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
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04
  • br Methods The study protocol was approved

    2019-06-26


    Methods The study protocol was approved by the ethics committee at Juntendo University Nerima Hospital. After informed consent was obtained, SBC measurement was performed using a blood sample from each participant. Plasma was separated from each sample immediately after collection by centrifugation at 3000rpm for 10–15min. All samples were stored at −20°C and were transferred on dry ice to Daiichi Sankyo RD Associe Co. Ltd., Tokyo, Japan. Each sample was thawed slowly at room temperature, and SBC was determined using high-performance liquid chromatography (HPLC). The SBC was measured twice in 3 patients who had changed their dose of Bep at least 4 weeks prior to the second sampling. The data for each of these 3 patients were evaluated at each sampling. The relationships between SBC and age, gender, body weight, liver function, renal function, underlying cardiovascular disease, cardiac function (i.e., left ventricular ejection fraction (LVEF) and left atrial dimension (LAD) examined by echocardiography), Bep dose, Bep dose per kilogram of body weight, and ECG parameters (RR interval, QRS duration, QT interval, and QTc) were studied. The glomerular KN-92 phosphate structure rate (GFR) was calculated as eGFR by the following formula: eGFR (ml/min/1.73m2)=0.741×5×age−0.203×serum creatinine−1.154. For female patients, the value was multiplied by 0.742. In all patients, 12-lead ECG was recorded with standard gain (0.1mV/mm) at a recording speed of 25mm/s on the same day as SBC measurement. The ECG parameters were measured or determined by 2 blinded investigators. When the decisions differed between them, the conclusion was made by a third blinded investigator. In addition, we divided the patients into two groups according to their SBC: a high-SBC (HSBC, SBC≥500ng/ml) and a low-SBC (LSBC, SBC<500ng/ml) group. The cutoff point was determined as 500ng/ml according to a report by Kurita et al. [16]. We also compared the clinical variables between the HSBC and LSBC groups.
    Results
    Discussion We demonstrated that SBC was positively correlated KN-92 phosphate structure with QT interval and QTc, and the HSBC group had a longer QT interval and included more patients with a QT interval>0.5s compared to the LSBC group. Measurement of the SBC appears useful for preventing proarrhythmias.
    Conclusions
    Conflict of interest
    Introduction
    Case report A 65-year-old man with a 6-year history of refractory paroxysmal atrial fibrillation (AF) underwent catheter ablation for persistent AF lasting 2 months. The left atrial (LA) and right atrial (RA) diameters were 39 and 32×43mm, respectively. Extensive encircling PV isolation was performed with the double Lasso technique using a CARTO three-dimensional electro-anatomical mapping system (Biosense-Webster, Diamond Bar, CA, USA). At the beginning of the procedure, disorganized AF was present (Figs. 1A and 2), which was confirmed by the recording of a random activation sequence of the atrial potentials in the coronary sinus (CS). AF was not terminated after complete isolation of the 4PVs. Instead, it was transformed to a sustained atrial tachyarrhythmia (ATA) with beat-to-beat variability of the atrial cycle length between 210ms and 260ms (Figs. 1B and 2). A 12-lead electrocardiogram during tachycardia showed negative flutter-like waves in the inferior leads and positive deflections in lead aV (Fig. 3). In contrast to AF before PV isolation, the irregular ATA exhibited a fixed proximal-to-distal CS activation sequence (Fig. 1B). The post-pacing interval following entrainment pacing of the anterior and posterior tricuspid annulus was nearly equal to the tachycardia cycle length (Fig. 4), consistent with irregular, cavotricuspid isthmus (CTI)-dependent, typical CCW AFL. Although the minimum cycle length of the tachycardia (210ms) was slightly shorter than the pacing cycle length (220ms), pacing during entrainment successfully captured the atrium. This was probably due to decremental conduction delay of the orthodromic wavefront. After the irregular ATA spontaneously transformed to regular ATA, we obtained an electro-anatomical activation map of the RA (Fig. 5), which showed a CCW tail-to-head activation sequence around the tricuspid annulus, confirming the diagnosis of typical AFL. Linear ablation of the CTI terminated AFL and restored sinus rhythm.