Open AccessMultiple Potential Molecular Contributors to Atrial Hypocontractility Caused by Atrial Tachycardia Remodeling in Dogs
Author(s) -
Reza Wakili,
YungHsin Yeh,
Xiao Yan Qi,
Maura Greiser,
Denis Chartier,
Kunihiro Nishida,
Ange Maguy,
Louis-Robert Villeneuve,
Peter Boknı́k,
Niels Voigt,
Judith Krysiak,
Stefan Kääb,
Ursula Ravens,
Wolfgang A. Linke,
Ger J.M. Stienen,
Yanfen Shi,
JeanClaude Tardif,
Ulrich Schotten,
Dobromir Dobrev,
Stanley Nattel
Publication year - 2010
Publication title -
circulation arrhythmia and electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.684
H-Index - 102
eISSN - 1941-3149
pISSN - 1941-3084
DOI - 10.1161/circep.109.933036
Subject(s) - contractility , medicine , myosin light chain kinase , endocrinology , protein kinase a , microbiology and biotechnology , chemistry , myosin , kinase , biology
Atrial fibrillation impairs atrial contractility, inducing atrial stunning that promotes thromboembolic stroke. Action potential (AP)-prolonging drugs are reported to normalize atrial hypocontractility caused by atrial tachycardia remodeling (ATR). Here, we addressed the role of AP duration (APD) changes in ATR-induced hypocontractility.
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