QT coupling interval can discriminate true from pseudo-torsade, finds EHJ study
Distinctive types of polymorphic ventricular tachycardia (VT) respond differently to different forms of therapy. For example in the setting of coronary artery disease, the entity of pseudo-torsade de pointes (showing QT prolongation) responds to quinidine while the same drug is contraindicated in true QT prolongation syndrome like drug-induced of congenital LQTS (long QT syndrome).
Rosso et al have shown in their recent study published in European Heart Journal that the coupling interval on surface ECG can help discriminate these two conditions as a longer QT and coupling intervals are a feature of true TdP.
In the past decades, several polymorphic VT entities have been recognized in the presence of structural, ischaemic, and primary electrical disorders. These entities can frequently be distinguished from one another by assessing the clinical characteristics of the, the baseline electrocardiogram, the initiation of the polymorphic VT, particularly whether or not the initiation is pause dependent, the coupling interval of the initiating ectopic beat, the initial rate, and the response to certain interventions.
Viskin and colleagues recently reported on the entity of polymorphic VT in patients with coronary artery disease in the absence of acute myocardial ischaemia which responded to quinidine therapy. A key issue in identifying this population to prevent further electrical storms and sudden cardiac arrests is to elucidate indicative clinical features.
In the present study, the authors further evaluated the electrocardiographic characteristics of 87 patients with this entity, in particular by focusing on the QT interval. In 32 patients, the QT interval was prolonged.
However, when comparing the polymorphic VTs of these patients, which were termed 'pseudo-TdP', with 53 patients with true TdP in the context of drug-induced LQTS, some key differences were noted:
1. The coupling interval of the initiating ectopic beat was shorter than 400 ms in pseudo-TdP and (much) longer than 400 ms in true TdP.
2. The QT interval in patients with pseudo-TdP was shorter, the mode of onset was less often pause dependent, and the initial R–R intervals were shorter than in true TdP.
3. Finally, patients with pseudo-TdP responded well to quinidine therapy, whereas quinidine is obviously detrimental in true TdP due to its QT-prolonging properties.
Thus, in patients with pseudo-TdP, polymorphic VTs occur in the presence of a prolonged QT interval, but not due to a prolonged QT interval.
"The importance of classifying and recognizing the aforementioned polymorphic VT subtypes is due to the different responses to pharmacological interventions", write Werf et al in an accompanying editorial (Figure 1).
Figure 1. Causes of polymorphic ventricular tachycardia (VT) and their treatment. Different types of polymorphic VTs based on the underlying substrate are shown, from polymorphic VTs with a short coupling interval of the initiating ectopic beat on the left to those with a relatively long coupling interval of the initiating ectopic beat on the right.
"It is paradoxical that a 'torsadogenic' drug such as quinidine can act as an antiarrhythmic in this context", add Werf et al.
The fact that quinidine, a 400-year-old drug derived from quinine used by South American Indians to treat malaria, is uniquely effective is remarkable, as it is also the only agent known to be of value in the Brugada and early repolarization syndromes.
The coupling interval thus helps discriminate between polymorphic VT that occurs despite a long QT interval (pseudo-TdP) and polymorphic arrhythmias striking because of a long QT (true TdP).
Source: European Heart Journal: