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  • Introduction Verapamil sensitive idiopathic left ventricular

    2019-05-06

    Introduction Verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) has been shown to be a clinical entity of left-sided idiopathic ventricular tachycardia (VT) [1,2]. In electrophysiological studies, two specific local potentials, the diastolic Purkinje (Pd) potential and presystolic Purkinje (Pp) potential, can be detected at the successful ablation site. The site is usually located in the left posterior septum, and these potentials are thought to be associated with the reentry circuit [3–5]. However, it remains uncertain whether these two potentials are critical for the induction and perpetuation of the tachycardia. Among these two potentials, the Pd potential is more likely to reflect a critical part of the reentry circuit (slow conduction zone, SCZ), and has been the target of catheter ablation with successful results [3–10]. The morphology of the Pd potential has been inconsistent in previous reports, showing a relatively spiky small potential [8,9], fragmented potential [10], or small slow potentials [3–7]. These might depend on individual electrophysiological properties of the Pd substrate, defined as an anatomical structure that produces a Pd potential by its electrical excitation. Entrainment pacing during tachycardia can sometimes selectively capture the Pd potential by local stimulation [5,7]. The Pd substrate is thus believed to be of a decent size, contain topoisomerase inhibitor tissue, and be insulated from the surrounding left ventricular myocardium. The tachycardia is successfully eliminated by radiofrequency (RF) deliveries targeting the Pd potential, which is commonly located in the left posterior or posteroseptal region [1–10]. Considering the anatomical features around this region, the most likely candidate for the Pd substrate might be a false tendon (FT), which has been shown to contain working myocardium or specialized conduction tissue such as Purkinje fibers [11,12]. However, the possibility that an FT forms a substantial part of the reentry circuit is controversial [13,14]. Therefore, we evaluated the spatial distribution and activation sequence of the Pd potential using a conventional 3-dimensional (3-D) electro-anatomical mapping (EAM) system. We then targeted the latest appearance of the Pd potential, which was usually fused with the Pp potential (spiky bundle potential), in the left ventricular posteroseptal region. From the theoretical point of view, such a potential should be recorded from the exit site of the SCZ (FT-septal connection). Finally, the aim of this study was to prove the electro-anatomical relationship between the Pd–Pp fusion potential and the septal connection of the FT using a new EAM system incorporating an intra-cardiac ultrasound system.
    Material and methods
    Results
    Discussion
    Acknowledgments
    Introduction Early repolarization (ER), a term classically used to refer to ST segment elevation on an electrocardiogram (ECG), is predominantly found in healthy young males and has traditionally been viewed as a completely benign entity [1,2]. However, it was recently reported that an ER ECG pattern in the inferior or lateral precordial leads is associated with ventricular fibrillation (VF), leading to the recognition of a pathological entity termed early repolarization syndrome (ERS) [3–8]. The Brugada syndrome (BrS) differs from ERS with respect to the magnitude and lead location of the abnormal J-wave; the two entities are thought to belong to a continuous spectrum of phenotypic expression known as “J-wave syndromes” [9]. Although ERS and BrS share similar clinical features including gender distribution and arrhythmia triggers, Kawata et al. hypothesized that different pathophysiological mechanisms were responsible for each condition based on their pharmacological responses [10]. It is known that in BrS, VF occurs more frequently during nighttime and from spring to early summer [11]. Our study aimed to investigate whether ERS has the same seasonal, weekly, and circadian distribution of VF events as BrS using data from the “J-wave associated with PRior cardiac EVENT” (J-PREVENT) registry [12].