ArticleAmerican journal of physiology. Heart and circulatory physiology2009
Status epilepticus induces cardiac myofilament damage and increased susceptibility to arrhythmias in rats.
Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 44 citations in OpenAlex.
- Epilepsy-induced heart damage and sudep risk: ion channelopathies, calcium homeostasis, and the therapeutic potential of resveratrol.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Impact of Cardiac Injury on the Clinical Outcome of Children with Convulsive Status Epilepticus.Children (Basel, Switzerland) · 2022Article
- Intramuscular atenolol and levetiracetam reduce mortality in a rat model of paraoxon-induced status epilepticus.Annals of the New York Academy of Sciences · 2020Article
- Myocardial remodeling and susceptibility to ventricular tachycardia in a model of chronic epilepsy.Epilepsia open · 2018Article
- Early cardiac electrographic and molecular remodeling in a model of status epilepticus and acquired epilepsy.Epilepsia · 2016Article
- Seizure-Induced Sympathoexcitation Is Caused by Activation of Glutamatergic Receptors in RVLM That Also Causes Proarrhythmogenic Changes Mediated by PACAP and Microglia in Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Atenolol offers better protection than clonidine against cardiac injury in kainic acid-induced status epilepticus.British journal of pharmacology · 2015Article
- Inhibition of the prostaglandin receptor EP2 following status epilepticus reduces delayed mortality and brain inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Autonomic boundary conditions for ventricular fibrillation and their implications for a novel defibrillation technique.The journal of physiological sciences : JPS · 2012Article
- Non-linear classification of heart rate parameters as a biomarker for epileptogenesis.Epilepsy research · 2012Article
- Article
- Methods for ECG evaluation of indicators of cardiac risk, and susceptibility to aconitine-induced arrhythmias in rats following status epilepticus.Journal of visualized experiments : JoVE · 2011Article
- Autonomic and cellular mechanisms mediating detrimental cardiac effects of status epilepticus.Epilepsy research · 2010Article
- Article
- Seizures, Epilepsy, and SUDEP: A Change of Heart?Epilepsy currentsArticle
Corrections and comments
- Commented on by
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Status epilepticus (SE) is a seizure or series of seizures that persist for >30 min and often results in mortality. Death rarely occurs during or immediately following seizure activity, but usually within 30 days. Although ventricular arrhythmias have been implicated in SE-related mortality, the effects of this prolonged seizure activity on the cardiac function and susceptibility to arrhythmias have not been directly investigated. We evaluated myocardial damage, alterations in cardiac electrical activity, and susceptibility to experimentally induced arrhythmias produced by SE in rats. SE resulted in seizure-related increases in blood pressure, heart rate, and the first derivative of pressure, as well as modest, diffuse myocyte damage assessed by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling staining. Ten to twelve days following seizures, electrocardiographic recordings showed arrhythmogenic alterations in cardiac electrical activity, denoted by prolonged QT interval corrected for heart rate and QT dispersion. Finally, SE increased susceptibility to experimentally induced (intravenous aconitine) cardiac arrhythmias. These data suggest that SE produces tachycardic ischemia following the activation of the sympathetic nervous system, resulting in cardiac myofilament damage, arrhythmogenic alterations in cardiac electrical activity, and increased susceptibility to ventricular arrhythmias.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.