Ibogaine QTc Risk Calculator

QTc is the heart-rate-corrected interval between the start of ventricular depolarisation (Q) and the end of repolarisation (T) on a 12-lead EKG. Ibogaine and its metabolite noribogaine block the cardiac hERG (IKr) potassium channel, slowing repolarisation and lengthening QTc — typically by 20-60 ms at peak plasma concentrations. Above approximately 500 ms, the risk of torsades de pointes (a polymorphic ventricular tachycardia) climbs sharply.

It is a conservative central estimate drawn from published flagship dosing studies — Glue 2016, Mash 2018, Davis 2017, Knuijver 2022 — where peak QTc prolongation clustered between +20 ms and +60 ms at clinically used doses. Poor CYP2D6 metabolisers and patients on CYP2D6 inhibitors fall toward the upper end of that range because plasma noribogaine is higher and stays elevated longer. Individual response varies — this calculator estimates a mean, not a guarantee.

International cardiology guidelines flag QTc above 450 ms in men and 470 ms in women as borderline, and 500 ms or higher as the torsades risk threshold. For ibogaine, our medical team typically requires baseline QTc below 440 ms in men and below 460 ms in women, with no QTc-prolonging co-medications, normal potassium and magnesium, and no family history of long QT syndrome before scheduling. The calculator's tiers reflect those clinical limits.

Amiodarone has an unusually long elimination half-life — 40 to 55 days — and dramatically prolongs QTc on its own. It cannot be washed out within any practical timeline, and combining it with ibogaine creates an unacceptable arrhythmia risk. Patients on amiodarone are typically ineligible for ibogaine until alternative antiarrhythmic management is established with their cardiologist.

Yes — many factors are modifiable. Repleting potassium and magnesium can restore QTc within hours. Tapering or transitioning QTc-prolonging co-medications (citalopram, methadone, atypical antipsychotics, ondansetron) under physician supervision returns QTc toward baseline over days to weeks. Discontinuing CYP2D6 inhibitors removes the multiplier on ibogaine plasma exposure. Our admissions physician walks through each factor individually and builds a pre-treatment optimisation plan.

The calculator estimates a mean expected peak QTc using literature-derived effect sizes. It is intended for pre-screening and patient education, not as a substitute for a 12-lead EKG and cardiology review. Real EKG values, electrolyte panels, and continuous telemetry on dosing day remain the source of truth. Use the calculator to identify risk factors worth optimising before scheduling.

Every patient receives a baseline 12-lead EKG, comprehensive metabolic panel (including potassium and magnesium), liver and kidney function panels, and — when indicated — echocardiogram, troponin, or 24-hour Holter monitor. CYP2D6 phenotyping is offered when poor-metaboliser status is suspected. On dosing day, continuous cardiac telemetry runs from pre-medication through full noribogaine clearance, with a physician at bedside.

We do not turn patients away on a single borderline reading. Borderline QTc is often driven by reversible factors — low potassium, undiagnosed hypothyroidism, sleep apnea, or a co-medication. Our team works with your prescriber to optimise these factors, repeats the EKG after intervention, and re-tiers eligibility. Some patients move from caution to eligible after a focused two-week workup.