ReviewFrontiers in physiology2014
Remodeling of cardiac passive electrical properties and susceptibility to ventricular and atrial arrhythmias.
Review in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- CLARISA: Connexin-43 Lateralization Automated ROI-Based Image Signal Analyzer.International journal of molecular sciences · 2026Article
- Myocardial disarray drives metabolic inefficiency in human cardiomyocytes.Communications biology · 2025Article
- Computational modelling of the impact of anatomical changes on ECGs in left ventricular hypertrophy.The Journal of physiology · 2025Article
- Severe Aortic Stenosis and Pre-Excitation Syndrome in Pregnancy-A Multidisciplinary Approach.Diagnostics (Basel, Switzerland) · 2025Article
- Translation of pathophysiological mechanisms of atrial fibrosis into new diagnostic and therapeutic approaches.Nature reviews. Cardiology · 2025Review
- Atrial Fibrosis in Atrial Fibrillation: Mechanistic Insights, Diagnostic Challenges, and Emerging Therapeutic Targets.International journal of molecular sciences · 2024Review
- 'Trapped re-entry' as source of acute focal atrial arrhythmias.Cardiovascular research · 2024Article
- Hygrothermal stress increases malignant arrhythmias susceptibility by inhibiting the LKB1-AMPK-Cx43 pathway.Scientific reports · 2024Article
- A simple approach for image-based modelling of the heart that enables robust simulation of highly heterogeneous electrical excitation.Scientific reports · 2023Article
- Cardiac Roles of Serotonin (5-HT) and 5-HT-Receptors in Health and Disease.International journal of molecular sciences · 2023Review
- Effects of ivabradine on ventricular electrophysiological remodeling after myocardial infarction in rats.Archives of medical science : AMS · 2023Article
- Lipomatous Metaplasia Enables Ventricular Tachycardia by Reducing Current Loss Within the Protected Corridor.JACC. Clinical electrophysiology · 2022Article
- Intracellular Redistribution of Left Ventricular Connexin 43 Contributes to the Remodeling of Electrical Properties of the Heart in Insulin-resistant Elderly Rats.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2022Article
- Atrioventricular accessory pathway unmasked by heart valve replacement.Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc · 2022Article
- Mechanisms Underlying Antiarrhythmic Properties of Cardioprotective Agents Impacting Inflammation and Oxidative Stress.International journal of molecular sciences · 2022Review
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- Ganglionated Plexi Ablation Suppresses Chronic Obstructive Sleep Apnea-Related Atrial Fibrillation by Inhibiting Cardiac Autonomic Hyperactivation.Frontiers in physiology · 2021Article
- Melatonin to Rescue the Aged Heart: Antiarrhythmic and Antioxidant Benefits.Oxidative medicine and cellular longevity · 2021Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coordinated electrical activation of the heart is essential for the maintenance of a regular cardiac rhythm and effective contractions. Action potentials spread from one cell to the next via gap junction channels. Because of the elongated shape of cardiomyocytes, longitudinal resistivity is lower than transverse resistivity causing electrical anisotropy. Moreover, non-uniformity is created by clustering of gap junction channels at cell poles and by non-excitable structures such as collagenous strands, vessels or fibroblasts. Structural changes in cardiac disease often affect passive electrical properties by increasing non-uniformity and altering anisotropy. This disturbs normal electrical impulse propagation and is, consequently, a substrate for arrhythmia. However, to investigate how these structural changes lead to arrhythmias remains a challenge. One important mechanism, which may both cause and prevent arrhythmia, is the mismatch between current sources and sinks. Propagation of the electrical impulse requires a sufficient source of depolarizing current. In the case of a mismatch, the activated tissue (source) is not able to deliver enough depolarizing current to trigger an action potential in the non-activated tissue (sink). This eventually leads to conduction block. It has been suggested that in this situation a balanced geometrical distribution of gap junctions and reduced gap junction conductance may allow successful propagation. In contrast, source-sink mismatch can prevent spontaneous arrhythmogenic activity in a small number of cells from spreading over the ventricle, especially if gap junction conductance is enhanced. Beside gap junctions, cell geometry and non-cellular structures strongly modulate arrhythmogenic mechanisms. The present review elucidates these and other implications of passive electrical properties for cardiac rhythm and arrhythmogenesis.
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