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
  • br Update on the diagnosis of

    2019-05-09


    Update on the diagnosis of ERS ERS is generally diagnosed in patients who display ER in the inferior and/or lateral leads presenting with aborted cardiac arrest, documented VF, or polymorphic VT. Consistent with the recent consensus report on ERP [24], ER is recognized if (1) there is an end QRS notch (J wave) or slur on the downslope of a prominent R wave with and without ST-segment elevation; (2) the peak of the notch or J wave (Jp) ≥0.1mV in ≥2 contiguous leads of the 12-lead ECG, excluding leads V1−V3; and (3) QRS duration (measured in leads in which a notch or slur is absent) o120 ms. Table 4 lists the exclusion criteria in the differential diagnosis trospium chloride of ERS. A proposed diagnostic score system for ERS, referred to as the Proposed Shanghai ERS Score, is presented in Table 5. The scoring system is based on evidence available in the literature to date. As in BrS, weighting of variables is based on expert opinion informed by cohort studies that do not include all variables presented. Thus, rigorous, objectively weighted coefficients were not derived from large-scale risk factor- and outcome-informed datasets. Nonetheless, the authors believed that some inferential weighting would be of benefit when applied to patients. As with all such recommendations, they will need to undergo initial and ongoing validation in future studies.
    Similarities and difference between BrS and ERS BrS and ERS display several clinical similarities, suggesting similar pathophysiology (Table 6) [19,21,103–105]. Males predominate in both syndromes, with BrS presenting in 71–80% among Caucasians and 94–96% among Japanese [106,107]. In the setting of ERP, VF occurred mainly in males (72%) when studied in an international cohort [2] but in a much higher percentage in a report by Japanese investigators [108]. BrS and ERS patients may be totally asymptomatic until they present with cardiac arrest. In both syndromes, the highest incidence of VF or SCD occurs in the third decade of life, perhaps related to trospium chloride levels in males [109]. In both syndromes, the appearance of accentuated J waves and ST-segment elevation is generally associated with bradycardia or pauses [110,111]. This can explain why VF in both syndromes often occurs during sleep or during a low level of physical activities [108,112]. The QT interval is relatively short in patients with ERS [2,113], and BrS who carry mutations in calcium channel genes [114]. As will be discussed in more detail later, ERS and BrS also share similarities with respect to the response to pharmacologic therapy. In both, electrical storms and associated J-wave manifestations can be suppressed using β- adrenergic agonists [115–118]. Chronic oral pharmacologic therapy using quinidine [119,120], bepridil [117], denopamine [115,121], and cilostazol [115,117,121–125] is reported to suppress the development of VT/VF in both ERS and BrS secondary to inhibition of Ito, augmentation of ICa, or both [3,122,126]. Differences between the 2 syndromes include (1) the region of the heart most affected (RVOT vs inferior LV); (2) the presence of (discrete) structural abnormalities in BrS but not in ERS; (3) the incidence of late potentials in signal- averaged ECGs (BrS 60% 4 ERS 7%) [108]; and (4) greater elevation of Jo, Jp, or Jt (ST-segment elevation) in response to sodium channel blockers in BrS vs ERS and higher prevalence of atrial fibrillation in BrS vs ERS [127]. Early studies suggested a different pathophysiologic basis for ERS and BrS based on the observation that sodium channel blockers unmask or accentuate J-wave manifestation in BrS but reduces the amplitude in ERS [108]. However, the recent study by Nakagawa et al. [357]. showed that J waves recorded using unipolar LV epicardial leads introduced into the left lateral coronary vein in ERS patients are indeed augmented, even though J waves recorded in the lateral precordial leads are diminished, due principally to engulfment of the surface J wave by the widened QRS [29,108]. The case report of Nakagawa et al. has recently been supplemented with additional cases in which this technique was used; 2 of these 3 cases showed pilsicainide-induced accentuation of the J waves in electrograms recorded from the epicardial surface of the LV (H. Morita, unpublished observations). Also in support of the thesis that these ECG patterns and syndromes are closely related are reports of cases in which ERS transitions into ERS plus BrS [105,128].