Torsades: adjacent and triggering electrocardiographic events

Abstract

Torsades de pointes (TdP) is a particular variant of ventricular arrhythmia associated with the long QT syndrome. The background of the latter is essentially 2-fold: patients under treatment with QT-prolonging drugs and subjects with congenital ionopathies. A third category is composed of subjects with both of these backgrounds. The fundamental feature of TdP is its provocation by pause-related augmentation of the repolarizing TU wave. The substrate electrocardiogram (ECG) shows prominent U waves in regular rhythm. The exaggeration of the U wave voltage following a pause is more marked the longer the pause and, for a given pause, more marked the faster the prepause rate. The pause-related sequences figure frequently adjacent to that which actually triggers the attack of TdP and continues to be seen after the event, serving to advise the physician as to the diagnosis, even following cardiac resuscitation, so that preventive measures can be taken (pacing, intravenous magnesium sulfate, or infusion with isoproterenol). The U wave of the regular rhythm ECG may show amplitude instability: an especially tall U triggering a premature ventricular complexe (PVC) that then in turn generates a pause-related sequence. TU alternans is common. Because these patients may not be in a monitored bed, recognition of pause-related phenomena in a patient with a long QT requires the ECG reader of the day to alert the floor as to the running danger. The mechanism of the pause-related TU augmentation is the generation of early afterdepolarizations.