Archives

  • 2018-07
  • 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
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04

    • In November a year old man with no family history

    2019-04-23

    In November 2011, a 19-year-old man with no family history of sudden death and a history of syncope was admitted to our hospital after experiencing a sudden cardiac arrest. He suddenly developed abnormal respiration and subsequently experienced convulsions while watching television. His friend, who was awakened by the unusual noise, found him unconscious, called emergency medical services immediately, and started cardiopulmonary resuscitation. Emergency medical services arrived 16min later and found that the patient had VF. The patient was successfully converted to sinus rhythm with an automated external defibrillator (Fig. 1A). He was intubated, transported to the intensive care unit, and initiated on a hypothermia protocol because of his decreased level of consciousness. At admission, his ECG showed sinus rhythm with PVBs, ER in the inferolateral leads, and a normal QT interval (Fig. 1B). Although ER in the inferolateral leads became prominent during hypothermic treatment, no arrhythmic event occurred at this time (Fig. 1C). The patient׳s cardiac evaluation during admission included cardiac catheterization, echocardiography, myocardial magnetic resonance imaging (MRI), and myocardial scintigraphy, which demonstrated no organic structural purchase AMN107 disease. In addition, a signal-averaged ECG was negative since all of three standard parameters showed normal values (the filtered QRS vector magnitude: 104ms (<105ms), the root mean square voltage of the terminal 40ms of the vector magnitude: 29.4μV (>11.0μV), the low-amplitude signal duration under 40μV in the terminal portion of the vector magnitude: 32ms (<44ms)). However, a Holter ECG documented PVBs and non-sustained VTs (NSVTs), which frequently appeared during the day or during heart rate increases. In addition, PVBs or the first initiating PVBs of NSVTs occasionally appeared with a short coupling interval (Fig. 1D-1). ER in the inferolateral leads diminished at that time, but became obvious during the night or at periods of decreased heart rate (Fig. 1D-2). Pharmacological stress testing was performed to assess the effects of anti-arrhythmic drugs on the J wave (Fig. 2) and PVBs (data not shown). The J points of the inferolateral leads were elevated after verapamil and propranolol infusion and depressed after isoproterenol and pilsicainide infusion. PVBs were increased after isoproterenol infusion and decreased after propranolol and verapamil infusion. An implantable cardioverter-defibrillator (ICD) was placed per current recommendations. After ICD placement, an electrophysiological study and radiofrequency catheter ablation were performed. Programmed ventricular stimulation was performed using a maximum of three extra stimuli (S4) at several different driven cycle lengths (CLs) from the right ventricular apex and outflow tract. However, because neither NSVT nor VF was induced, the stimulation was repeated during isoproterenol infusion (1–3μg/min). Isoproterenol infusion mildly increased the occurrence of clinical PVBs or NSVT with the same QRS morphology as the spontaneous clinical PVBs. Because the PVBs were not bidirectional and a ryanodine receptor gene mutation was not detected later on, we excluded catecholaminergic polymorphic VT. The clinical PVBs had a left bundle branch block configuration with a left-axis deviation. At the time of PVB, an early activated lesion was explored using an A-20 electrode catheter placed at the right ventricular septum. Then, an earliest activated site (EAS) located at the inferior septum of the right ventricle and preceding QRS onset by 32ms with presystolic Purkinje potentials and a unipolar QS pattern was detected with an ablation catheter (Fig. 3A and B). Furthermore, paced mapping at the EAS showed a QRS morphology nearly identical to that of the spontaneous PVBs (Fig. 3A). Purkinje potentials during sinus rhythm were also recorded at the EAS (Fig. 3C). Radiofrequency energy was delivered to the EAS in the temperature-controlled mode with a target temperature of 55–60°C and a maximum power of 45W using a conventional 4-mm tip ablation catheter. Although ectopic NSVTs were temporally induced just after starting energization, they completely disappeared 30s later (Fig. 4A). Clinical PVBs remained, but NSVT and the couplets of PVBs completely disappeared and were not inducible by isoproterenol. No low voltage area in the right ventricle was confirmed by electroanatomical mapping (Fig. 4B). Holter monitoring and an exercise stress test after ablation showed no PVB couplets or NSVT. During the 8-month follow-up examination at which time the patient received no drug therapy, no episodes of syncope or VF recurrence were observed.