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|Title:||Absence of calcium channel α1C-subunit mutation in human atrial fibrillation||Authors:||Soon, J.-L.
|Issue Date:||Aug-2010||Citation:||Soon, J.-L., Ping, L., Chua, Y.-L., Soong, T.-W., Yoong-Kong, K.S. (2010-08). Absence of calcium channel α1C-subunit mutation in human atrial fibrillation. Asian Cardiovascular and Thoracic Annals 18 (4) : 349-353. ScholarBank@NUS Repository. https://doi.org/10.1177/0218492310375749||Abstract:||L-type voltage-gated calcium channel mutation or phenotypical variation resulting from alternative splicing has been associated with sudden arrhythmogenic death and heart failure. Changes in calcium current density, protein and mRNA expression have been associated with atrial fibrillation. We studied human atrium harvested from 16 cardiac surgery patients (coronary bypass and/or valve procedures) for mutation of Cav1.2 α1C (the main pore-forming subunit of L-type voltage-gated calcium channel) for an association with atrial fibrillation. Seven patients had persistent atrial fibrillation and one was resuscitated from ventricular arrhythmia. Clinical data were collected and prospectively updated for the development of arrhythmia. Four (25%) patients had new-onset postoperative paroxysmal atrial fibrillation. DNA from all atrial specimens was amplified, extracted, and sequenced. The α1C- subunit mutation was absent in all specimens obtained from all patients, regardless of heart rhythm. This suggests that atrial fibrillation is not associated with loss-of-function mutation of the main poreforming subunit of the L-type voltage-gated calcium channel. © 2010 SAGE Publications.||Source Title:||Asian Cardiovascular and Thoracic Annals||URI:||http://scholarbank.nus.edu.sg/handle/10635/109152||ISSN:||02184923||DOI:||10.1177/0218492310375749|
|Appears in Collections:||Staff Publications|
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