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

    • The morphology and degree of ST segment

    2019-05-17

    The morphology and degree of ST-segment elevation may also be influenced by the position of the recording electrodes. A higher right precordial lead placement than the conventional position at V1−V3 can also be used to unmask the Brugada-type ECG in subjects without typical ECG changes or unequivocal signs [40–42]. Demonstration and unmasking of the type 1 ECG pattern at the higher lead positions also have diagnostic value for Brugada syndrome, similar to its appearance at the conventional lead position of V1−V3 [40–42].
    Differential diagnosis of Brugada-type ECG ECG changes that are similar to those of Brugada syndrome are observed in various normal and abnormal conditions, including early repolarization in apparently healthy individuals and young athletes as well as cases of left ventricular hypertrophy, acute myocardial infarction, pericarditis, variant nop receptor pectoris, arrhythmogenic right ventricular cardiomyopathy (ARVC), pulmonary embolism, and hyperkalemia [3,4,9,10,43–45]. Differential diagnoses for patients showing ST-segment elevation in the right precordial leads are shown in Table 1. In particular, differential diagnosis between Brugada syndrome and ARVC on ECG may be difficult. Common ECG features of ARVC represent depolarization/repolarization abnormalities such as an epsilon wave, prolongation of the QRS interval, late potential, and an inverted T wave in the right precordial leads [9,10] (Fig. 4A). Moreover, monomorphic VT with left bundle branch block morphology facilitated occasionally by catecholamines and exercise is observed in patients with ARVC, and its mechanism involves scar-related reentry. In contrast, the electrogenesis of polymorphic ventricular tachycardia degenerating into VF in Brugada syndrome patients is thought to involve phase-2 reentry [9,10]. ST-segment elevation in the right precordial leads is often enhanced by vagotonic agents and life-threatening ventricular arrhythmias frequently occur at rest, after meals, or during sleep. Unlike ARVC, the level and morphology of ST elevation spontaneously fluctuate over multiple days and within a single day, and the typical ECG changes do not exhibit a stable expression pattern. A type 1 ECG is unmasked by administration of sodium channel blockers in Brugada syndrome patients, whereas ARVC patients do not exhibit ST–T wave changes related to repolarization abnormalities during drug challenge testing. The morphologies of ST-segment elevation in Brugada syndrome are also similar to those observed during variant angina and SCD occurs during sleep in both diseases, which is often due to polymorphic ventricular tachycardia degenerating into VF [46,47]. Moreover, the coexistence of both diseases in the same patients has been observed occasionally. [43–45] ST-segment elevation in variant angina patients is detected briefly during spontaneous chest pain or intracoronary injection of acetylcholine in the precordial and inferior leads, accompanied by reciprocal ST–T wave changes (Fig. 4B). Furthermore, unlike Brugada syndrome, administration of sodium channel blockers does not affect ST-segment changes in patients with variant angina. On the other hand, ECG manifestations in Brugada syndrome patients represent persistent or fluctuating ST-segment elevation in the right precordial leads from V1 to V3, which is improved during exercise testing. The reciprocal ST–T wave change is not recognized on ECG in Brugada syndrome.
    Manifestations of Brugada-type ECG
    Clinical implications In large cohort studies, the spontaneous appearance of a type 1 ECG pattern associated with symptoms of aborted sudden death or unexplained syncope is indicative of a poor prognosis for Brugada syndrome patients [7,8,12,54]. Moreover, the incidence of cardiac events in symptomatic patients with only a drug-induced type 1 ECG was 3–17% during the follow-up period [8,13,14,48,54]. In contrast, there is a low incidence of arrhythmic events in asymptomatic patients with either a spontaneous or drug-induced type 1 ECG as compared to symptomatic subjects. Specifically, asymptomatic patients with only a drug-induced type 1 ECG have a very low incidence of cardiac events (0–1%) [8,13,14,48,54]. Therefore, a drug-induced type 1 ECG in asymptomatic patients does not appear to increase the arrhythmic risk. Considering the infrequent appearance of a type 1 ECG pattern in baseline recordings and its significance for the detection of arrhythmic events, the frequency and number of ECG recordings used to judge whether individuals show a type 1 or non-type 1 ECG at baseline are quite important [54].