Ventricular arrhythmias complicating weight reduction therapy in a patient with a prolonged QT interval

Abstract

Summary: Serious ventricular arrhytlmias are known to occur in patients with long QT intervals. We describe a case of torsade de pointes occurring in a patient with a prolonged QT interval while taking a 1000 calorie diet, diethylpropion hydrochloride (Tenuate Dospan) and bendrofluazide. In patients with long QT intervals, hypokalaemia and drugs which further delay repolarization may facilitate the development of life threatening arrhythmias.Case report A 35 year old housewife presented with a 24 h history ofbriefepisodes ofloss ofconsciousness. She had been taking a 1000 calorie diet for 3 weeks; bendrofluazide 5 mg/d and diethylpropion hydrochloride 75 mg/d were added for 10 d prior to admission. On admission the pulse was irregular and the blood pressure was 120/ 80 mm Hg. Cardiovascular and neurological findings were otherwise normal. Biochemical investigations revealed a reduced serum potassium of 2.4 mmol/l (normal range 3.5-4.5 mmol/l). All other biochemical and haematological tests were normal. The electrocardiogram revealed sinus rhythm, with frequent unimorphological ventricular ectopics. The measured QT interval (QTm) was 0.4s during a heart rate of 100 beats/min, and the corrected QT interval (QTc) according to Bazett (1920) was 0.52s (normal less than 0.44 s). The QRS and ST segments were normal and U waves were present. Chest radiograph and echocardiogram were normal.Cardiac monitoring showed episodes of ventricular tachycardia, of a torsade de pointes morphology (Figure 1), associated with episodes of loss of consciousness. Treatment included the withdrawal of bendrofluazide and diethylpropion hydrocholoride, potassium replacement and an intravenous infusion of mexiletine which suppressed ventricular arrhythmias. Two days later when the patient was normokalaemic, the QTc was prolonged at 0.50 s (QTm, 0.42 s, heart rate 85 beats/min) and U waves were absent (Figure 2).Three months later investigations were performed when the serum potassium was 3.9 mmol/l. The electrocardiogram revealed that QTc was persistently prolonged to 0.48 s (QTm 0.42 s, heart rate 77 beats/ min). No ventricular arrhythmias were induced by maximal treadmill exercise testing. An intracardiac electrophysiological study revealed normal conduction times and no ventricular arrhythmias were induced with programmed right ventricular stimulation, either before or after intravenous isoprenaline (7 ,Lg/ min for 5 min). The QTm during identical rates of atrial pacing was unchanged following the isoprenaline infusion. Subsequently. 100 mg/d of atenolol has shortened the QTc to 0.42 s (QTm 0.43 s, heart rate 51 beats/min) and the patient has remained asymp-