• S Banai and D Tzivoni.
• Heiden Department of Cardiology, Bikur-Cholim Hospital, Jerusalem, Israel.
• J. Cardiovasc. Electrophysiol. 1993 Apr 1;4(2):206-10.

AbstractTorsade de pointes is an uncommon and unique type of ventricular tachycardia. It differs from other forms of ventricular tachycardia by its morphological features, underlying mechanism, and modes of therapy. Recognizing torsade de pointes is of major clinical importance, as standard antiarrhythmic regimens might not only be ineffective in abolishing this life-threatening arrhythmia but may aggravate it. Torsade de pointes is most commonly precipitated by QT prolonging drugs, mainly type IA antiarrhythmic therapy such as quinidine and disopyramide, and other antiarrhythmic agents are reported to cause torsade de pointes as well. Predisposing factors known to increase the likelihood of developing torsade de pointes are: electrolyte imbalance (hypokalemia, hypomagnesemia, or both) and slow heart rate induced either by sinus bradycardia or heart block. Treatment of torsade de pointes is aimed at shortening the QT interval. By acceleration of the heart rate, the QT interval is shortened, thus preventing the recurrence of the arrhythmia. Treatment of torsade de pointes includes: isoproterenol infusion, cardiac pacing, and intravenous atropine. Intravenous magnesium sulfate, a relatively new mode of therapy for torsade de pointes, was proven to be extremely effective and is now regarded as the treatment of choice for this arrhythmia.

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