BACKGROUND
Torsades de pointes (TdP) is a life-threatening form of ventricular tachycardia characterized by QRS complexes twisting around the isoelectric line on electrocardiography and can be associated with a prolonged QT interval. Management of these combined conditions can be challenging. This report presents 2 cases of refractory torsades de pointes arising from distinct mechanisms—short-coupled variant TdP and acquired long QT syndrome—following myocardial infarction.
CASE REPORT
Case 1 was a 53-year-old woman with a prior unexplained cardiac arrest who presented with a TdP electrical storm in the context of short-coupled premature ventricular contractions (coupling interval 200 ms) and a corrected QT interval (QTc) within normal limits (459 ms), consistent with short-coupled variant TdP. Sequential pharmacological therapy and overdrive ventricular pacing escalated to 150 beats per minute both failed; arrhythmia cessation was temporally associated with subsequent intravenous lidocaine, an agent historically among the least effective for this entity. A dual-chamber implantable cardioverter-defibrillator was implanted. Case 2 was a 79-year-old woman who developed extreme QTc prolongation (708 ms) 4 days after primary percutaneous coronary intervention for anterior ST-elevation myocardial infarction, sustaining more than 50 daily TdP episodes refractory to pharmacological therapy; overdrive pacing at 100 beats per minute abolished the arrhythmia, with the QTc normalizing to 461 ms at 3-month follow-up.
CONCLUSIONS
These cases illustrate how distinguishing the likely electrophysiological mechanism of refractory TdP may help guide rescue therapy. Overdrive pacing was effective in the acquired long QT case and ineffective in the short-coupled case, in which the arrhythmia was controlled only after lidocaine was added—an unusual observation in this setting.

Keywords: Death, Sudden, Cardiac; Long QT Syndrome; Torsades de Pointes; Ventricular Fibrillation; Ventricular Premature Complexes