Lessons from a lethal prolongation

Abstract

A 61-year-old male was brought into the emergency department after an out-of-hospital cardiac arrest. The patient’s history consisted of previous heroin abuse, for which he had been taking methadone 120 mg/day for years. Two years prior, the patient had a first syncope, which was adjudicated to be an epileptic seizure. After a second syncope, an implantable loop recorder (ILR) was implanted.

After waking up, the patient asked for the time and subsequently lost consciousness. The arrest was witnessed by the spouse who alerted emergency services and started basic life support. Ventricular fibrillation was the first rhythm documented, and after a third shock, there was return of spontaneous circulation. The patient was intubated and transported to the emergency department. Blood tests revealed low potassium (2.9 mmol/L, reference 3.5–5.1 mmol/L) and normal magnesium levels. Interrogation of the ILR demonstrated polymorphic ventricular tachycardia (Figure 1A). An electrocardiogram (ECG) recorded 2 years previously already showed significant QTc prolongation while patient was on methadone, but this was unfortunately not recognized as such (Figure 1B). An ECG pre-dating his methadone use showed no QTc prolongation. The patient was admitted to the intensive care unit, and after correction of the hypokalaemia, additional ECGs confirmed the long QT interval in the absence of any QT-prolonging drugs other than methadone (Figure 1C). Unfortunately, electroencephalography demonstrated absent electrical brain activity, and the patient died after termination of supportive treatment. At autopsy, no structural heart disease was found, and genetic testing did not reveal any long QT syndrome (LQTS)–related mutation.