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Tack-Ki Leung

Researcher at Montreal Heart Institute

Publications -  21
Citations -  1418

Tack-Ki Leung is an academic researcher from Montreal Heart Institute. The author has contributed to research in topics: Atrial fibrillation & Angioplasty. The author has an hindex of 11, co-authored 21 publications receiving 1358 citations. Previous affiliations of Tack-Ki Leung include Université de Montréal.

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Journal ArticleDOI

Evolution of the atrial fibrillation substrate in experimental congestive heart failure: angiotensin-dependent and -independent pathways.

TL;DR: AC inhibition prevented increases in tissue angiotensin II concentration, phosphorylated ERK expression, Bax/Bcl-2 ratio, and cellular apoptosis, but did not affect total cell death, leukocyte infiltration, JNK or p38 activation, and reduced butdid not eliminate tissue fibrosis.
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Differences in atrial versus ventricular remodeling in dogs with ventricular tachypacing-induced congestive heart failure

TL;DR: There are qualitative and quantitative differences in atrial versus ventricular remodeling in experimental ventricular tachypacing-induced CHF, with potentially important consequences for understanding underlying mechanisms and developing new therapeutic approaches.
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Dynamic nature of atrial fibrillation substrate during development and reversal of heart failure in dogs.

TL;DR: Reversal of CHF is followed by normalized atrial function and decreased duration of AF; however, fibrosis and conduction abnormalities are not reversible, and a substrate that can support prolonged AF remains.
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Effects of simvastatin on the development of the atrial fibrillation substrate in dogs with congestive heart failure

TL;DR: CHF-induced atrial structural remodeling and AF promotion are attenuated by simvastatin, but not fenofibrate, and Statin-induced inhibition of profibrotic atrial fibroblast responses and attenuation of left-ventricular dysfunction may contribute to preventing the CHF- induced fibrotic AF substrate.
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Ionic current abnormalities associated with prolonged action potentials in cardiomyocytes from diseased human right ventricles

TL;DR: I(K1, I(to1), and I(Ks) are down-regulated in AH cells of human heart failure, which contributes to APD prolongation that favors the occurrence of arrhythmogenic EADs and suggests a link between human cardiac histopathologic/functional abnormalities and arrh rhythmogenic ionic remodeling.