Torsades de pointes

ECG: On these Holter tracings, we find the different elements of torsade de pointes: 1) a long QT on the sinus rhythm; 2) minimally premature ventricular extrasystoles but falling on the T wave because of its prolonged duration; extrasystoles in couplets or bursts; 3) onset of a tachycardia on a ventricular extrasystole; wide QRS tachycardia between 170 and 200 bpm; polymorphic irregular tachycardia with rotation of QRS complexes around the “isoelectric” baseline with change of axis (positive QRS, then negative, then positive) approximately every 20 ventricular complexes; 4) a spontaneous termination of the episode explaining the occurrence of a syncope and not of a sudden death;

Comments: Torsade de pointes corresponds to a tachycardia with intermediate properaties positioned between ventricular fibrillation and ventricular tachycardia with a characteristic clinical and electrocardiographic presentation:

1. circumstances of occurrence: between the tachycardia attacks, a bradycardia as well as significant repolarization abnormalities are most often observed in the presence of an elongated QT interval. The various etiologies of torsade de pointes have therefore as common grounds either to prolong the QT interval or to slow the heart rate, or both at the same time. The most frequently observed etiologies are the atrioventricular block (10 to 15% of Adam Stokes-type syncopes observed in this setting are related to a torsade de pointes), the post termination pause of atrial fibrillation (particularly in patients treated with diuretics and/or amiodarone), hypokalemia, an iatrogenic origin (series of drugs prolonging the QT), the presence of a congenital long QT. Several causes may be associated, such as the addition of hypokalemia and a QT-prolonging treatment.
2. A triggering factor: the tachycardia episode is triggered by the occurrence of ventricular extrasystoles not necessarily very early but occurring during the T wave of the previous complex because of its marked prolongation. The occurrence of ventricular bigeminy in a patient with prolonged QT interval should suspect the worrisome occurrence of a torsade de pointes, the prolongation of the diastole being linked to the post-extrasystolic pause prolonging the repolarization of the conducted complex. Similarly, the alternation of the T wave or the U wave is an electrocardiographic precursor sign of torsade. These extrasystoles are generally related to the occurrence of early post-depolarizations.
3. A very evocative tachycardia pattern: the tachycardia is rapid and polymorphic, marked by the rapid succession (generally between 50 and 250 bpm) of broad ventricular ectopic complexes of variable polarity with progressive and cyclic rotation around the isoelectric line. Repolarization generally remains identifiable, the differentiation of QRS complexes and T waves being most often possible, which differs from a ventricular fibrillation pattern (the impossibility of identifying QRS complexes and T waves). A twisting around the baseline is at the origin of the term “torsade de pointes”, the direction of the “pointes” suddenly reversing every 5 to 10 complexes (or more), sometimes at a time of a brief slowing of the rate. The characteristic undulation pattern of the tracing may appear only in certain leads, the simultaneous recording of several leads (in particular the frontal leads) being necessary in order to demonstrate the helical appearance of the tracing. The P waves are dissociated but are not visible. While the arrhythmia is generated by the occurrence of an extrasystole during a vulnerable period, its perpetuation is linked to reentry circuits favored by the inhomogeneity of the refractory periods (long QT pattern), which are relatively slow and few due to long refractory periods. Electrical activation is less disorganized than in an episode of ventricular fibrillation and progresses more coherently, explaining the clear differentiation of QRS complexes. There is no convincing explanation for the alternating direction of the QRS complexes (presence of two different undulations, one left ventricular, the other right ventricular, alternatively expressed). Clinically, this rhythm disorder entails, if prolonged, a cardiovascular inefficiency generating loss of consciousness.
4. Spontaneously resolving episodes: torsades de pointes generally occurs as attacks lasting from a few seconds to a few tens of seconds reducing spontaneously. The spontaneous and often sudden cessation of attacks after a short ventricular pause is characteristic of this form of arrhythmia, which explains the frequent occurrence of a syncope (with spontaneous return to consciousness) rather than sudden death. There is a marked tendency for recurrence and some prolonged attacks can eventually degenerate into ventricular fibrillation.

The spontaneous cessation of attacks is likely due to the presence of long refractory periods, a limited number of reentry circuits, long refractory periods opposing an electrical barrier to the propagation and the maintenance of reentry circuits.

Take-home message: a torsade of points corresponds to an irregular, polymorphic wide QRS tachycardia with a characteristic twisting pattern around the baseline, most often spontaneously resolving and occurring in a setting of long QT and bradycardia.