ArticleEpilepsia open2018
Myocardial remodeling and susceptibility to ventricular tachycardia in a model of chronic epilepsy.
Article in Epilepsia open, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Neurocardiology: Brain-Heart Interactions in the Heart.MedComm · 2026Review
- The mechanism of sudden unexpected death in epilepsy: A mini review.Frontiers in neurology · 2023Review
- Epilepsy duration is an independent factor for electrocardiographic changes in pediatric epilepsy.Epilepsia open · 2021Article
- Cardiac dysregulation following intrahippocampal kainate-induced status epilepticus.Scientific reports · 2020Article
- Genetic ablation or pharmacological inhibition of Kv1.1 potassium channel subunits impairs atrial repolarization in mice.American journal of physiology. Cell physiology · 2019Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
objectiveSympathetic predominance and ventricular repolarization abnormalities represent epilepsy-associated cardiac alterations and may underlie seizure-induced ventricular arrhythmias. Myocardial ion channel and electrical remodeling have been described early in epilepsy development and may contribute to ventricular repolarization abnormalities and excitability. Using the pilocarpine-induced acquired epilepsy model we sought to examine whether altered myocardial ion channel levels and electrophysiological changes also occur in animals with long-standing epilepsy.
methodsWe examined myocardial adrenergic receptor and ion channel protein levels of epileptic and age-matched sham rats (9-20 months old) using western blotting. Cardiac electrical properties were examined using optical mapping ex vivo and electrophysiology in vivo. We investigated the propensity for ventricular tachycardia (VT) and the effects of β-adrenergic blockade on ventricular electrical properties and excitability in vivo.
resultsIn animals with long-standing epilepsy, we observed decreased myocardial voltage-gated K SIGNIFICANCE: Our findings demonstrate that myocardial ion channel remodeling and sympathetic predominance, risk factors for increased ventricular excitability and arrhythmias, persist in chronic epilepsy. The beneficial effects of β-adrenergic antagonist treatment late in the course of epilepsy suggest that attenuating elevated sympathetic tone may represent a therapeutic target for ameliorating epilepsy-associated cardiac morbidity.
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Registered trials
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