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Circulating KCNH2 current-activating factor in patients with heart failure and ventricular tachyarrhythmia.

Hiroki Sugiyama | Kazufumi Nakamura | Hiroshi Morita | Satoshi Akagi | Yoshinori Tani | Yusuke Katayama | Nobuhiro Nishii | Toru Miyoshi | Satoshi Nagase | Kunihisa Kohno | Kengo Fukushima Kusano | Tohru Ohe | Junko Kurokawa | Tetsushi Furukawa | Hiroshi Ito
PloS one | 2011

It is estimated that approximately half of the deaths in patients with HF are sudden and that the most likely causes of sudden death are lethal ventricular tachyarrhythmias such as ventricular tachycardia (VT) or fibrillation (VF). However, the precise mechanism of ventricular tachyarrhythmias remains unknown. The KCNH2 channel conducting the delayed rectifier K(+) current (I(Kr)) is recognized as the most susceptible channel in acquired long QT syndrome. Recent findings have revealed that not only suppression but also enhancement of I(Kr) increase vulnerability to major arrhythmic events, as seen in short QT syndrome. Therefore, we investigated the existence of a circulating KCNH2 current-modifying factor in patients with HF.

Pubmed ID: 21625547

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RRID:CVCL_0045

Cell line HEK293 is a Transformed cell line with a species of origin Homo sapiens (Human)

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