Drug-induced Brugada syndrome: Clinical characteristics and risk factors

Konigstein, Maayan; Rosso, Raphaël; Topaz, Guy; Postema, Pieter G.; Friedensohn, Limor; Heller, Karin; Zeltser, David; Belhassen, Bernard; Adler, Arnon; Viskin, Sami

doi:10.1016/j.hrthm.2016.03.016

Cited by 45 publications

(26 citation statements)

References 34 publications

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“…antibiotics (erythromycin), antimycotics (fluconazole), antihistaminics (astemizole), antiemetics (cisapride), antimalarial agents (chloroquine), neuroleptic drugs (risperidone) and antidepressant drugs (fluoxetine) [for recent review see (Schwartz and Woosley 2016)]. Conversely, in Brugada syndrome, men are at higher risk of developing a fully-blown ECG phenotype and even cardiac events in response to drugs class-1 antiarrhythmic drugs (sodium channel blockers) but also following exposure to tricyclic antidepressants, fluoxetine, lithium, trifluoperazine, antihistamines, or cocaine (Konigstein et al 2016;Yap et al 2009).…”

Section: Differences Between Men and Women In Susceptibility To Drug mentioning

confidence: 99%

Sex differences in cardiac electrophysiology

Ravens

2018

Can. J. Physiol. Pharmacol.

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Women have a longer QT interval than men, which appears to evolve after puberty suggesting that sex hormones have an influence on cardiac electrophysiology. Sex hormones do in fact regulate cardiac ion channels via genomic and nongenomic pathways. Women are at greater risk for life-threatening arrhythmias under conditions that prolong the QT interval. In addition, women exhibit greater sensitivity to QT interval-prolonging drugs. Female sex has also an impact on propensity to cardiovascular disease, including atrial fibrillation. However, ex vivo recorded atrial action potentials (APs) from female and male patients in atrial fibrillation did not exhibit significant differences in shape, except that APs from women had slower upstroke velocity. It is concluded that sex-related differences should be taken into account not only in the clinics, but also in basic research.

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Section: Differences Between Men and Women In Susceptibility To Drug mentioning

confidence: 99%

Sex differences in cardiac electrophysiology

Ravens

2018

Can. J. Physiol. Pharmacol.

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“…The clinical significance of drug-induced Brugada pattern in the absence of symptoms, family history of BrS, or family with Brugada ECG is undetermined. [ 34 ]…”

Section: Diagnosismentioning

confidence: 99%

Brugada syndrome in children - Stepping into unchartered territory

Behere

Weindling

2017

Ann Pediatr Card

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Brugada syndrome (BrS) is an autosomal dominant inherited channelopathy. It is associated with a typical pattern of ST-segment elevation in the precordial leads V1–V3 and potentially lethal ventricular arrhythmias in otherwise healthy patients. It is frequently seen in young Asian males, in whom it has previously been described as sudden unexplained nocturnal death syndrome. Although it typically presents in young adults, it is also known to present in children and infants, especially in the presence of fever. Our understanding of the genetic pathogenesis and management of BrS has grown substantially considering that it has only been 24 years since its first description as a unique clinical entity. However, there remains much to be learned, especially in the pediatric population. This review aims to discuss the epidemiology, genetics, and pathogenesis of BrS. We will also discuss established standards and new innovations in the diagnosis, prognostication, risk stratification, and management of BrS. Literature search was run on the National Center for Biotechnology Information's website, using the Medical Subject Headings (MeSH) database with the search term “Brugada Syndrome” (MeSH), and was run on the PubMed database using the age filter (birth–18 years), yielding 334 results. The abstracts of all these articles were studied, and the articles were categorized and organized. Articles of relevance were read in full. As and where applicable, relevant references and citations from the primary articles were further explored and read in full.

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“…The only characteristics that differentiated patients who developed arrhythmias from those who did not were younger age and non-oral route of administration for the culprit drugs. Both in those with and without arrhythmias, duration of exposure to the drug before the BrS ECG developed was weeks to years, making ECG screening at the time of drug initiation impractical (Konigstein et al, 2016).…”

Section: -4 Treatment and Prevention Of Drug-induced Brsmentioning

confidence: 99%

Drug-induced fatal arrhythmias: Acquired long QT and Brugada syndromes

Turker

Itoh

et al. 2017

Pharmacology & Therapeutics

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Since the early 1990s, the concept of primary "inherited" arrhythmia syndromes or ion channelopathies has evolved rapidly as a result of revolutionary progresses made in molecular genetics. Alterations in genes coding for membrane proteins such as ion channels or their associated proteins responsible for the generation of cardiac action potentials (AP) have been shown to cause specific malfunctions which eventually lead to cardiac arrhythmias. These arrhythmic disorders include congenital long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, short QT syndrome, progressive cardiac conduction disease, etc. Among these, long QT and Brugada syndromes are the most extensively studied, and drugs cause a phenocopy of these two diseases. To date, more than 10 different genes have been reported to be responsible for each syndrome. More recently, it was recognized that long QT syndrome can be latent, even in the presence of an unequivocally pathogenic mutation (silent mutation carrier). Co-existence of other pathological conditions in these silent mutation carriers may trigger a malignant form of ventricular arrhythmia, the so called torsade de pointes (TdP) that is most commonly brought about by drugs. In analogy to the drug-induced long QT syndrome, Brugada type 1 ECG can also be induced or unmasked by a wide variety of drugs and pathological conditions; so physicians may encounter patients with a latent form of Brugada syndrome. Of particular note, Brugada syndrome is frequently associated with atrial fibrillation whose therapeutic agents such as Vaughan Williams class IC drugs can unmask the dormant and asymptomatic Brugada syndrome. This review describes two types of drug-induced arrhythmias: the long QT and Brugada syndromes.

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Drug-induced Brugada syndrome: Clinical characteristics and risk factors

Cited by 45 publications

References 34 publications

Sex differences in cardiac electrophysiology

Sex differences in cardiac electrophysiology

Brugada syndrome in children - Stepping into unchartered territory

Drug-induced fatal arrhythmias: Acquired long QT and Brugada syndromes

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