Laila Guzadhur

Falstaff House, Bardolph Road
Richmond, ENG, United Kingdom

Last Updated: 09/26/2026

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Found 11 publications

Response to: Depolarization vs. repolarization: what is the mechanism of ventricular arrhythmogenesis underlying sodium channel haploinsufficiency in mouse hearts?

Response to: Depolarization vs. repolarization: what is the mechanism of ventricular arrhythmogenesis underlying sodium channel haploinsufficiency in mouse hearts?

Journal: Acta physiologica (Oxford, England)

Published: June 09, 2016

The RyR2-P2328S mutation downregulates Nav1.5 producing arrhythmic substrate in murine ventricles.

The RyR2-P2328S mutation downregulates Nav1.5 producing arrhythmic substrate in murine ventricles.

Journal: Pflugers Archiv : European journal of physiology

Published: July 19, 2015

Sodium channel haploinsufficiency and structural change in ventricular arrhythmogenesis.

Sodium channel haploinsufficiency and structural change in ventricular arrhythmogenesis.

Journal: Acta physiologica (Oxford, England)

Published: May 13, 2015

Flecainide exerts paradoxical effects on sodium currents and atrial arrhythmia in murine RyR2-P2328S hearts.

Flecainide exerts paradoxical effects on sodium currents and atrial arrhythmia in murine RyR2-P2328S hearts.

Journal: Acta physiologica (Oxford, England)

Published: October 03, 2014

Arrhythmic substrate, slowed propagation and increased dispersion in conduction direction in the right ventricular outflow tract of murine Scn5a+/- hearts.

Arrhythmic substrate, slowed propagation and increased dispersion in conduction direction in the right ventricular outflow tract of murine Scn5a+/- hearts.

Journal: Acta physiologica (Oxford, England)

Published: August 23, 2013

Action potential wavelength restitution predicts alternans and arrhythmia in murine Scn5a(+/-) hearts.

Action potential wavelength restitution predicts alternans and arrhythmia in murine Scn5a(+/-) hearts.

Journal: The Journal of physiology

Published: July 10, 2013

Conduction slowing contributes to spontaneous ventricular arrhythmias in intrinsically active murine RyR2-P2328S hearts.

Conduction slowing contributes to spontaneous ventricular arrhythmias in intrinsically active murine RyR2-P2328S hearts.

Journal: Journal of cardiovascular electrophysiology

Published: November 08, 2012

The age-dependence of atrial arrhythmogenicity in Scn5a+/- murine hearts reflects alterations in action potential propagation and recovery.

The age-dependence of atrial arrhythmogenicity in Scn5a+/- murine hearts reflects alterations in action potential propagation and recovery.

Journal: Clinical and experimental pharmacology & physiology

Published: April 11, 2012

Nonlinearity between action potential alternans and restitution, which both predict ventricular arrhythmic properties in Scn5a+/- and wild-type murine hearts.

Nonlinearity between action potential alternans and restitution, which both predict ventricular arrhythmic properties in Scn5a+/- and wild-type murine hearts.

Journal: Journal of applied physiology (Bethesda, Md. : 1985)

Published: March 31, 2012

Reduced Na(+) and higher K(+) channel expression and function contribute to right ventricular origin of arrhythmias in Scn5a+/- mice.

Reduced Na(+) and higher K(+) channel expression and function contribute to right ventricular origin of arrhythmias in Scn5a+/- mice.

Journal: Open biology

Published: March 21, 2012

Frequency distribution analysis of activation times and regional fibrosis in murine Scn5a+/- hearts: the effects of ageing and sex.

Frequency distribution analysis of activation times and regional fibrosis in murine Scn5a+/- hearts: the effects of ageing and sex.

Journal: Mechanisms of ageing and development

Published: October 28, 2011

Showing 1-11 of 11

Last Updated: 09/26/2026