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    • The prevalence of drug induced type Brugada

    2019-06-18

    The prevalence of drug-induced type 1 Brugada pattern among patients with clinical AVNRT was found to be 27.1% by our group [17]. This high prevalence has important implications in terms of the epidemiology of BrS. The prevalence of paroxysmal supraventricular tachycardia (PSVT) (AVNRT and AVRT) in the general population in the US has been reported to be approximately 2.25/1000 persons [36]. If these results are extrapolated to the entire US population, we estimate nearly 140,000 new cases of PSVT per year. AVNRT comprises 60% of all PSVT cases. If a high prevalence of drug-induced type 1 Brugada pattern in patients with spontaneous AVNRT is confirmed by further studies, the prevalence of drug-induced type 1 Brugada pattern may reach approximately 21,000 new cases per year.
    Clinical characteristics The Butaprost of AF is more likely to occur during night time in patients with BrS [9]. Studies wherein an association between AF and BrS has been evaluated have involved mostly male patients. Therefore, the involvement of a sex predilection for the development of AF in patients with BrS is not clear [1]. Clinical AFL has been anecdotally reported either in young patients (<20 years old) as an isolated arrhythmia, or coexisting with AF in adults, or as a part of atrial myopathy and progressive cardiac conduction disorder in patients with BrS [37–45]. Our group recently showed that patients with AVNRT and drug-induced type 1 Brugada pattern were predominantly women (88.5% versus 62.9%, p=0.015) and had higher prevalence of chest pain (38.5% versus 18.6%, p=0.042) and migraine headaches (38.4% versus 14.2%, p=0.008) than patients without concealed BrS. Drug-induced initiation and/or worsening of duration and/or frequency of palpitations (along with documented AVNRT) were observed more frequently in patients with concealed BrS than in patients without concealed BrS (15.4% versus 1.4%, p=0.006) [17]. AF can be the first mode of presentation in SQTS particularly in patients with lone AF [2]. Sinus node dysfunction coexisting with AF can be observed particularly in patients with type 2 SQTS [30]. Sinus node dysfunction can be a clinical manifestation in patients with CPVT either as a part of a primary genetic defect or atrial myopathy coexisting with AF and/or AFL [46].
    Genetics of atrial arrhythmias In BrS, a decrease in cardiac sodium (INa) or calcium (ICa) channel current or augmentation of any one of a number of outward cardiac potassium channel currents, including IKr, IKs, and Ito, can cause preferential abbreviation of the right ventricular epicardial action potential secondary to all-or-none repolarization of the action potential at the end of phase 1 [47]. The substrate responsible for the development of ventricular arrhythmias also may contribute to arrhythmogenesis in the atria of the heart [1]. Two cardiac potassium channel currents, Ito and IKur are known to be major repolarizing currents in the human atrium. Nav1.5 has been demonstrated as the predominant channel followed by Nav1.1, Nav1.3, and Nav1.6 in humal atrial cells [48]. Loss-of-function mutations in the INa channel α-subunit (SCN5A) is the most common (~20%) etiology of BrS [49]. Recently, SCN10A, a neuronal sodium channel gene encoding Nav1.8 has been identified as a major susceptibility gene (~16%) for BrS [50]. In addition, loss-of-function mutations in the ICa,L channel α- and β-subunits cause BrS in a significant number of patients (~10%) [51]. Loss-of-function mutations in the INa channel α- and β-subunits (SCN5A, SCN1B, SCN2B, and SCN3B) and ICa,L channel α- and β-subunits (CACNA1C and CACNB2) have been identified in patients with both BrS and AF [9,12,52–55]. A missense mutation (S422L) in the cardiac KATP channel (KCNJ8) has been identified as the cause of ERS associated with AF [56,57]. The role of SCN5A mutations in the development of AF in patients with BrS remains unclear. Two studies showed that the prevalence of AF is not different in patients with BrS with or without SCN5A mutation [9,12]. The presence of SCN5A mutations have been associated with lower number of premature atrial contractions on Holter monitoring, longer intra-atrial conduction time, and structural remodeling (higher left atrial volume index) but not with AF episodes [11]. A reduced number of potentially triggering premature atrial contractions in the presence of a more extensive substrate in SCN5A mutation carriers hypothetically account for AF not being more prevalent in patients with SCN5A mutations than in those without them [12,58].