Drug-induced QT prolongation: consequences and current dilemma

Abstract

An 86-year-old woman was admitted with falls. She was taking no medication and had no family history of long QT syndrome. An electrocardiogram (ECG) revealed atrial fibrillation at 160 beats per minute. Rate control was commenced with digoxin and metoprolol, to a total dosage of 625 μg and 137.5 mg respectively. On day 8, the therapy was changed to attempt chemical cardioversion with sotalol at a dosage of 40 mg daily. After a cumulative sotalol dosage of only 120 mg, given over 3 days, the ECG showed extreme QT interval prolongation (800 msec) and bizarre T, or TU wave inversion (Figure 1). Blood tests were normal (K+ 5.3 mmol/litre, Mg++ 0.97 mmol/litre, Ca++ 2.45 mmol/litre) and troponin T was negative. An echocardiogram showed normal dimensions and function. The patient experienced numerous runs of polymorphic ventricular tachycardia (torsade de pointes) precipitated by repeated ‘R on T’ events (Figure 2). Intravenous magnesium had no effect. Temporary pacing was used to overdrive pace the patient. The patient was commenced on a low dose of bisoprolol and made a complete recovery to sinus rhythm and a normal QT interval.