ArticleJournal of cardiovascular translational research2014
Atrial tachyarrhythmias induced by the combined effects of β1/2-adrenergic autoantibodies and thyroid hormone in the rabbit.
Article in Journal of cardiovascular translational research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed, 11 citations in OpenAlex.
- Autoantibodies in Atrial Fibrillation-State of the Art.International journal of molecular sciences · 2023Review
- Review
- Elevated β1-Adrenergic Receptor Autoantibody Levels Increase Atrial Fibrillation Susceptibility by Promoting Atrial Fibrosis.Frontiers in physiology · 2020Article
- Adrenergic Autoantibody-Induced Postural Tachycardia Syndrome in Rabbits.Journal of the American Heart Association · 2019Article
- A peptidomimetic inhibitor suppresses the inducibility of β1-adrenergic autoantibody-mediated cardiac arrhythmias in the rabbit.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2015Article
- Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Activating autoantibodies (AAb) to β-adrenergic receptors (βAR) are associated with atrial fibrillation in patients with Graves' disease. In the present study, we examined the interaction of thyroid hormone with β1/2AR-AAb in inducing atrial tachyarrhythmias in the rabbit. Immunization of rabbits with a β1AR or β2AR second extracellular loop peptide produced high titers of β1AR-AAb or β2AR-AAb. Thyroid hormone in combination with β1AR-AAb or β2AR-AAb induced a significant number of sustained sinus tachycardia and atrial tachycardia, respectively. Both combinations resulted in significantly increased inductions of sustained arrhythmias compared to AAb alone. Thyroid hormone alone induced sustained sinus and junctional tachycardia. Sera from immunized rabbits specifically bound to and activated β1AR or β2AR in transfected cells in vitro. This study demonstrates thyroid hormone qualitatively accentuates the specific arrhythmogenic action of these AAb and quantitatively enhances their rate. Our data support a dual role of AAb and thyroid hormone in Graves'-associated tachyarrhythmias.
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Registered trials
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