ArticleJACC. Clinical electrophysiology2016
Enhancement of Gap Junction Function During Acute Myocardial Infarction Modifies Healing and Reduces Late Ventricular Arrhythmia Susceptibility.
Article in JACC. Clinical electrophysiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- Gap junctional and ephaptic coupling in cardiac electrical propagation: homocellular and heterocellular perspectives.The Journal of physiology · 2026Review
- Protective effect of ursodeoxycholic acid upon the post-myocardial infarction heart.Cardiovascular research · 2025Article
- The Role of Infarct Border Zone Remodelling in Ventricular Arrhythmias: Bridging Basic Research and Clinical Applications.Journal of cellular and molecular medicine · 2025Review
- Acute ischaemia and gap junction modulation modify propagation patterns across Purkinje-myocardial junctions.Frontiers in physiology · 2025Article
- Identification of Cx43 variants predisposing to ventricular fibrillation in the acute phase of ST-elevation myocardial infarction.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2023Article
- Uncovering potential diagnostic biomarkers of acute myocardial infarction based on machine learning and analyzing its relationship with immune cells.BMC cardiovascular disorders · 2023Article
- Serine-threonine protein phosphatase regulation of Cx43 dephosphorylation in arrhythmogenic disorders.Cellular signalling · 2021Review
- Rotigaptide Infusion for the First 7 Days After Myocardial Infarction-Reperfusion Reduced Late Complexity of Myocardial Architecture of the Healing Border-Zone and Arrhythmia Inducibility.Journal of the American Heart Association · 2021Article
- Ventricular fibrillation mechanism and global fibrillatory organization are determined by gap junction coupling and fibrosis pattern.Cardiovascular research · 2021Article
- Multiplexing physical stimulation on single human induced pluripotent stem cell-derived cardiomyocytes for phenotype modulation.Biofabrication · 2021Article
- Cross-Priming Dendritic Cells Exacerbate Immunopathology After Ischemic Tissue Damage in the Heart.Circulation · 2021Article
- Fibroblast Growth Factor 21 Ameliorates NaFrontiers in pharmacology · 2021Article
- Classification of Fibrillation Organisation Using Electrocardiograms to Guide Mechanism-Directed Treatments.Frontiers in physiology · 2021Article
- Prolonged ursodeoxycholic acid administration reduces acute ischaemia-induced arrhythmias in adult rat hearts.Scientific reports · 2020Article
- Granger Causality-Based Analysis for Classification of Fibrillation Mechanisms and Localization of Rotational Drivers.Circulation. Arrhythmia and electrophysiology · 2020Article
- Standardised Framework for Quantitative Analysis of Fibrillation Dynamics.Scientific reports · 2019Article
- Danqi soft capsule prevents infarct border zone remodelling and reduces susceptibility to ventricular arrhythmias in post-myocardial infarction rats.Journal of cellular and molecular medicine · 2019Article
- Article
- Interventricular Differences in Action Potential Duration Restitution Contribute to Dissimilar Ventricular Rhythms inFrontiers in cardiovascular medicine · 2019Article
- Therapeutic strategies targeting connexins.Nature reviews. Drug discovery · 2018Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
objectivesThe purpose of this study was to investigate the effects of enhancing gap junction (GJ) coupling during acute myocardial infarction (MI) on the healed infarct scar morphology and late post-MI arrhythmia susceptibility.
backgroundIncreased heterogeneity of myocardial scarring after MI is associated with greater arrhythmia susceptibility. We hypothesized that short-term enhancement of GJ coupling during acute MI can produce more homogeneous infarct scars, reducing late susceptibility to post-MI arrhythmias.
methodsFollowing arrhythmic characterization of a rat 4-week post-MI model (n = 24), another 27 Sprague-Dawley rats were randomized to receive rotigaptide to enhance GJ coupling (n = 13) or to saline control (n = 14) by osmotic minipump immediately prior to and for the first 7 days following surgically induced MI. At 4 weeks post-MI, hearts were explanted for ex vivo programmed electrical stimulation (PES) and optical mapping. Heterogeneity of infarct border zone (IBZ) scarring was quantified by histomorphometry.
resultsDespite no detectable differences in infarct size at 4 weeks post-MI, rotigaptide-treated hearts had reduced arrhythmia susceptibility during PES (inducibility score for rotigaptide: 2.4 ± 0.8; for control: 5.0 ± 0.6; p = 0.02) and less heterogeneous IBZ scarring (dispersion of IBZ complexity score: rotigaptide: 1.1 ± 0.1; control: 1.4 ± 0.1; p = 0.04), associated with an improvement in IBZ conduction velocity (rotigaptide: 43.1 ± 3.4 cm/s; control: 34.8 ± 2.0 cm/s; p = 0.04).
conclusionsEnhancement of GJ coupling for only 7 days at the time of acute MI produced more homogeneous IBZ scarring and reduced arrhythmia susceptibility at 4 weeks post-MI. Short-term GJ modulation at the time of MI may represent a novel treatment strategy to modify the healed infarct scar morphology and reduce late post-MI arrhythmic risk.
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