Elevated ventricular repolarization lability is believed to be linked to the risk of ventricular tachycardia/ventricular fibrillation. However, ventricular repolarization is a complex electrical phenomenon, and abnormalities in ventricular repolarization are not completely understood. To evaluate repolarization lability, vectorcardiography (VCG) is an alternative approach where the electrocardiographic (ECG) signal can be considered as possessing both magnitude and direction. Recent research has shown that VCG is advantageous over ECG signal analysis for identification of repolarization abnormality. One of the key reasons is that the VCG approach does not rely on exact identification of the T-wave offset, which improves the reproducibility of the VCG technique. However, beat-to-beat variability in VCG is an emerging area for the investigation of repolarization abnormality though not yet fully realized. Therefore, the purpose of this review is to explore the techniques, findings, and efficacy of beat-to-beat VCG parameters for analyzing repolarization lability, which may have potential utility for further study.
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http://dx.doi.org/10.1515/bmt-2015-0005 | DOI Listing |
Heart Rhythm
January 2025
Office of Science and Engineering Laboratories, Center for Devices and Radiological Health, Food and Drug Administration, Silver Spring, MD, USA. Electronic address:
Background: Spontaneously occurring life threatening reentrant arrhythmias result when a propagating premature beat encounters a region with significant dispersion of refractoriness. Although localized structural tissue heterogeneities and prescribed cell functional gradients have been incorporated into computational electrophysiological models, a quantitative framework for the evolution from normal to abnormal behavior that occurs via disease is lacking.
Objective: The purpose of this study was to develop a probabilistic modeling framework that represents the complex interplay of cell function and tissue structure in health and disease which predicts the emergence of premature beats and the initiation of reentry.
Heart Rhythm
January 2025
Department of Molecular Biosciences, University of California, Davis, CA, USA; Department of Basic Sciences, California Northstate University, Elk Grove, CA. Electronic address:
Background: Friedreich's ataxia (FA) is a rare inherited neuromuscular disorder, where most patients die from lethal cardiomyopathy and arrhythmias. Mechanisms leading to arrhythmic events in FA patients are poorly understood.
Objective: This study aims to examine cardiac electrical signal propagation in mouse model of FA with severe cardiomyopathy and evaluate effects of omaveloxolone (OMAV), the first FDA-approved therapy.
Circ Res
December 2024
Department of Biology and Genetics, McAllister Heart Institute, University of North Carolina, Chapel Hill. (W.S., J.P.-L., W.G.W., W.F.M., F.L.C.).
Background: Males and females exhibit distinct anatomic and functional characteristics of the heart, predisposing them to specific disease states.
Methods: We identified microRNA (miRNAs/miR) with sex-differential expression in mouse hearts.
Results: Four conserved miRNAs are present in a single locus on the X-chromosome and are expressed at higher levels in females than males.
Biomolecules
December 2024
Department of Anatomy, Animal Physiology and Biophysics, Faculty of Biology, University of Bucharest, Splaiul Independentei 91-95, 050095 Bucharest, Romania.
Cenobamate is a novel third-generation antiepileptic drug used for the treatment of focal onset seizures and particularly for multi-drug-resistant epilepsy; it acts on multiple targets: GABA receptors (EC 42-194 µM) and persistent neuronal Na currents (IC 59 µM). Side effects include QT interval shortening with >20 ms, but not <300 ms. Our in vitro cardiac safety pharmacology study was performed via whole-cell patch-clamp on HEK293T cells with persistent/inducible expression of human cardiac ion channel isoforms hNav1.
View Article and Find Full Text PDFBackground: Long QT Syndrome Type-2 (LQT2) is due to loss-of-function variants. encodes K 11.1 that forms a delayed-rectifier potassium channel in the brain and heart.
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