ArticleJournal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing2009
Lack of gelsolin promotes perpetuation of atrial fibrillation in the mouse heart.
Article in Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 10 citations in OpenAlex.
- Sex-specific response to A1BG loss results in female dilated cardiomyopathy.Biology of sex differences · 2025Article
- Allele-specific expression in the human heart and its application to postoperative atrial fibrillation and myocardial ischemia.Genome medicine · 2016Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeGelsolin (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.
methodsUsing 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.
resultsThe 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.
conclusionsGsn 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.
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