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Acquired long-QT syndrome with recurrent pause-dependent torsades de pointes — ABIM Board MCQ

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HardArrhythmiaAcquired long-QT syndrome with recurrent pause-dependent torsades de pointesABIM Board

A 72-year-old woman is hospitalized for dofetilide initiation for persistent symptomatic atrial fibrillation. After the third dose, she converts to sinus rhythm. Telemetry subsequently shows sinus bradycardia at 42/min, frequent premature ventricular complexes, and several self-terminating episodes of polymorphic ventricular tachycardia initiated after long pauses. A 12-lead ECG between episodes shows a QTc interval of 620 milliseconds. Dofetilide is discontinued. Serum potassium is increased from 3.6 to 4.6 mEq/L, and serum magnesium is 2.3 mg/dL after intravenous magnesium sulfate administration. Despite these measures, she has two additional pause-dependent episodes. Between episodes, blood pressure is 124/68 mm Hg, and she has no chest pain; serial troponin concentrations are normal. She has no prior syncope or family history of sudden cardiac death. Which of the following is the most appropriate next intervention to prevent further episodes?

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Correct answer: C — Initiate temporary transvenous overdrive pacing

This patient has acquired long-QT syndrome with recurrent, pause-dependent torsades de pointes caused by dofetilide. The diagnostic discriminators are marked QTc prolongation, polymorphic ventricular tachycardia beginning after long pauses, and postconversion bradycardia. The offending medication has been stopped, potassium and magnesium have been repleted, and intravenous magnesium has failed to suppress recurrence. The next step is to increase the heart rate with temporary overdrive pacing, which shortens repolarization and prevents the pauses that trigger torsades. Amiodarone can further prolong repolarization and may worsen torsades; it is more appropriate for recurrent polymorphic ventricular tachycardia when the QT interval is not prolonged. Lidocaine may be used for polymorphic ventricular tachycardia associated with acute ischemia or a normal QT interval, neither of which is present here. Esmolol can worsen the bradycardia and pause dependence; beta-blockers are important in many congenital long-QT syndromes but are not the acute solution to bradycardia-mediated acquired torsades. A permanent pacemaker is premature because the bradycardia and QT prolongation have an identifiable, potentially reversible drug-related cause. Any episode that becomes sustained would require immediate unsynchronized defibrillation, but pacing is the appropriate intervention to prevent further recurrence while dofetilide clears.

Reference: Part 9: Adult Advanced Life Support (2025) — https://cpr.heart.org/en/resuscitation-science/cpr-and-ecc-guidelines/adult-advanced-life-support 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death (2017) — https://professional.heart.org/en/science-news/-/media/372e5f2704ae40b593b80f4d2a155e60.ashx