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  • A year old man was admitted to our hospital

    2019-04-16

    A 49-year-old man was admitted to our hospital for SMVT treatment. He was diagnosed with DHCM at the age of 45 years in the referring hospital. His chief complaint was palpitations, and he was conscious and hemodynamically stable during the VT. A 12-lead electrocardiogram (ECG) during sinus rhythm revealed an unusual R wave progression in the precordial leads and a tall R wave in aVR (Fig. 1A, left panel). An rS pattern was observed in lead V1, and a QS pattern in leads V2–V6; northwest axis deviation in the 12-lead ECG (Fig. 1A, right panel) suggested that the VT originated from the ventricular apical septum. The VT order EPZ004777 length (VTCL) was prolonged to 630ms following intravenous amiodarone infusion. Cardiac computed tomography imaging demonstrated a thick left ventricular (LV) wall (~20mm), and the LV ejection fraction was reduced to 40% (Fig. 1B). Delayed contrast-enhanced cardiac magnetic resonance (CMR) imaging showed an enlarged delayed-enhanced region in the apical septum and lateral wall (Fig. 1C). The VT recurred immediately following cardioversion, and amiodarone administration failed to resolve it. Therefore, we performed an electrophysiological study and catheter ablation after obtaining written informed consent. Endocardial activation mapping of the right (RV) and left ventricles during VT using an electroanatomic map (EAM) (CARTO3, Biosense Webster Inc., Diamond Bar, CA, USA) showed a focal activation pattern, wherein the site of earliest activation was located in the apical septum of both ventricles (Fig. 2A). However, the VT mechanism was considered as reentry because manifest entrainment was observed by burst pacing during VT. No diastolic potential was observed during the VT in the endocardium of either ventricle. Despite the remote location of the earliest activation sites in the RV and LV (the distance measured on the EAM was 17mm), QRS morphologies during pacing from the earliest activation sites were almost identical to those observed during VT (Fig. 2B). Furthermore, the postpacing intervals (PPI) minus the order EPZ004777 VTCL following entrainment pacing from the RV and LV were 30ms and 28ms, respectively. Radiofrequency (RF) energy delivered (Navistar ThermoCool, Biosense Webster Inc.) at the earliest RV site did not affect the VT, whereas RF energy delivered at the earliest LV site resulted in temporary VT termination (maximum power of 50W). However, VT recurred a few minutes after removing the RF energy delivery. We suspected that the VT circuit was located in a deep layer of the ventricular septum. Therefore, bipolar ablation between the RV and LV was attempted. Two irrigated catheters (LV: Navistar ThermoCool, RV: Cool Path Duo, St. Jude Medical) were placed at the contralateral site of the earliest activation in each ventricle (Fig. 2C), and RF energy was delivered between the two catheters (maximum power of 35W). However, bipolar ablation did not completely resolve the VT. As a result, we hypothesized that the main VT circuit may be located in the epicardium, and performed epicardial voltage mapping using a subxiphoid puncture. A wide low-voltage area (<1.5mV) was identified on the lateral epicardial wall during sinus rhythm (Fig. 3A), and diastolic potentials were recorded during the VT in this area. We performed detailed mapping of the diastolic potentials using EAM, and the critical isthmus was revealed on the anterolateral epicardial wall (Fig. 3B). At the center of the critical isthmus (Figs. 3B arrowhead, and 4A), concealed entrainment was observed (PPI=VTCL, stim-QRS interval=egm-QRS interval) (Fig. 4B). The initial RF energy (maximum power of 35W) was delivered at this site, which completely resolved the VT after 21s (Fig. 4C). We added bonus applications at an adjacent site. Subsequently, VT could not be induced by programmed electrical stimuli. No complications were observed following the procedure, and the patient was discharged 5 days after catheter ablation.