• 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
  • br Methods br Results The clinical genetic electrocardiograp


    Results The clinical, genetic, electrocardiographic, and electrophysiological characteristics of the study patients are shown in Table 1. Eight of the 45 patients were symptomatic, having a history of syncope (n=3) or aborted SCD (n=5). The remaining 37 patients were asymptomatic, although 4 had a family history of SCD. The ECGs of 26 patients showed a type 1 basal ECG pattern, and 19 showed a type 1 ECG pattern after a challenge test. An SCN 5A bet bromodomain was found in 1 patient. Positive ventricular late potentials were detected in 26 of 44 (59.1%) patients. Among the 28 patients in whom an electrophysiological study was performed, VF was induced in 25 (89.3%). The clinical, genetic, electrocardiographic, and electrophysiological characteristics of the patients in each group (symptomatic and asymptomatic patients) are shown in Table 2. A family history of sudden cardiac death (SCD) at age <45 years, spontaneous type 1 ECG, and positive ventricular late potentials were significantly more prevalent in the group of symptomatic patients. However, the AH interval, HV interval, and inducibility of VF/polymorphic VT did not differ between the 2 groups of patients.
    Discussion In the present study, we showed that average T(p-e)-c interval, RT-c dispersion, and corrected average repolarization dispersion were greater in patients with a type 1 ECG than in patients with a type 2/3 ECG. However, no differences were noted in other variables representing other parameters of repolarization interval and spatial and transmural dispersion of repolarization between patients with a type 1 and those with a type 2/3 ECG. Furthermore, no differences in spatial and transmural dispersion variables were observed between symptomatic and asymptomatic patients, although the prevalence of positive late ventricular potentials was significantly higher in symptomatic patients. The prevalence of positive ventricular late potential in type 1 ECG was marginally higher compared to that in type 2/3 ECG (16/26vs. 6/18, P=0.062), and both repolarization and depolarization abnormalities may constitute a type 1 ECG. Qualitative analysis showed that late potentials were located adjacent to the V2–V3 ECG position, whereas the distribution of the RT-c, RTe-c, and T(p-e)-c dispersion was more widespread, and usually located left inferior to the late potential location. The dispersion of the depolarization and repolarization indices suggests a different pathogenesis of these abnormalities. Transmural dispersion of repolarization within the ventricular myocardium has been suggested to underlie arrhythmogenesis in Brugada, short QT, or long QT syndrome, and in SCD [12,13]. Three electrophysiologically distinct cell types have been identified in the ventricular myocardium: endocardial, epicardial, and M cells. Differences in the time course of repolarization of these 3 ventricular myocardial cell types contribute prominently to inscription of the electrocardiographic T-wave [14]. In isolated ventricular wedge preparations, the peak of the T-wave was shown to coincide with epicardial repolarization and the end of the T-wave with repolarization of the M cells; thus, Tp-e provides a measure of transmural dispersion of repolarization [15]. These and other studies have suggested that although Tp-e on the surface ECG may not be equivalent to transmural dispersion of repolarization, this interval may serve as an index of transmural dispersion of repolarization and thus be helpful in forecasting risk for the development of life-threatening arrhythmias [13,15]. Evidence in support of this hypothesis has been provided in hypertrophic cardiomyopathy, congenital, and acquired long QT syndrome, and other pathologic conditions [7]. The reported cellular basis of BS is marked dispersion of repolarization in the right ventricular epicardium and transmurally [16–18]. Previous studies showed that the T peak-end interval and T peak-end dispersion on the 12-lead ECG are potential risk factors for VT/VF and VT/VF inducibility in patients with the Brugada ECG phenotype [8,19]. Studies have reported that QT/RR and T peak-end/RR slopes show loss of rate-dependency in VF(+) BS patients than in VF(−) BS patients and control patients, and the T peak-end interval correlated negatively with the RR interval in the VF(+) Brugada group and positively with the RR interval in the VF(−) Brugada and control groups [20]. However, an experimental study comparing epicardial electrograms and surface electrograms showed that T peak-end does not correlate with transmural dispersion of repolarization but rather is an index of total dispersion of repolarization [21]. In the present study, average T(p-e)-c interval, corrected maximum T peak-end dispersion, and corrected average T peak-end dispersion from the 187-channel SAVP-ECG did not differ between symptomatic and asymptomatic BS patients. However, average T(p-e)-c interval was marginally increased in patients with type 1 ECG compared to that in patients with type 2/3 Brugada type ECG. Additionally, corrected maximum RT interval dispersion and corrected average RT interval dispersion were greater in patients with a type 1 ECG compared to those in patients with a type 2/3 Brugada type ECG. However, the parameters on the absolute value and dispersion of repolarization did not differ between symptomatic and asymptomatic BS patients. Therefore, the ECG manifestation of type 1 Brugada ECG may be related to the longer transmural repolarization interval and greater spatial dispersion of refractoriness. Recent studies have shown that right ventricular fibrosis and conduction delay without a transmural repolarization gradient are the dominant pathophysiologic mechanisms for type 1 ECG and the origin of VF in BS [22–25]. We previously reported the presence of right ventricular outflow tract endocardial conduction delay and right ventricular septal histopathological abnormalities in patients with BS [26,27]. Furthermore, Nademanee et al. reported that the electrophysiological mechanism in patients with BS is delayed depolarization over the anterior aspect of the right ventricular outflow tract, and catheter ablation of this area of abnormal depolarization results in normalization of the Brugada ECG pattern and prevents VT/VF [28]. In our patient series, the prevalence of ventricular late potentials was significantly higher in symptomatic patients than in asymptomatic patients.