highlight that prior reports often lacked detailed QT recovery documentation. From these observations they recommend urgent critical care admission and prolonged cardiac monitoring until complete QT normalisation in cases of ibogaine intoxication, because malignant ventricular arrhythmia may occur early or late after ingestion. They conclude that, although uncommon, ibogaine intoxication can be life‑threatening due to its high cardiotoxic potential.