Article
In vivo effect of a dominant negative Kv4.2 loss-of-function mutation eliminating I(to,f) on atrial refractoriness and atrial fibrillation in mice.
Circulation journal : official journal of the Japanese Circulation Society - 1 Mar 2009
Odening Katja E, Nerbonne Jeanne M, Bode Christoph, Zehender Manfred, Brunner Michael
Abstract excerpt
BACKGROUND: Gain-of-function K(+) channel mutations cause familial atrial fibrillation (AF) by shortening of the atrial action potential duration (APD). APD-prolonging K(+) channel blockers are an effective therapeutic option in AF. In vitro, the dominant negative Kv4.2W362F mutation (Kv4DN) eliminates I(to,f) in murine atrial myocytes and markedly prolongs the APD, so whether this loss-of-function of I(to,f)...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.