Observations on the onset of Torsade de Pointes arrhythmias in the acquired long QT syndrome

doi:10.1016/S0008-6363(00)00192-9

Cardiovascular Research 2000 48(3):421-429; doi:10.1016/S0008-6363(00)00192-9
© 2000 by European Society of Cardiology

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Observations on the onset of Torsade de Pointes arrhythmias in the acquired long QT syndrome

Marc A. Vos^a^,*, B. Gorenek^b, S.Cora Verduyn^a, Ferenc F. van der Hulst^a, Jet D. Leunissen^a, Leon Dohmen^a and Hein J. Wellens^a

^aDepartment of Cardiology, Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands
^bDepartment of Cardiology, Osmangazi University Hospital, Eskisehir, Turkey

^* Corresponding author. Tel.: +31-4338-75-101; fax: +31-4338-75-104 m.vos{at}cardio.azm.nl

Objective: Premature ectopic beats may create a specific sequenceof events (e.g. short–long–short) preceding Torsadede Pointes arrhythmias (TdP) in the long QT syndrome. The relevanceof this sequence for the initiation of TdP is not clear. Inour dog model of TdP, interventricular dispersion ( ${Delta}$ APD=left–rightventricular monophasic action potential duration: APD) is associatedwith TdP, therefore we tested the hypothesis that the ectopicbeats contributes to ${Delta}$ APD. Methods: In 17 anaesthetized dogswith chronic AV-block, which showed spontaneous TdP after classIII medication, APD was analyzed to 1. quantitate the alterationsdue to (multiple) ectopic beats on the left and right APD (measuredwith endocardial catheters) and 2. compare the ${Delta}$ APD prior tothe occurrence of premature beats (steady state) in dogs withnon-sudden onset of TdP (n = 10) and sudden onset TdP (n = 7).Three phases were distinguished: phase 1: steady state beatsprior to ectopic beats, phase II: the beat(s) belonging to thedynamic phase, and phase III: the beat causing TdP. Becausethe coupling interval of premature beats in this condition oftenfalls within the APD, the ${Delta}$ APD₅₀ was validated as an alternativefor the previously applied ${Delta}$ APD₁₀₀ (r = 0.51, P<0.01). Results:In steady state (phase I) ${Delta}$ APD₅₀ is longer in the sudden onsetTdP (130±35 ms) as in the non-sudden onset TdP (65±40ms). In the non-sudden TdP group the dynamic phase II contributeto the heterogeneity in APD, i.e. LV-APD increases more thanRV-APD leading to a ${Delta}$ APD₅₀ increase to 130±100 ms (P<0.01)just preceding TdP (phase III). Conclusion: The synergism betweenectopic beats (short–long–short sequence) and ${Delta}$ APDcreate the circumstances for TdP initiation.

KEYWORDS Ventricular arrhythmias; ECG; Long QT syndrome; Antiarrhythmic agents; Arrhythmia (mechanisms); Repolarization

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