Asymptomatic Brugada Syndrome Case Unmasked During Dimenhydrinate Infusion

Pastor, Agustı́n; Núñez, Ambrosio; Cantale, Carina; Cosío, Francisco G.

doi:10.1046/j.1540-8167.2001.01192.x

Cited by 58 publications

(22 citation statements)

References 2 publications

(3 reference statements)

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“…ST segment elevation in BS is often dynamic. The Brugada ECG may often be concealed, but can be unmasked or modulated by sodium channel blockers, a febrile state, vagotonic agents, α-adrenergic agonists, β-adrenergic blockers, tricyclic or tetracyclic antidepressants, firstgeneration antihistaminics (dimenhydrinate), a combination of glucose and insulin, hyperkalemia, hypokalemia, hypercalcemia, and by alcohol and cocaine toxicity [37][38][39][40][41][42][43][44][45][46][47]. These agents may also induce acquired forms of BS.…”

Section: Antidepressant and Antipsychotic Drug-induced Brugada Syndromementioning

confidence: 99%

Sudden cardiac death secondary to antidepressant and antipsychotic drugs

Sicouri

Antzelevitch

2008

Expert Opinion on Drug Safety

101

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A number of antipsychotic and antidepressant drugs are known to increase the risk of ventricular arrhythmias and sudden cardiac death. Based largely on a concern over QT prolongation and the development of life-threatening arrhythmias, a number of antipsychotic drugs have been temporarily or permanently withdrawn from the market or their use restricted. Some antidepressants and antipsychotics have been linked to QT prolongation and the development of Torsade de pointes arrhythmias, whereas others have been associated with a Brugada syndrome phenotype and the development of polymorphic ventricular arrhythmias. This review examines the mechanisms and predisposing factors underlying the development of cardiac arrhythmias, and sudden cardiac death, associated with antidepressant and antipsychotic drugs in clinical use.

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Section: Antidepressant and Antipsychotic Drug-induced Brugada Syndromementioning

confidence: 99%

Sudden cardiac death secondary to antidepressant and antipsychotic drugs

Sicouri

Antzelevitch

2008

Expert Opinion on Drug Safety

101

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“…The ECG characteristics exhibit day-to-day variation and may not always be present [Veltmann et al, 2006]. However, they may be unmasked by administration of sodium channel blockers, for example, ajmaline or flecainide [Brugada et al, 2000a,b;Shimizu et al, 2000], fever Dumaine et al, 1999], vagotonic agents [Mizumaki et al, 2004;Wichter et al, 2002], a-adrenergic agonists [Pastor et al, 2001], b-adrenergic blockers [Miyazaki et al, 1996], cyclic antidepressants [Goldgran-Toledano et al, 2002], hyper-and hypokalemia [Araki et al, 2003;Littmann et al, 2007a], hypercalcemia [Littmann et al, 2007b], alcohol [Pilz and Luft, 2003], and cocaine [Ortega-Carnicer et al, 2001]. The current diagnostic criteria for BrS are given in Box 1.…”

Section: Introductionmentioning

confidence: 99%

The genetic basis of Brugada syndrome: A mutation update

et al. 2009

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Brugada syndrome (BrS) is a condition characterized by a distinct ST-segment elevation in the right precordial leads of the electrocardiogram and, clinically, by an increased risk of cardiac arrhythmia and sudden death. The condition predominantly exhibits an autosomal dominant pattern of inheritance with an average prevalence of 5:10,000 worldwide. Currently, more than 100 mutations in seven genes have been associated with BrS. Loss-of-function mutations in SCN5A, which encodes the a-subunit of the Na v 1.5 sodium ion channel conducting the depolarizing I Na current, causes 15-20% of BrS cases. A few mutations have been described in GPD1L, which encodes glycerol-3-phosphate dehydrogenase-1 like protein; CACNA1C, which encodes the a-subunit of the Ca v 1.2 ion channel conducting the depolarizing I L,Ca current; CACNB2, which encodes the stimulating b2-subunit of the Ca v 1.2 ion channel; SCN1B and SCN3B, which, in the heart, encodes b-subunits of the Na v 1.5 sodium ion channel, and KCNE3, which encodes the ancillary inhibitory b-subunit of several potassium channels including the Kv4.3 ion channel conducting the repolarizing potassium I to current. BrS exhibits variable expressivity, reduced penetrance, and ''mixed phenotypes,'' where families contain members with BrS as well as long QT syndrome, atrial fibrillation, short QT syndrome, conduction disease, or structural heart disease, have also been described.

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“…A sedating, first-generation histaminic H1 receptor antagonist (dimenhydrinate; [22]) and cocaine [23] intoxication are also reported to cause the electrocardiographic sign of the Brugada syndrome.…”

Section: Acquired Brugada Syndromementioning

confidence: 99%

Brugada syndrome

Francis

Antzelevitch

2005

International Journal of Cardiology

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The Brugada syndrome is an autosomal dominant disease with incomplete penetrance that may cause syncope and sudden cardiac death in young individuals with a normal heart. It is characterized by an electrocardiographic pattern of complete or incomplete right bundle branch block and ST segment elevation in leads V1-V3. One of the genes linked to this syndrome is SCN5A, the gene encoding for the cardiac sodium channel. Mutations in SCN5A cause a functional reduction in the availability of cardiac sodium current in Brugada syndrome. However, only 20-25% of patients affected by this syndrome have mutations on this gene. A novel gene locus on chromosome 3, distinct from SCN5A, has been identified recently. The relative male preponderance of the phenotype, despite equal inheritance of the gene in males and females, has led to the speculation of a role for testosterone in the phenotype. The disease could manifest at first time as cardiac arrest without any previous symptom, and the electrocardiographic pattern could be intermittent, requiring a pharmacological challenge with Class I antiarrhythmic drugs to unmask ST elevation. Several conditions producing Brugada-like electrocardiographic patterns should be borne in mind and excluded while making a diagnosis of the Brugada syndrome. The management is difficult as pharmacological agents are not universally effective. The mode of treatment recommended by the majority of cardiac electrophysiologists is the implantation of a cardioverter defibrillator. Symptomatic patients with inducible ventricular arrhythmias and a positive family history should be considered for prophylactic implantation of a cardioverter defibrillator.

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Asymptomatic Brugada Syndrome Case Unmasked During Dimenhydrinate Infusion

Cited by 58 publications

References 2 publications

Sudden cardiac death secondary to antidepressant and antipsychotic drugs

Sudden cardiac death secondary to antidepressant and antipsychotic drugs

The genetic basis of Brugada syndrome: A mutation update

Brugada syndrome

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