Article
Loss-of-Function KCNE2 Variants: True Monogenic Culprits of Long-QT Syndrome or Proarrhythmic Variants Requiring Secondary Provocation?
Circulation. Arrhythmia and electrophysiology - 1 Aug 2017
Roberts Jason D, Krahn Andrew D, Ackerman Michael J, Rohatgi Ram K, Moss Arthur J, Nazer Babak, Tadros Rafik, Gerull Brenda, Sanatani Shubhayan, Wijeyeratne Yanushi D, Baruteau Alban-Elouen, Muir Alison R, Pang Benjamin, Cadrin-Tourigny Julia, Talajic Mario, Rivard Lena, Tester David J, Liu Taylor, Whitman Isaac R, Wojciak Julianne, Conacher Susan, Gula Lorne J, Leong-Sit Peter, Manlucu Jaimie, Green Martin S, Hamilton Robert, Healey Jeff S, Lopes Coeli M, Behr Elijah R, Wilde Arthur A, Gollob Michael H, Scheinman Melvin M
Abstract excerpt
BACKGROUND: Insight into type 6 long-QT syndrome (LQT6), stemming from mutations in the KCNE2-encoded voltage-gated channel β-subunit, is limited. We sought to further characterize its clinical phenotype. METHODS AND RESULTS: Individuals with reported pathogenic KCNE2 mutations identified during arrhythmia evaluation were collected from inherited arrhythmia clinics and the Rochester long-QT syndrome (LQTS)...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.