Not all that twist is Torsades de Pointes

This tracing was sent to me by a friend.

 

Figure 1

It started and ended with a regular wide QRS rhythm at a rate of about 70 bpm. This rhythm is most likely a ventricular-paced rhythm in the setting atrial fibrillation (AF) rather than AF with CHB with wide ventricular escape. In the middle strip is a wide QRS rhythm with different morphology that seemed to be twisting. They thought this was Torsades de Pointes. However, the corrected QT is 435 ms. This should be labeled as polymorphic ventricular tachycardia.

Torsades de Pointes (TdP) was coined by Dessertnne in 1966 as a polymorphic ventricular tachycardia (VT) characterized by twisting of points. It was originally described in the setting of bradycardia caused by complete heart block. Other predisposing factor aside from severe bradycardia is potassium depletion, use of medications that prolong the QT (acquired) and congenital (idiopathic) long-QT syndrome. 

Tdp is not simply an ECG description but as a syndrome characterized by prolonged ventricular repolarization with QT intervals generally exceeding 500 ms. The long-short RR cycle sequences commonly precede TdP.

It should also be remembered that the risk of developing TdP in patient with idiopathic long-QT syndrome is related to the length of the QTc interval and not the QT itself. There are several methods that are used to compute for the QTc but the famous one is the Bazett's method (QTc = QT/ √RR). The risk is increased at QTc at values of 500 ms or longer.

There is a less common form of TdP which is initiated by a close-coupled PVC and does not involve the preceding pauses or bradycardia.

A VT that looked like TdP without QT prolongation should be classified as polymorphic VT and not as TdP.

Why distinguish TdP and polymorphic VT?

The intervention of VT with polymorphic pattern depends whether it occurs in the setting of prolonged QT interval. In all patients with TdP, administration of class IA, possible some class IC and class III antiarrhythmic agents (eg amiodarone, dofetilide, sotalol) can increase the abnormal QT interval and worsen the arrhythmia. Intravenous magnesium is the initial treatment of choice from an acquired cause followed by temporary ventricular pacing. When the QT interval is normal, polymorphic VT resembling TdP, the standard antiarrhythmic drugs can be used. TdP resulting from congenital long-QT syndrome is treated with beta blockade, pacing and ICD. Thus, it important to classify a VT (without QT prolongation) that looked morphologically as TdP as polymorphic VT because of the above therapeutic considerations.

References:

Drew B et al. 2010. AHA/ACCF Scientific Statement Prevention of Torsade de Pointes in Hospital Settings. Circulation  121: 1047-1060

Zipes et al. 2015. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 10th ed.  ElSevier PA

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