br Discussion Catheter ablation has played an
Discussion Catheter ablation has played an increasingly important role in controlling VT episodes in patients with structural glucosamine sulfate disease who have an ICD [6–10]. LPs recorded at an endocardial ventricular site reflect slow conduction into a protected zone. Strategies for the successful ablation of poorly tolerated, scar-based VTs often involve the identification and ablation of LPs during sinus rhythm [4,5,11], on the basis that they are critical sites for maintenance of the VT. In this case, high-density mapping with a multipolar catheter facilitated the delineation of the heterogeneous infarct architecture and detection of the LPs , and those sites were identified as putative isthmuses. The dissociation of LPs after catheter ablation of the scar-based VT in this patient with ischemic cardiomyopathy was a unique observation. An externally irrigated ablation catheter design has been shown to create deeper and larger volume lesions compared with the nonirrigated catheter design . It can be speculated that conduction through the entrance site was modified by the RF application, resulting in conduction block to the LPs. Large prospective studies are needed to determine whether the emergence of dissociated LPs is a prognostic indicator of successful ablation in patients with postinfarction VT.
Conflict of interest
Introduction Idiopathic ventricular tachycardia (VT) can occur in patients with structurally normal hearts. Idiopathic VT is classified into several subtypes according to its mechanism, QRS morphology, and site of origin . The His-Purkinje system (HPS) has been found to be responsible for some forms of idiopathic VT. One form, verapamil-sensitive idiopathic left VT, arises close to or in the left posterior fascicle. It is the most common form of HPS-related VT and is considered a re-entrant mechanism. Another rare form of HPS-related VT is focal Purkinje VT, which is due to abnormal automaticity or triggered activity in the ventricular conducting system . Focal Purkinje VT arises from both the left bundle branch (LBB) and right bundle branch (RBB) and may be abolished by radiofrequency (RF) catheter ablation at the site of the earliest Purkinje potential during VT [3,4]. In the present report, we describe a case of HPS-related VT, with a narrow QRS configuration, that was successfully ablated in the left coronary cusp (LCC).
Case report A 23-year-old woman, with a 5-year history of repetitive palpitation and an otherwise unremarkable medical history, was admitted to our hospital. Clinical examination and echocardiography findings ruled out structural heart disease. A 12-lead electrocardiography (ECG) during tachycardia revealed frequent and incessant narrow QRS tachycardia, with only short-duration, intervening episodes of junctional rhythm (Fig. 1A). Ambulatory monitoring of the patient showed frequent episodes of narrow QRS tachycardia, with junctional rhythm accounting for approximately 65% of the total heartbeats per day. After written informed consent was obtained, an electrophysiological study was performed. The patient׳s basic rhythm was junctional rhythm. Repetitive, short-duration, narrow QRS tachycardia appeared during junctional rhythm. The R–R interval of the tachycardia was irregular (Fig. 1B). Two quadripolar 5-Fr catheters were positioned in the His-bundle region and in the right ventricular apex, and an octapolar 5-Fr catheter was placed in the coronary sinus. An intracardiac ECG during tachycardia showed ventriculoatrial (VA) dissociations and His deflections preceding each QRS complex (Fig. 1B). During pacing from the atrium, the HV interval – the time from the initial deflection of the His bundle (H) potential and the onset of ventricular activity (V) – was 43ms, whereas during tachycardia, the HV interval was 27ms. The tachycardia could not be induced or terminated by programmed ventricular stimulation. The Purkinje potentials of the RBB, recorded in the right ventricle, showed antegrade conduction of RBB signals; none of these Purkinje potentials were preceded by His deflections. Consequently, left ventricle (LV) mapping was performed, which showed antegrade conduction of the Purkinje potentials of the left anterior fascicle (LAF) during tachycardia. A tiny single potential (TSP) was recorded in the LCC (Figs. 2A, B, and 3A) and preceded the His deflection by 15ms during tachycardia. During pacing from the atrium, the activation sequence of the TSP and His deflection was reversed (Fig. 3B). Furthermore, the TSP–His deflection interval was unchanged during the different pacing cycle lengths. These findings indicated that the TSP was connected with the HPS.