What is the clinical evidence from this study?

Study design: Other. Population: Wolff-Parkinson-White (WPW) syndrome. Intervention: Mutant PRKAG2 gene (Arg302Gln) expression vs. Wild-type PRKAG2 gene expression (TG(WT)). Primary outcome: PR interval (ms) (p=<0.05).

December 21, 2004CirculationOpen Access

Transgenic Mouse Model of Ventricular Preexcitation and Atrioventricular Reentrant Tachycardia Induced by an AMP-Activated Protein Kinase Loss-of-Function Mutation Responsible for Wolff-Parkinson-White Syndrome

Q: What are the key findings of this study?

Transgenic mice expressing the mutant PRKAG2 gene exhibited ventricular preexcitation with a shortened PR interval (10 vs 33 ms, P<0.05) and prolonged QRS (20 vs 10 ms, P<0.05) compared to wild-type.

View Full Paper

Ask AI

Bookmark

Key result

Transgenic mice expressing the mutant PRKAG2 gene exhibited ventricular preexcitation with a shortened PR interval (10 vs 33 ms, P<0.05) and prolonged QRS (20 vs 10 ms, P<0.05) compared to wild-type.

Population

Transgenic mice generated by cardiac-restricted expression of the wild-type (TG) and mutant (TG) PRKAG2 gene…

Comparison

Expression of mutant PRKAG2 gene responsible for… vs Expression of wild-type PRKAG2 gene (TG) and…

Design

Preclinical

Authors

JSJasvinder SidhuElectrophysiology YRYadavendra S. RajawatBaylor College of Medicine TRTapan G. RamiHouston Methodist

Discussion

Member takes

Implication

Establishes a PRKAG2-mutant WPW mouse model; leaves open AMPK-targeted therapy translation to humans.

Structured PICO

Population

Transgenic mice expressing wild-type or mutant (Arg302Gln) PRKAG2 gene to model familial Wolff-Parkinson-White syndrome.

Intervention

Expression of mutant PRKAG2 gene (Arg302Gln) responsible for familial Wolff-Parkinson-White (WPW) syndrome (TG(R302Q))

Comparator

Expression of wild-type PRKAG2 gene (TG(WT)) and nontransgenic mice

Outcome

Electrophysiological phenotype (ventricular preexcitation, QRS duration, AV accessory pathway), AMPK enzymatic activity, and cardiac hypertrophysurrogate

Main Result

Absolute Event Rate: 10% vs 33%

p-value: p=<0.05

A transgenic mouse model expressing the PRKAG2 Arg302Gln mutation successfully replicates the human Wolff-Parkinson-White syndrome phenotype, demonstrating that the defect is driven by AMPK loss of function.

Cite This Study

Sidhu et al. (2004) studied Wolff-Parkinson-White (WPW) syndrome. Mutant PRKAG2 gene (Arg302Gln) expression vs. Wild-type PRKAG2 gene expression (TG(WT)) was evaluated on PR interval (ms) (p=<0.05). Transgenic mice expressing the mutant PRKAG2 gene exhibited ventricular preexcitation with a shortened PR interval (10 vs 33 ms, P<0.05) and prolonged QRS (20 vs 10 ms, P<0.05) compared to wild-type.

synapsesocial.com/papers/6a97debbb58c727d448bf9c8 https://doi.org/10.1161/01.cir.0000151291.32974.d5

View Full Paper

Ask AI

Bookmark

Transgenic Mouse Model of Ventricular Preexcitation and Atrioventricular Reentrant Tachycardia Induced by an AMP-Activated Protein Kinase Loss-of-Function Mutation Responsible for Wolff-Parkinson-White Syndrome

Discussion

Member takes

Implication

Structured PICO

Main Result

Cite This Study

Transgenic Mouse Model of Ventricular Preexcitation and Atrioventricular Reentrant Tachycardia Induced by an AMP-Activated Protein Kinase Loss-of-Function Mutation Responsible for Wolff-Parkinson-White Syndrome

Discussion

Member takes

Implication

Structured PICO

Main Result

Cite This Study

Also Consider

Also Consider