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    • Letsas et al reported that the prevalence of Brugada type

    2019-04-30

    Letsas et al. reported that the prevalence of Brugada-type ECG was 0.34% in men and 0.04% in women in the Greek population [19]. Despite the similar BS gender differences between the Greeks and the Japanese, many multicenter studies performed in Western countries indicated that the frequency of men with BS (72–80%) [35–39] was much lower than that of the Japanese population (94–96%) [31,32]. The reason for this national difference in gender-related frequency in BS is not completely understood. Racial difference or higher BMI in Caucasian men might have an influence on the severity of Brugada phenotype manifestation. Another reason may be the difference of BS cohorts between Western multicenter studies and Japanese BS registries. The former included a significant number of family members in whom type 1 ECG was induced by drug provocation tests, while the latter mainly consisted of probands who had spontaneous type 1 ECG. The fact that patients with a milder phenotypic expression of BS make up a considerable proportion of subjects in studies from Western countries, may result in the higher rate of inclusion of women in Western registries.
    Prognosis of healthy individuals showing Brugada-pattern ECG The prognosis of healthy subjects with Brugada-pattern ECG or Brugada-type ECG is favorable. Miyasaka et al. reported that one of 98 subjects with Brugada-pattern ECG with a J-point elevation ≥1mm and 139 of 13,831 controls died during 2.6±0.3 years of follow-up [8]. Matsuo et al. reported that seven of 32 subjects with Brugada-pattern ECG developed unexpected death in Yeast Extract to 20 of 4736 subjects with normal ECG during 40 years of follow-up [11]. Cox survival analysis revealed that mortality was significantly higher in subjects with Brugada-pattern ECG than in control subjects. Sakabe et al. reported that one of 69 subjects with Brugada-type ECG with a J-wave amplitude ≥2mm had an episode of ventricular fibrillation during 4 years of follow-up [13]. Tsuji et al. reported that one of 98 subjects with Brugada-type ECG and 142 of 13,806 controls developed cardiovascular death during 7.8±1.6 years of follow-up, although no one with type 1 ECG died [9]. With regard to juveniles, Oe et al. [14] reported that none of the four subjects with Brugada-type ECG had an episode of sudden death or syncope during 6.8±1.0 years of follow-up. The outcome of healthy subjects with Brugada-type ECG is much better in Western countries. No cardiovascular death or life-threatening ventricular arrhythmia was observed in 25 individuals during 29.7±10.7 months of follow-up in a Greek population [19], in 15 subjects during 19±2 years of follow-up in a Finnish population [17], and in seven subjects for more than 30 years of follow-up in a Danish population [16]. However, one of 31 subjects died suddenly during 10.1±5.5 years of follow-up in an English and an Italian population [20]. Sixty-one subjects showing Brugada-pattern ECG in a French population did not die from cardiovascular disease during 49±30 months of follow-up [23]. To summarize, the annual death rate of healthy adults with Brugada-pattern or Brugada-type ECG is estimated to be less than 0.5%.
    Conclusions
    Conflict of interest
    Diagnostic ECG criteria for Brugada syndrome
    Multiple factors influencing Brugada-type ECG The ECG pattern is dynamic, variable, and often concealed. Multiple factors have been shown to influence ST-segment elevation in Brugada syndrome patients and suspected cases. These factors include changes in heart rate, body temperature, autonomic imbalance, glucose-induced insulin secretion, sodium channel blockers, and so others [3,4,10,26–36] (Fig. 3). Among these factors, sodium channel blockers have the most critical influence on patients with Brugada syndrome and related conditions because of their actions of unmasking ST elevation and inducing serious arrhythmic events as unexpected or side effects [3,4,10,26,27]. Other classes and types of drugs are also known to affect ST-segment elevation and arrhythmia development in manifest and latent Brugada syndrome patients. Recently, drugs that should be avoided by Brugada syndrome patients have been listed on a website (〈http://www.brugadadrugs.org〉) due to the occasional and unexpected development of Brugada-type ST elevation and ventricular tachyarrhythmias [37]. Drugs used in Brugada syndrome patients and suspected cases are categorized into four groups: (1) drugs to be avoided; (2) drugs to be preferably avoided; (3) antiarrhythmic drugs; and (4) diagnostic drugs. Sodium channel blockers are recommended diagnostic drugs for Brugada syndrome. Pilsicainide exhibits the properties of a pure sodium channel blocker and has been recommended for the diagnosis of suspected cases in Japan. On the other hand, quinidine is classified as a sodium channel blocker and has been shown to be effective in suppressing ST-segment elevation and preventing VTs. [38,39] The preventive effects of quinidine are supposedly exerted through its action on the specific K+ current, Ito.