Overdose of Cyclic Antidepressants and the Brugada Syndrome

Goldgran-Tolédano, Dany; Sidéris, Georgios; Kévorkian, Jean-Philippe

doi:10.1056/nejm200205163462020

Cited by 124 publications

(65 citation statements)

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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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Section: Introductionmentioning

confidence: 99%

The genetic basis of Brugada syndrome: A mutation update

et al. 2009

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“…1,3 In a study of 98 patients experiencing an overdose of tricyclic antidepressants, Goldgran-Toledano et al 18 reported that overall mortality among all patients was 3%, but among patients who displayed a Brugada phenotype it was 6.7%. Rouleau et al 3 reported 3 cases of psychotropic drug-induced Brugada ECG, occurring during coadministration of amitriptyline and other antipsychotic drugs.…”

Section: Discussionmentioning

confidence: 99%

“…18 Tricyclic antidepressants, including amitriptyline, have been reported to block I Na among other actions. 19,20 The drug has also been shown to potently inhibit I to .…”

Section: Introductionmentioning

confidence: 99%

Ionic and Cellular Mechanisms Underlying the Development of Acquired Brugada Syndrome in Patients Treated with Antidepressants

Minoura¹,

Diego²,

Barajas-Martínez³

et al. 2011

J Arrhythmia

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Introduction-Tricyclic antidepressants are known to induce cardiac arrhythmias at therapeutic or supratherapeutic doses. The tricyclic antidepressant, amitriptyline, is reported to induce ST segment elevation in the right precordial electrocardiogram (ECG) leads, thus unmasking Brugada syndrome (BrS). The mechanism by which antidepressants induce the BrS phenotype and associated sudden death is not well established.

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“…Hypotension, widened QRS duration, and seizures were more commonly found in patients with BEP after TCA overdose. A case series of BEP after TCA overdose showed that there was no statistically significant increase in the risk of death from cardiac causes related to the development of BEP after TCA overdose (5). The mechanism of BEP after TCA overdose is not well known.…”

Section: Discussionmentioning

confidence: 99%