• 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • As Okishige et al described patients


    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 tubulin 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
    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.
    Case report A 73-year-old man with HCM experienced palpitations for 6 months. A 12-lead electrocardiogram (ECG) obtained at a medical clinic showed a first-degree atrioventricular block (PR interval, 260ms), left ventricular hypertrophy (LVH) with strain-type negative T waves in V2–6 leads, and monomorphic PVCs. The PVCs had a right bundle branch block (RBBB) morphology and an inferior axis (Fig. 1A), suggesting that the origin was the anterior portion of the basal left ventricle (LV). A Holter ECG showed a total of 5101 PVCs (6% of the total beats) and 9 VT runs. Oral administration of a β-blocker did not suppress the PVCs. A signal-averaged ECG showed negative late potentials. Transthoracic echocardiography showed LVH with normal LV systolic function (LV ejection fraction, 70.6%; interventricular septum thickness, 15mm; posterior wall thickness, 12.7mm). The patient had no history of hypertension. Cardiac magnetic resonance imaging showed global LV hypertrophy and mild hypokinesis of the apex (Fig. 2A). Late gadolinium enhancement (LGE) was observed in the LV apex region (Fig. 2B). The coronary angiography findings were normal, and left ventriculography showed no obstruction of the LV outflow or middle portions. In an electrophysiologic study, three diagnostic catheters were inserted from the femoral veins and placed in the high right atrium, His bundle position, and right ventricular apex. Endocardial bipolar electrograms were recorded at a filter bandwidth of 30–500Hz. Electrograms were simultaneously recorded using the 12-lead surface ECG and stored in a computer system (LabSystem PRO; Bard Electrophysiology). A spontaneous clinical PVC with an RBBB QRS morphology and inferior axis was observed. LV mapping and catheter ablation were performed with a 7-Fr deflectable quadripolar catheter (4mm distal tip electrode, 1–7–4mm interelectrode spacing, and embedded with a thermistor for the CARTO system [Biosense Webster Inc., Diamond Bar, CA, USA]). LV mapping during sinus rhythm identified a low voltage zone only in the anterior-to-lateral portions of the basal LV (Fig. 3A). Intracardiac ECG recorded a sharp presystolic Purkinje potential that preceded the earliest ventricular activation on the surface ECG by 32ms during the PVC (Fig. 3B). During sinus rhythm, this site exhibited a small Purkinje potential just before the local ventricular activation (Fig. 3B) near the border zone around the low-voltage area (Fig. 3A). Pacing from that site exhibited a 11/12 pace match with the clinical PVC (Fig. 1B). RF delivery (60°C, 50W, 60s) at that site abolished the PVC without any recurrence during rapid ventricular pacing, and no recurrence of the PVCs/NSVT was observed for 10 months without the use of any antiarrhythmic drugs or β-blockers.