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    • The electrocardiogram showed narrow QRS complex regular tach

    2019-06-24

    The electrocardiogram showed narrow QRS complex regular tachycardia, which was terminated by rapid injection of adenosine triphosphate. During the tachycardia, the P wave was not identifiable and was likely hidden completely in the QRS complex (Fig. 1). As the patient desired complete cure of the tachycardia, an electrophysiological study (EPS) was performed. In the EPS, a 4 French decapolar electrode catheter was easily inserted via the right subclavian vein through the coronary sinus but was not stabilized. The Alfacalcidol what medium injected from the long sheath inserted in the right femoral vein revealed a PLSVC and significantly enlarged coronary sinus (Fig. 2). An appropriate atrial end of slow pathway (Asp) potential was identified at the anterosuperior aspect of the coronary sinus ostium and RF energy was delivered (Fig. 3A and B). The junctional accelerated rhythm was acquired at the eighth time of delivery (maximal temperature: 55°C; duration: 32s; power: 30W). After the ablation, the jump-up phenomenon provoked by the programmed atrial extrastimuli disappeared, and the tachycardia was not inducible at any stimulation before and after isoproterenol administration. Therefore, the ablation was considered successful, and the patient was discharged from the hospital 2 days after the procedure. The intracardiac electroanatomical mapping revealed a gigantic coronary sinus ostium and PLSVC (Fig. 4). The upward shift of the His bundle was also observed. The site where the Asp potential was recorded existed at the upper one-third of the enlarged ostium of coronary sinus (Fig. 3C and D and Fig. 4). The distance between the His bundle and Asp site was 14.8mm. The site was nearly the same as the previous ablation site but slightly more proximal to the His bundle electrode. The RF energy was delivered without any concerns for damaging the His bundle because the site was adequately distant from the His bundle (Fig. 4). The movement of ablation catheter was easily observed before and during RF delivery by the CARTO system. The accelerated AV junctional rhythm was obtained at the first RF delivery (maximal temperature: 55°C; duration: 35s; power: 25W). The RF energy was delivered again for confirmation (maximal temperature: 55°C; duration: 47s; power: 30W). After the ablation, no jump-up phenomenon was observed, and the AVNRT was no longer inducible at any atrial stimulation even after isoproterenol administration. The patient remained asymptomatic for at least 6 months following the second procedure.
    Discussion The coexistence of PLSVC and AVNRT is rare and has only been reported in a few case reports [1–5]. In these few cases, the successful ablation sites varied among the significantly dilated ostia of the coronary sinus. As Okishige et al. described [1], patients with PLSVC have significantly enlarged coronary sinus ostia, and therefore, the course of the slow pathway may be displaced from its normal alignment. The position of the His bundle may also be displaced, increasing the risk of damaging the AV nodal conduction during an ablation of the atrial end of slow pathway. In this case, RF energy was delivered in the first ablation session for a short duration, as we remained cognizant of the possibility of damaging the His bundle. Moreover, the contact of the ablation catheter to the endocardium may have been insufficient because the anatomical relationship between Koch\'s triangle and the coronary sinus was difficult to comprehend. Hence, these uncertainties resulted in an unsuccessful ablation.
    Conflict of interest
    Acknowledgments
    Introduction Sudden cardiac death, the most devastating feature of the natural history of hypertrophic cardiomyopathy (HCM), can be the first clinical manifestation of the disease in previously asymptomatic patients with HCM [1]. These observations have led to the use of antiarrhythmic treatment or radiofrequency (RF) ablation in patients with HCM and premature ventricular contractions (PVCs)/ventricular tachycardia (VT). Monomorphic VT in the presence of structural heart disease is mainly due to reentry involving the bundle branches or myocardial scar regions [2]. In contrast, episodes of repetitive idiopathic right and left ventricular outflow tract VT are attributable to abnormal automaticity or triggered activity of the ventricular myocardium [2]. Evidence shows that PVCs originating from the distal Purkinje arborization play an important role in the initiation of malignant arrhythmias such as polymorphic VT and ventricular fibrillation (VF) in patients with or without structural heart disease [2]. In the clinical setting of HCM, the mechanism underlying VT is often scar-related reentry [3,4]. However, here, we report the case of a patient who had HCM and developed symptomatic repetitive monomorphic PVC and nonsustained VT (NSVT), the mechanism of which was suggested to involve the Purkinje fibers.