"Torsade de pointes" tachycardia. Re-entry or focal activity?

Abstract

SUMMARY Paroxysms of ventricular tachycardia in which the amplitude and the direction of QRS complexes change periodically are defined as "torsade de pointes" tachycardias. The mechanism of this atypical ventricular arrhythmia has not yet been elucidated. The aim of our study was to induce "torsade de pointes" tachycardia experimentally, in order to gain insight into its possible mechanism. The experiments were carried out with isolated porcine hearts, perfused by the Langendorff technique. Epicardial electrocardiograms were recorded by unipolar leads. The specific pattern of "torsade de pointes" tachycardia could be induced by stimulation of the right and left ventricles in phase. From our experimental observations we conclude that a possible cause of "torsade de pointes" tachycardia is the interaction of two ectopic ventricular foci.Rapid ventricular tachycardias, with periodic change of amplitude and direction of the QRS complexes, are defined as "torsade de pointes" tachycardias.1 A detailed description of this serious arrhythmia has been given by Dessertenne,2 who also created the term "torsade de pointes" (twisted tips). The precise mechanism of this atypical ventricular arrhythmia has not been completely clarified. Prolongation of the QT interval and inhomogeneous repolarisation of neighbouring areas of the myocardium are believed to be of major importance for its genesis.' I "Torsade de pointes" has been recognised during hypokalaemia,F6 hypomagnesaemia,78 acute ischaemia,9 myocardial infarction,'0 myocarditis,' during the use of various antiarrhythmic agents, for example quinidine," I lignocaine,' mexiletine,'2 disopyramide,'3 14 and could be initiated by electrical ventricular stimulation.'5 Thus, aetiology of this rhythm disorder is diverse; its characteristic electrocardiographic appearance, however, suggests a specific mechanism. The aim of our study was to induce "torsade de pointes" tachycardias experimentally in order to gain insight into its possible mechanism. MethodsThe experiments were carried out in isolated pig hearts (n=7). The animals (weight 20±1 kg) were Supported by Deutsche Forschungsgemeinschaft. Accepted for publication 8 April 1982 anaesthetised by intravenous injection of sodium pentobarbitone (15 mg/kg). After intubation and artificial respiration the thorax was opened by a midsternal incision and the heart was rapidly removed and fixed to a heart lung machine where it was perfused with the blood of the same pig using the Langendorff technique. 16 The temperature was 37°C, and the coronary flow was set at 200 m/min. The hearts were paced electrically from the epicardium with two independent stimulation generators at one and a half times the diastolic threshold. Unipolar electrocardiograms were recorded by means of non polarisable cotton wick electrodes from the epicardium and were recorded on an Elema ink writer (Fig. 1). ResultsIf paced from the right ventricle the electrocardiogram recorded within the area of the left anterior descending artery showed a positive deflection (...

Early afterdepolarizations and cardiac arrhythmias

“…Experimentally, TdP can be produced by pacing the ventricle at two separate sites at different pacing rates, so that the mass of ventricular tissue captured by the two sites fluctuates as they shift in and out of phase 36. Alternatively, a nonstationary reentrant rotor which meanders rapidly over the surface of the ventricle can also produce a shifting electrical axis characteristic of TdP and PVT 34.…”

Perpetuation of torsade de pointes in heterogeneous hearts: competing foci or re‐entry?

“…The latter is supported by early work in which ECGs with typical TdP appearance could be reproduced by pacing the left ventricle at a constant cycle length of 245 ms while pacing the right ventricle at slightly variable cycle lengths (230–260 ms) (D'Alnoncourt et al . ). In a recent study we found that in the drug‐induced CAVB dog, 90% of the cases of self‐terminating TdP are perpetuated by ectopic activity (Boulaksil et al .…”

Cytosolic Ca2+ triggers early afterdepolarizations and torsade de pointes in rabbit hearts with type 2 long QT syndrome

“…The original hypothesis of Dessertenne (1966) is that two or more automatic foci firing impulses at slightly different frequencies are responsible for TdP. This was substantiated experimentally when stimulation of the right and left ventricles at slightly different rates produced ECG patterns classically associated with TdP (D'Alnoncourt et al 1982). An alternative explanation of TdP is that the QT prolongation is a manifestation of prolonged APDs and that an enhanced dispersion of repolarization is required to increase the vulnerability to reentrant arrhythmias (Kuo et al 1985).…”