ORIGINAL ARTICLE The site of origin of torsade de pointes Edo Y Birati, 1 Bernard Belhassen, 1 Abdennasser Bardai, 2 Arthur A M Wilde, 2 Sami Viskin 1 ABSTRACT Objective The electrocardiographic (ECG) characteristics and mode of onset of torsade de pointes (TdP) are well described. Less is known about the site of onset of this arrhythmia. This study was conducted to determine if arrhythmias in the long QT syndrome (LQTS) have a predominant site of origin. Design A retrospective analysis of all episodes of LQTS- related arrhythmias recorded in two university hospitals. Patients Patients with LQTS and no structural heart disease, for whom simultaneous 6e12 leads ECG recording of the onset of TdP was available, were included. Interventions None. Main outcome measures The site of origin of TDP was defined according to the morphology of the initiating ventricular complex based on validated criteria. Multiple- lead recordings of 1025 LQTS-related arrhythmias, including 151 episodes of TdP and 874 QT-related extrasystoles (impending TdP) were available for 50 patients. Results The site of origin of TdP was not homogeneously distributed (p<0.001). Instead, the majority of episodes of TdP (56%) and most QT-related extrasystoles (70%) originated from the outflow tract. There was no correlation between site of origin and the aetiology of LQTS or the QT duration. On a given patient, multiple episodes of TdP tended to originate from the same area and the site of origin of QT-related extrasystoles correlated with the site of origin of TdP. Conclusion The most frequent site of origin of TdP is the outflow tract. Further studies are needed to understand why this relatively small area of the ventricle is a predominant site of origin of diverse ventricular arrhythmias. Torsade de pointes (TdP) is a polymorphic ventric- ular tachycardia (VT) that occurs in the setting of a long QT syndrome (LQTS). 1 Prolongation of the QT interval may be due to an inherited disorder (congenital LQTS) 2 or may be acquired (secondary to metabolic abnormalities, bradyarrhythmias or due to drugs that prolong ventricular repolarisation). 1 The electrocardiographic (ECG) characteristics 3e5 and mode of onset 46e8 of TdP have been well described. Specifically, drug-induced 46 and bradycardia-induced TdP 9 are essentially always ‘pause-dependent’ (ie, they are preceded by heart rate deceleration or ‘short- long’ sequences), 46 whereas TdP in the congenital LQTS may be ‘pause-dependent’ or ‘tachycardia- dependent’ depending on the genotype. 78 Less is known, however, about the site of origin of TdP. Determining the site of origin of TdP is of scientific interest. Tissue models of LQTS show that the abnormal prolongation of the action potential (the hallmark of the LQTS) creates the trigger (early after-depolarisations) and the substrate (abnormal dispersion of repolarisation) that start and perpetuate TdP. 10 Yet, it is unknown if some areas of the human cardiac ventricle are more sensitive to this process than others. In this regard, it is intriguing to determine if TdP predominantly begins at the ventricular outflow tract. The right ventricular outflow tract (RVOT) is not only the site of origin of the most common form of idiopathic monomorphic VT, 11 but has also been described as a predominant site of origin for malignant polymorphic ventricular arrhythmias like catecholaminergic polymorphic VT, 12 Brugada syndrome 13 14 and some cases of idiopathic ventricular fibrillation. 15 16 Furthermore, deter- mining the site of origin of TdP has potentially important clinical implications. Radiofrequency ablation of the site of arrhythmia origin is the first line of therapy for idiopathic monomorphic VT and has also been used successfully to treat poly- morphic ventricular arrhythmias. 15 16 In fact, radiofrequency ablation of the zone triggering TdP has already been performed in isolated cases of LQTS. 14 We therefore performed the present study to determine if TdP has a predominant site of origin and if this region is disease-specific (ie, differs according to the aetiology of LQTS) or patient- specific (if multiple episodes of TdP in the same patient originate from the same region). METHODS We reviewed all the traces of TdP collected over the years in the Tel-Aviv Medical Center (Israel) and the Academic Medical Center of Amsterdam (The Netherlands), and selected for this study those traces showing the onset of TdP in 6e12 leads in patients without structural heart disease affecting ventricular function. Absence of ventricular dysfunction was specified as part of the inclusion criteria because the criteria for correlating QRS morphology with the site of origin of a VT differ for patients with and without ventricular scar. TdP was a polymorphic VT lasting three or more beats occurring in a patient with congenital or acquired LQTS. QT-related extrasystoles were ventricular extrasystoles originating from the terminal part of the obviously prolonged QT interval (mostly in sinus complexes following post-extrasystolic pauses). Such extrasystoles were saved to our archives because they were recorded shortly before the onset of TdP and were considered signs of ‘impending TdP ’. 1 Most of the patients in this study have been described in previous studies reporting the mode of onset of TdP. 57e9 See Editorial, p 1631 1 Department of Cardiology, Tel-Aviv Sourasky Medical Center and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel 2 Academic Medical Center, Amsterdam, The Netherlands Correspondence to Sami Viskin, Department of Cardiology, Tel-Aviv Sourasky Medical Center, 6 th Weizman Street, Tel-Aviv 64239, Israel; samiviskin@gmail.com Accepted 28 March 2011 Published Online First 10 May 2011 1650 Heart 2011;97:1650e1654. doi:10.1136/hrt.2010.212381 Heart rhythm disorders group.bmj.com on November 15, 2011 - Published by heart.bmj.com Downloaded from