Electrophysiological Substrates for Gender Difference in the Incidence of Torsades de Pointes Arrhythmias

El‐Sherif, Nabil; Himel, Herman D.; Yue, Yuan; Boutjdir, Mohamed; Restivo, Mark

doi:10.1002/9781119152637.ch24

Cited by 3 publications

(2 citation statements)

References 33 publications

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“…[51] The underlying mechanisms can be summarised as follows:[52] an estradiol-induced decrease in Ikr as well as increase of ICaL, NCX expression and activity, RyR2 leakiness, Ca2+ transient amplitude, and a1- and b2-adrenoreceptor responsiveness; a testosterone-induced increase in Ikr, Iks, and Ik1, increased SERCA activity, and shortened Ca2+ transient; and a progesterone-induced increase in Iks, increased CERCA expression and activity, and increased ICA-L current sensitivities with reduced Ca2+ oscillations upon sympathetic stimulation. In a recent study, we have shown that modulation of voltage-Ca 2+ uncoupling[53] may provide one more attractive electrophysiological mechanism for the increased vulnerability of female to drug-induced LQTS.…”

Section: Acquired Long Qt Syndromementioning

confidence: 99%

Acquired Long QT Syndrome and Electrophysiology of Torsade de Pointes

El‐Sherif

Turitto

Boutjdir

2019

Arrhythm Electrophysiol Rev

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Congenital long QT syndrome (LQTS) has been the most investigated cardiac ion channelopathy. Although congenital LQTS remains the domain of cardiologists, cardiac electrophysiologists and specialised centres, the much more frequently acquired LQTS is the domain of physicians and other members of healthcare teams required to make therapeutic decisions. This paper reviews the electrophysiological mechanisms of acquired LQTS, its ECG characteristics, clinical presentation, and management. The paper concludes with a comprehensive review of the electrophysiological mechanisms of torsade de pointes.

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Section: Acquired Long Qt Syndromementioning

confidence: 99%

Acquired Long QT Syndrome and Electrophysiology of Torsade de Pointes

El‐Sherif

Turitto

Boutjdir

2019

Arrhythm Electrophysiol Rev

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“…However, recent experimental data that included, among others, estrogen upregulation of Ica‐L by a classical genomic mechanism, may challenge the concept of repolarization reserve. Instead, Ca 2+ homeostasis, and voltage‐Ca 2+ uncoupling may provide more attractive electrophysiological mechanisms for the increased vulnerability of female to drug‐induced LQTS.…”

Section: Ethnicity and Gender Differences In Drug‐induced Lqtsmentioning

confidence: 99%

Acquired long QT syndrome and torsade de pointes

El‐Sherif

Turitto

Boutjdir

2018

Pacing Clinical Electrophis

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Since its initial description by Jervell and Lange-Nielsen in 1957, the congenital long QT syndrome (LQTS) has been the most investigated cardiac ion channelopathy. Although congenital LQTS continues to remain the domain of cardiologists, cardiac electrophysiologists, and specialized centers, the by far more frequent acquired drug-induced LQTS is the domain of all physicians and other members of the health care team who are required to make therapeutic decisions. This report will review the electrophysiological mechanisms of LQTS and torsade de pointes, electrocardiographic characteristics of acquired LQTS, its clinical presentation, management, and future directions in the field.

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