Familial atrial fibrillation: simulation of the mechanisms and effects of a slow rectifier potassium channel mutation in human atrial tissue

2005 ◽  
Author(s):  
G. Seemann ◽  
D.L. Weib ◽  
F.B. Sachse ◽  
O. Dossel
Keyword(s):  
Atrial Fibrillation ◽  
Potassium Channel ◽  
Atrial Tissue ◽  
Familial Atrial Fibrillation ◽  
Channel Mutation ◽  
Rectifier Potassium Channel

scholarly journals Mutations in the potassium channel subunit KCNE1 are associated with early-onset familial atrial fibrillation

2012 ◽  
Vol 13 (1) ◽  
Author(s):  
Morten S Olesen ◽  
Bo H Bentzen ◽  
Jonas B Nielsen ◽  
Annette B Steffensen ◽  
Jens-Peter David ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Potassium Channel ◽  
Early Onset ◽  
Familial Atrial Fibrillation

scholarly journals MinkS38G Gene Polymorphism and Atrial Fibrillation in the Chinese Population: A Meta-Analysis of 1871 Participants

2014 ◽  
Vol 2014 ◽  
pp. 1-6
Author(s):  
Yan-yan Li ◽  
Lian-sheng Wang ◽  
Xin-zheng Lu
Keyword(s):  
Atrial Fibrillation ◽  
Gene Polymorphism ◽  
Potassium Channel ◽  
Chinese Population ◽  
Meta Analysis ◽  
Delayed Rectifier ◽  
Channel Current ◽  
Delayed Rectifier Potassium Channel ◽  
The Individual ◽  
Rectifier Potassium Channel

Minkgene S38G polymorphism in theβ-subunit of slow activating component of the delayed rectifier potassium channel current potassium channel has been associated with increased atrial fibrillation (AF) risk. However, the individual studies results were still controversial. To investigate the association ofMinkS38G gene polymorphisms with AF, a meta-analysis including 1871 subjects from six individual studies was conducted.MinkS38G gene polymorphism was significantly related to AF under allelic (OR: 1.380, 95% CI: 1.200–1.600,P<0.00001), recessive (OR: 1.193, 95% CI: 1.033–1.377,P=0.017), dominant (OR: 1.057, 95% CI: 1.025–1.089,P<0.00001), additive (OR: 1.105, 95% CI: 1.036–1.178,P=0.002), homozygous (OR: 1.128, 95% CI: 1.068–1.191,P<0.00001), and heterozygous genetic models (OR: 1.078, 95% CI: 1.014–1.146,P=0.016). A significant association betweenMinkS38G gene polymorphism and AF risk was found. G allele carriers may predispose to AF.

scholarly journals Adrenergic regulation of a key cardiac potassium channel can contribute to atrial fibrillation: evidence from an IKstransgenic mouse

2008 ◽  
Vol 586 (2) ◽  
pp. 627-637 ◽  
Author(s):  
Kevin J. Sampson ◽  
Cecile Terrenoire ◽  
Daniel O. Cervantes ◽  
Riyaz A. Kaba ◽  
Nicholas S. Peters ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Potassium Channel ◽  
Adrenergic Regulation

scholarly journals TASK-1 current is inhibited by phosphorylation during human and canine chronic atrial fibrillation

2015 ◽  
Vol 308 (2) ◽  
pp. H126-H134 ◽  
Author(s):  
Erin Harleton ◽  
Alessandra Besana ◽  
Parag Chandra ◽  
Peter Danilo ◽  
Tove S. Rosen ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Normal Sinus Rhythm ◽  
Human Subjects ◽  
Phosphorylation Site ◽  
Chronic Atrial Fibrillation ◽  
Resting Membrane Potential ◽  
Atrial Remodeling ◽  
Protein Levels ◽  
Atrial Tissue ◽  
Normal Sinus

Atrial fibrillation (AF) is a common arrhythmia with significant morbidities and only partially adequate therapeutic options. AF is associated with atrial remodeling processes, including changes in the expression and function of ion channels and signaling pathways. TWIK protein-related acid-sensitive K+ channel (TASK)-1, a two-pore domain K+ channel, has been shown to contribute to action potential repolarization as well as to the maintenance of resting membrane potential in isolated myocytes, and TASK-1 inhibition has been associated with the induction of perioperative AF. However, the role of TASK-1 in chronic AF is unknown. The present study investigated the function, expression, and phosphorylation of TASK-1 in chronic AF in atrial tissue from chronically paced canines and in human subjects. TASK-1 current was present in atrial myocytes isolated from human and canine hearts in normal sinus rhythm but was absent in myocytes from humans with AF and in canines after the induction of AF by chronic tachypacing. The addition of phosphatase to the patch pipette rescued TASK-1 current from myocytes isolated from AF hearts, indicating that the change in current is phosphorylation dependent. Western blot analysis showed that total TASK-1 protein levels either did not change or increased slightly in AF, despite the absence of current. In studies of perioperative AF, we have shown that phosphorylation of TASK-1 at Thr383 inhibits the channel. However, phosphorylation at this site was unchanged in atrial tissue from humans with AF or in canines with chronic pacing-induced AF. We conclude that phosphorylation-dependent inhibition of TASK-1 is associated with AF, but the phosphorylation site responsible for this inhibition remains to be identified.

Familial atrial rapid fibrillation associated with double mutations of SCN5A and KCNQ1

2021 ◽  
pp. 1-3
Author(s):  
Miwa Kanai ◽  
Keiko Toyohara ◽  
Morio Shoda
Keyword(s):  
Atrial Fibrillation ◽  
Paediatric Population ◽  
Familial Case ◽  
Familial Atrial Fibrillation

Abstract Familial atrial fibrillation is inherited and sporadically occurs in the paediatric population. Generally, fibrillated wavelets are reported at a frequency of approximately 6 Hz. Herein, we report a familial case presenting rapidly fibrillated wavelets at frequencies of approximately 12 to 30 Hz associated with KCNQ1 and SCN5A mutations.

scholarly journals Anti-Arrhythmic Action of an ATP-Sensitive Potassium Channel Blocker Against Atrial Fibrillation Associated with Beta-Adrenergic Stress in Rat Hearts

2011 ◽  
Vol 100 (3) ◽  
pp. 197a
Author(s):  
Andrew F. James ◽  
Shang Jin Kim ◽  
Haifei Zhang ◽  
Stephanie C. Choisy ◽  
Hua Lin ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Potassium Channel ◽  
Channel Blocker ◽  
Beta Adrenergic ◽  
Potassium Channel Blocker ◽  
Rat Hearts
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