Chronic heart failure slows late sodium current in human and canine ventricular myocytes: implications for repolarization variability.
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The role of late I Na in development of cardiac arrhythmiasRegulation of intracellular Na(+) in health and disease: pathophysiological mechanisms and implications for treatmentThe late Na+ current--origin and pathophysiological relevanceTowards a better understanding of QT interval variabilityNa+ channel function, regulation, structure, trafficking and sequestrationNew treatment options for late Na current, arrhythmias, and diastolic dysfunctionLate Sodium Current in Human Atrial Cardiomyocytes from Patients in Sinus Rhythm and Atrial FibrillationLate Na(+) current and protracted electrical recovery are critical determinants of the aging myopathyPost-translational modifications of the cardiac Na channel: contribution of CaMKII-dependent phosphorylation to acquired arrhythmiasExperimentally-Based Computational Investigation into Beat-To-Beat Variability in Ventricular Repolarization and Its Response to Ionic Current InhibitionSimulation and mechanistic investigation of the arrhythmogenic role of the late sodium current in human heart failureMicrodomain-Specific Modulation of L-Type Calcium Channels Leads to Triggered Ventricular Arrhythmia in Heart Failure.miR-19b Regulates Ventricular Action Potential Duration in Zebrafish.Basal late sodium current is a significant contributor to the duration of action potential of guinea pig ventricular myocytes.There goes the neighborhood: pathological alterations in T-tubule morphology and consequences for cardiomyocyte Ca2+ handling.Verapamil suppresses cardiac alternans and ventricular arrhythmias in acute myocardial ischemia via ryanodine receptor inhibitionElectrophysiological remodeling in heart failureInhibition of the late sodium current slows t-tubule disruption during the progression of hypertensive heart disease in the rat.Late sodium current contributes to diastolic cell Ca2+ accumulation in chronic heart failure.Calpain inhibition reduces amplitude and accelerates decay of the late sodium current in ventricular myocytes from dogs with chronic heart failureEffects of ranolazine on torsades de pointes tachycardias in a healthy isolated rabbit heart modelElectrophysiological and structural remodeling in heart failure modulate arrhythmogenesis. 1D simulation study.Post-transcriptional silencing of SCN1B and SCN2B genes modulates late sodium current in cardiac myocytes from normal dogs and dogs with chronic heart failure.Calcium-voltage coupling in the genesis of early and delayed afterdepolarizations in cardiac myocytesHuman Na(v)1.8: enhanced persistent and ramp currents contribute to distinct firing properties of human DRG neurons.Targeting cardiomyocyte Ca2+ homeostasis in heart failure.A mathematical model for active contraction in healthy and failing myocytes and left ventricles.Reduced response to IKr blockade and altered hERG1a/1b stoichiometry in human heart failureLate sodium current in failing heart: friend or foe?Modulation of late sodium current by Ca2+, calmodulin, and CaMKII in normal and failing dog cardiomyocytes: similarities and differences.Chronic inhibition of the Na+/H+ - exchanger causes regression of hypertrophy, heart failure, and ionic and electrophysiological remodelling.Molecular identity of the late sodium current in adult dog cardiomyocytes identified by Nav1.5 antisense inhibition.Myocyte repolarization modulates myocardial function in aging dogsLate sodium current is a new therapeutic target to improve contractility and rhythm in failing heart.Inhibition of late sodium current to reduce electrical and mechanical dysfunction of ischaemic myocardium.Role of late sodium current as a potential arrhythmogenic mechanism in the progression of pressure-induced heart disease.Ranolazine combined with enalapril or metoprolol prevents progressive LV dysfunction and remodeling in dogs with moderate heart failure.Pathophysiology of the cardiac late Na current and its potential as a drug target.The arrhythmogenic consequences of increasing late INa in the cardiomyocyte.Late Na+ current produced by human cardiac Na+ channel isoform Nav1.5 is modulated by its beta1 subunit.
P2860
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P2860
Chronic heart failure slows late sodium current in human and canine ventricular myocytes: implications for repolarization variability.
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
2006年论文
@zh
2006年论文
@zh-cn
name
Chronic heart failure slows la ...... or repolarization variability.
@ast
Chronic heart failure slows la ...... or repolarization variability.
@en
type
label
Chronic heart failure slows la ...... or repolarization variability.
@ast
Chronic heart failure slows la ...... or repolarization variability.
@en
prefLabel
Chronic heart failure slows la ...... or repolarization variability.
@ast
Chronic heart failure slows la ...... or repolarization variability.
@en
P2093
P2860
P1476
Chronic heart failure slows la ...... for repolarization variability
@en
P2093
Albertas I Undrovinas
Hani N Sabbah
Norman Silverman
P2860
P304
P356
10.1016/J.EJHEART.2006.08.007
P577
2006-10-24T00:00:00Z