Lack of gelsolin promotes perpetuation of atrial fibrillation in the mouse heart.
OBJECTIVE
Gelsolin (gsn) is involved in the reorganization of the cytoskeleton, thereby modulating cardiomyocytal L-type Ca(2+) channels. We investigated global cardiac electrophysiological characteristics in a gsn-deficient (gsn(-/-)) mouse strain.


METHODS
Using transvenous catheterization, atrial and ventricular stimulation were performed in 15 male mice [eight gsn(-/-), seven wild-type (gsn(+/+))]. Surface ECG, standard electrophysiological parameters, and inducibility of atrial fibrillation (AF) were evaluated.


RESULTS
The surface ECG showed shorter PQ (37.8 +/- 4.6 versus 42.9 +/- 2.7 ms; P = 0.02), but longer QRS (16.5 +/- 1.8 versus 13.9 +/- 1.2 ms; P = 0.005) and QT intervals (38.5 +/- 2.2 versus 35.6 +/- 2.4 ms, P = 0.03) in gsn(-/-). Gsn(-/-) exhibited significantly higher susceptibility to induction of prolonged AF episodes > or =60 s [six of eight gsn(-/-) versus one of seven gsn(+/+); P = 0.04]. Sustained AF episodes > or =10 min were observed in 50% of the gsn-deficient animals.


CONCLUSIONS
Gsn deficiency results in perpetuation of inducible episodes of atrial fibrillation. Altered L-type Ca(2+) currents and disturbed Ca(2+) handling known to be associated to gsn deficiency likely contribute to this effect.
Schrickel
Jan Wilko
JW
Department of Medicine-Cardiology, University of Bonn, Sigmund Freud Strasse 25, 53105, Bonn, Germany. jan.schrickel@ukb.uni-bonn.de
Fink
Klaus
K
Meyer
Rainer
R
Grohé
Christian
C
Stoeckigt
Florian
F
Tiemann
Klaus
K
Ghanem
Alexander
A
Lickfett
Lars
L
Nickenig
Georg
G
Lewalter
Thorsten
T
D000200:Action Potentials; D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology*; D018780:Body Surface Potential Mapping; D018260:Gelsolin / Q000235:genetics / Q000378:metabolism*; D006329:Heart Conduction System / Q000503:physiopathology*; D006339:Heart Rate; D008297:Male; D051379:Mice; D018345:Mice, Knockout
D018260:Gelsolin