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In their paper published in Heart, Birati and colleagues report the cardiac location from which arise the premature ventricular beats initiating torsades de pointes (TdP) in patients with long QT syndrome (in press).1 Interestingly, they demonstrate that these foci preferentially cluster in some areas of the heart, mainly in the ventricular outflow tracts. Even if ECG characteristics of TdP have been largely described, this work is the first one dedicated to the morphologies of the initiating premature beats. The authors should be congratulated for such a challenging task, and their findings raise the question why some cardiac areas such as the right ventricular outflow tract (RVOT) are more ‘arrhythmogenic’ than others.
As recalled by the authors, many ventricular arrhythmias seem to come from the right ventricle and particularly from the RVOT. Of course, right ventricular structural heart diseases such as arrhythmogenic right ventricular dysplasia or congenital heart diseases are responsible for some ventricular arrhythmias. However, the prominence of the right ventricle in arrhythmogenesis is otherwise best highlighted in many various clinical settings.
First of all, the RVOT is usually considered to be the preferential location for ‘benign’ ventricular premature beats (VPB) as initially described by Rosenbaum.
VPB in Brugada syndrome predominantly arise from different right ventricular sites—mainly at the RVOT—as well as the rare cases of sustained monomorphic ventricular tachycardia (VT). Arrhythmias induced during drug challenge also predominantly arise from the RVOT,2 and the ventricular fibrillation (VF) induction rate by programmed ventricular stimulation is higher when the protocol is performed at the RVOT than at the right ventricular apex, while VF is scarcely ever induced at the left ventricle.3
The most common form of idiopathic VT occurring in normal hearts also originates from the RVOT, and most of the time, the adenosine-sensitive repetitive monomorphic VT …
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