Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04

    • br Conflict of interest br Introduction Idiopathic left

    2019-04-20


    Conflict of interest
    Introduction Idiopathic left ventricular tachycardia (ILVT) with a right bundle-branch block (RBBB) configuration and superior or left axis is a distinct entity that arises in the left ventricle, mostly because of a reentry mechanism and is usually verapamil sensitive [1–6]. Although this type of tachycardia has been suggested to originate from the Purkinje network [1,5], its precise re-entry circuit and slow conduction zone remain unclear. However, radiofrequency (RF) catheter ablation has been reported to successfully eliminate this arrhythmia from the left-hand side of the interventricular septum, where the earliest Purkinje potential (PP) and late diastolic potential are recorded during ventricular tachycardia (VT). In addition, catheter ablation targeting of the left posterior fascicle was shown to be another therapeutic strategy for curing ILVT [7]. These observations raise the possibility that anterior or posterior fascicles compose a critical part of the re-entry circuit of ILVT. However, there have been no reports describing the role of the main trunk of the left bundle branch in the mechanism of ILVT. In this report, we present results indicating the role of main trunk of the left bundle branch in the re-entry circuit of ILVT in a patient.
    Case report A 19-year-old man was referred to our hospital in June 2006 with a 3-year history of paroxysmal palpitations. An ambulatory electrogram monitor showed a regular wide QRS tachycardia. The patient was admitted to our hospital for an electrophysiological study and RF catheter ablation. An initial physical examination revealed normal findings and the laboratory parameters were within normal limits. A standard 12-lead electrocardiogram obtained during sinus rhythm showed no abnormalities; other examinations, including a chest roentgenogram and echocardiogram, showed no evidence of structural serotonin receptor disease or other abnormalities. After obtaining written informed consent, we performed an electrophysiological study and catheter ablation for the regular wide QRS tachycardia. Under fluoroscopic guidance, a 4-Fr quadripolar electrode catheter, two 5-Fr decapolar electrode catheters, a 5-Fr quadripolar electrode catheter (Irvine Biomedical Inc., Irvine, CA, USA), and a 2.5-Fr micro-sized mapping catheter with 8 electrodes (Cardima Inc., Fremont, CA, USA) were introduced into the high right atrium, His-bundle region, left ventricular septum, right ventricular apex, and coronary sinus, respectively, through the femoral veins and artery. The intracardiac electrocardiogram showed an atrial-His interval of 85ms and a His-ventricular interval of 47ms at baseline. Right atrial burst pacing and right and left ventricular burst pacing easily induced tachycardia with a QRS duration of 125ms, an RBBB pattern, inferior axis, and a cycle length of 320ms (Fig. 1). Ventriculoatrial dissociation was observed during tachycardia and the diagnosis of VT was subsequently established. Ventricular stimulations from the right ventricular apex with constant cycle lengths 10, 20, and 30ms shorter than that of the VT cycle length were performed during VT and manifest entrainment was confirmed. In addition, a PP preceding ventricular activation and dull mid-diastolic potential preceding PP (pre-PP) were recorded simultaneously during the VT at the mid-septum of the left ventricle, which is characteristic of verapamil-sensitive ILVT. During left ventricular outflow mapping, we observed a slight spontaneous conversion of the QRS morphology during VT with prolongation of the QRS duration from 125ms to 143ms and an identical inferior axis and tachycardia cycle length. A reverse morphological change of the QRS was observed as well. Intracardiac electrograms showed that there were no differences in the left ventricular activation sequences between VT with narrow QRS duration and that with wide duration (Fig. 2). RF catheter ablation and left ventricular mapping were performed using a 7-Fr quadripolar ablation catheter with a 4-mm distal electrode, an embedded thermistor, and a deflectable tip (Marin®, Medtronic Inc., Minneapolis, MN, USA). Left ventricular endocardial mapping at the left ventricular outflow tract accidentally produced a complete left bundle-branch block (CLBBB), and thereafter, only VT with a wide QRS duration of 143ms was induced (Fig. 3). In addition, no conversions of the QRS morphology and no changes of the VT cycle length were observed. The earliest ventricular activation during VT was found at the apical septum of the left ventricle, and RF catheter ablation at the basal third of the mid-septum, where pre-PP and PP were recorded during tachycardia, successfully eliminated the VT. After ablation, a new diastolic potential appeared during sinus rhythm at the lower and more basal site compared with the successful ablation site; this has been observed in some patients with verapamil-sensitive ILVT after successful ablation [8].