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    • Thieno-GTP manufacturer br Case report A year old man with

    2019-06-19


    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 Thieno-GTP manufacturer 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.
    Discussion Here, we reported a case of PVCs/NSVT in a patient with nonobstructive HCM. This patient presented with PVCs/NSVT with a RBBB and inferior axis morphology that was successfully cured by targeting of the proximal portion of the anterior left bundle branch. HCM-related VT has been shown to result from scar-related reentry, the circuits of which originate from the LV-right ventricle junction around the interventricular septum and sometimes involve an LV aneurysm [4]. In dilated-phase HCM, the VT reentrant circuits are located in the basal septum or basal anterior-to-anterolateral LV area [5]. In this scar-related reentry in HCM, targeting the channel by using a combination of voltage-based substrate late/fractionated potential mapping during sinus rhythm and activation and entrainment mapping during VT effectively eliminates VT [3]. Regardless of the origin of the HCM-related VT, the VT circuits often involve the epicardium and endocardium [3,4]. Such arrhythmogenic substrates and increased LV thickness cause difficulties in performing endocardial ablation of VT in patients with HCM [3,4]. In the present case, delayed-enhanced magnetic resonance imaging (MRI) showed an LGE in the LV apex (Fig. 2B), but intracardiac mapping showed a low voltage area only in the basal anterior-to-lateral LV area (Fig. 3A). In addition, a spike potential preceding the ventricular potential at that site during the PVC and sinus rhythm was reproducibly observed. Delivery of RF energy to that site terminated the PVCs/NSVT. These observations suggest that the PVCs/NSVT originated from the anterior fascicular Purkinje network area. Although the exact mechanism underlying the PVCs/VT remains unclear, the PVCs/VT occurred spontaneously, suggesting that its mechanism was triggered activity, abnormal automaticity, or (less possibly) unstable reentry within the Purkinje network.