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Yung-Hsin Yeh

Researcher at Chang Gung University

Publications -  44
Citations -  2825

Yung-Hsin Yeh is an academic researcher from Chang Gung University. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 19, co-authored 27 publications receiving 2548 citations. Previous affiliations of Yung-Hsin Yeh include Université de Montréal & Montreal Heart Institute.

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Journal ArticleDOI

Arrhythmogenic Ion-Channel Remodeling in the Heart: Heart Failure, Myocardial Infarction, and Atrial Fibrillation

TL;DR: The changes in ion channel and transporter properties associated with three important clinical and experimental paradigms: congestive heart failure, myocardial infarction, and atrial fibrillation are reviewed and important opportunities for improved therapeutic approaches are highlighted.
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Calcium-Handling Abnormalities Underlying Atrial Arrhythmogenesis and Contractile Dysfunction in Dogs With Congestive Heart Failure

TL;DR: Congestive heart failure causes profound changes in Ca2-handling and -regulatory proteins that produce atrial fibrillation–promoting atrial cardiomyocyte Ca2+-handing abnormalities, arrhythmogenic triggered activity, and contractile dysfunction.
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Pulmonary vein region ablation in experimental vagal atrial fibrillation: role of pulmonary veins versus autonomic ganglia.

TL;DR: Intact PVs are not needed for maintenance of experimental cholinergic AF and ablation of the autonomic ganglia at the base of the PVs suppresses vagal responses and may contribute to the effectiveness of PV-directed ablation procedures in vagal AF.
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Changes in Connexin Expression and the Atrial Fibrillation Substrate in Congestive Heart Failure

TL;DR: CHF causes atrial connexin changes, but these are not essential for CHF-related conduction disturbances and AF promotion, which are rather related primarily to fibrotic interruption of muscle bundle continuity.
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Cellular signaling underlying atrial tachycardia remodeling of L-type calcium current

TL;DR: Rapid atrial cardiomyocyte activation causes Ca2+ loading, which activates the Ca2-dependent calmodulin–calcineurin–NFAT system to cause transcriptional downregulation of ICaL, restoring Ca 2+i to normal at the cost of APD reduction.