Shahid Hameed, Asma Sharif, Tariq Mahmood Malik.
Non-Cardiac Drugs Causing Ventricular Arrhythmias.
Pak J Med Sci Jan ;17(1):45-9.

A 22 years old woman, mother of two children, was brought to the emergency department on a hot summer day. Her family gave history of sudden onset of drowsiness accompanied by high-grade fever of three hours duration. In the past history, she had tonsillectomy five years back, and had deflected nasal septum, for which she was awaiting surgery. For her nasal problem she was advised rhizin (cetirizine) two weeks before presentation. There was no history of sudden death in the family. At the time of presentation her peripheral pulses were not palpable and blood pressure was not recordable. Cardiac monitor showed episodes of bradycardia with prolonged QT interval and polymorphic broad complex tachycardia. The standard 12-lead electrocardiogram (ECG) recorded sustained ventricular tachycardia. She had immediate direct current (DC) cardioversion (3 shocks), following which sinus rhythm was restored, and hemodynamic stability achieved. The ECG in sinus rhythm was normal with rate corrected QT (QTc) of 460 ms. The patients was later managed in the coronary care unit. She was a little agitated though fully conscious. Her physical examination was normal, with a pulse rate of 108 per minute, a blood pressure of 115/70 mm Hg, and a temperature of 102 F. Her neurological examination was normal; she had no signs of meningeal irritation. A complete blood count showed leukocytosis of 11,000. Microscopic examination of the urine showed large number of pus cells. Serum sodium was 127 mmol/L, and potassium 2.7 mmol/L. Serum calcium and magnesium were within normal range. Computerized tomographic scan (CT) of the brain was normal. Lumbar puncture was carried out and cerebrospinal fluid analysis revealed no abnormality. The patient received immediate treatment with intravenous saline and potassium chloride to correct electrolyte imbalance. She was not given antiarrhythmic drugs and had no recurrence of ventricular tachycardia. Her pyrexia was treated with intravenous ceftriaxone 1 gram twice a day, and in view of possibility of malaria, fansidar was also given. The fever subsided after 48 hours. A normal echocardiogram out ruled structural heart disease and normal coronary angiography excluded anomalous coronary circulation as a possible cause of ventricular arrhythmia. The final diagnosis in this case is torsade de pointes, possibly precipitated by either the antihistamine or extremely low potassium level or both. The patients was asymptomatic when reviewed a month later. Her 24 hours holter monitor revealed no cardiac arrhythmia.

Case 2 : A 30 years old woman, mother of 5 children, was brought to a peripheral hospital in an unconscious state, early in the morning. She had collapsed at home 15 minutes earlier followed by a seizure like activity associated with tongue bite and urinary incontinence. The previous evening she had been prescribed an antimalarial, halofantrine, by a local practitioner for low grade pyrexia. At presentation, she was described to have cardiopulmonary arrest with no spontaneous breathing and absent pulses. Cardiopulmonary resuscitation was carried out after which she achieved hemodynamic stability (without DC shock or antiarrhythmic). Her ECG at that time showed polymorphic ventricular tachycardia and a sinus beat showing prolonged QT interval of 500 ms. On recovery her physical examination was normal, as was her blood count, blood urea and serum electrolytes. A CT scan of the brain was also done, which was normal. A week later, she was transferred to our care for further management. At that time she was on amiodarone (antiarrhythmic) and sodium valproate (antiepileptic). ECG still showed prolonged QT of 500ms. After carefully analyzing the data, we were convinced of the diagnosis of torsade de pointes caused by administration of halofantrine, so antiepileptic and antiarrhythmic therapy was stopped. She remained well and her QT interval normalized after two days.

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