Increased right ventricular repolarization gradients promote arrhythmogenesis in a murine model of Brugada syndrome.
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Molecular and genetic basis of sudden cardiac deathElectrophysiological Mechanisms of Brugada Syndrome: Insights from Pre-clinical and Clinical StudiesRecent developments in the management of patients at risk for sudden cardiac death.Sudden cardiac death and inherited channelopathy: the basic electrophysiology of the myocyte and myocardium in ion channel disease.Delayed conduction and its implications in murine Scn5a(+/-) hearts: independent and interacting effects of genotype, age, and sexArrhythmic substrate, slowed propagation and increased dispersion in conduction direction in the right ventricular outflow tract of murine Scn5a+/- hearts.Mapping of reentrant spontaneous polymorphic ventricular tachycardia in a Scn5a+/- mouse model.Nonlinearity between action potential alternans and restitution, which both predict ventricular arrhythmic properties in Scn5a+/- and wild-type murine heartsReduced Na(+) and higher K(+) channel expression and function contribute to right ventricular origin of arrhythmias in Scn5a+/- mice.Inherited Arrhythmias: Of Channels, Currents, and Swimming.Mouse Models of SCN5A-Related Cardiac ArrhythmiasCardiac electrophysiology in mice: a matter of size.Refractory dispersion promotes conduction disturbance and arrhythmias in a Scn5a (+/-) mouse modelMurine Electrophysiological Models of Cardiac Arrhythmogenesis.Multiple targets for flecainide action: implications for cardiac arrhythmogenesis.Spatial and temporal heterogeneities are localized to the right ventricular outflow tract in a heterozygotic Scn5a mouse model.In vivo studies of Scn5a+/- mice modeling Brugada syndrome demonstrate both conduction and repolarization abnormalities.Variability in local action potential durations, dispersion of repolarization and wavelength restitution in aged wild-type and Scn5a+/- mouse hearts modeling human Brugada syndrome.Determination of action potential wavelength restitution in Scn5a+/- mouse hearts modelling human Brugada syndrome.Normal interventricular differences in tissue architecture underlie right ventricular susceptibility to conduction abnormalities in a mouse model of Brugada syndrome.
P2860
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P2860
Increased right ventricular repolarization gradients promote arrhythmogenesis in a murine model of Brugada syndrome.
description
2010 nî lūn-bûn
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2010年の論文
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2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
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2010年论文
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2010年论文
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name
Increased right ventricular re ...... ine model of Brugada syndrome.
@en
Increased right ventricular re ...... ine model of Brugada syndrome.
@nl
type
label
Increased right ventricular re ...... ine model of Brugada syndrome.
@en
Increased right ventricular re ...... ine model of Brugada syndrome.
@nl
prefLabel
Increased right ventricular re ...... ine model of Brugada syndrome.
@en
Increased right ventricular re ...... ine model of Brugada syndrome.
@nl
P2093
P2860
P1476
Increased right ventricular re ...... ine model of Brugada syndrome.
@en
P2093
Andrew A Grace
Christopher L-H Huang
Claire A Martin
Yanmin Zhang
P2860
P304
P356
10.1111/J.1540-8167.2010.01767.X
P577
2010-10-01T00:00:00Z