A Case of Sudden Cardiac Death due to Pilsicainide-Induced Torsades de Pointes
An 84-year-old male visited our hospital due to palpitations and shortness of breath that began two days previously. He underwent physical examination, 12-lead ECG, chest X-ray, and blood tests. The patient's heart rate was 150 beats/min, and his blood pressure was 126/76 mm Hg. Chest X-ray revealed no cardiomegaly (cardiothoracic index=46%) and no congestion. An ECG examination showed atrial fibrillation, which was considered to be of recent onset (within 48 hours). Although ECG showed a tendency for poor progression of R in V 1-3, the patient had no chest pain and no history of coronary artery disease. In addition, an echocardiography, which was performed in a private clinic two months before the patient visited our hospital, showed normal left ventricular wall motion; during the past two months, there were no significant differences of ST-T changes in ECG. Routine laboratory tests revealed serum sodium of 142 mEq/L, potassium of 4.8 mEq/L (no hypokalemia and hyperkalemia) and creatinine of 1.0 mg/dL, which were indicative of mild renal dysfunction. Thus, oral low-dose pilsicainide at 50 mg twice daily was prescribed to convert atrial fibrillation to a sinus rhythm, and a Holter ECG was ordered in the outpatient clinic. In addition, he started anticoagulant treatment with warfarin but did not receive any other drugs, including any other antiarrhythmic drugs.\nOne day after receiving an oral administration of pilsicainide, he visited our hospital again, and a Holter monitor was fitted to evaluate the efficacy of pilsicainide and initiated at 13:30 in the afternoon. At this time, he felt no palpitations and showed a sinus rhythm with normal QT and QTc intervals (320 msec and 400 msec, respectively) in the CM5 lead of the Holter ECG (). However, the patient died during his sleep 18 hours after the Holter ECG was started. He reported no discomfort during the day or before his sudden death.\nThe analysis of the Holter ECG recording revealed that the cause of sudden death was an episode of TdP (). The Holter ECG showed that the patient developed atrial fibrillation followed by repetitive non-sustained and sustained TdP ( and ). As shown in , the QTc interval in the Holter ECG showed gradual elongation from 13:30 at the start until 6:00 the next day. At 7:00 the next day, TdP was observed, and it continued for approximately one hour; at 8:00, cardiac arrest was detected in the Holter ECG. The electrophysiological parameters, QRS complexes, RR, and QTc interval were measured. The segments with excessive noise, ectopic activity and atrial fibrillation were excluded from the analysis. illustrates the trend of the electrophysiological parameters. The QTc interval was clearly prolonged compared with that of initial Holter ECG. At the same time, the width of the QRS complexes was slightly prolonged compared with that of the initial Holter ECG.