Electrical alternations in cardiac action potential duration have been shown to be a precursor to arrhythmias and sudden cardiac death. Through the mechanism of excitation-contraction coupling, the presence of electrical alternans induces alternations in the heart muscle contractile activity. Also, contraction of cardiac tissue affects the process of cardiac electric wave propagation through the mechanism of the so-called mechanoelectrical feedback. Electrical excitation and contraction of cardiac tissue can be linked by an electromechanical model such as the Nash-Panfilov model. In this work, we explore the feasibility of suppressing cardiac alternans in the Nash-Panfilov model which is employed for small and large deformations. Several electrical pacing and mechanical perturbation feedback strategies are considered to demonstrate successful suppression of alternans on a one-dimensional cable. This is the first attempt to combine electrophysiologically relevant cardiac models of electrical wave propagation and contractility of cardiac tissue in a synergistic effort to suppress cardiac alternans. Numerical examples are provided to illustrate the feasibility and the effects of the proposed algorithms to suppress cardiac alternans.
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http://dx.doi.org/10.1016/j.compbiomed.2015.05.011 | DOI Listing |
Physiol Rep
December 2024
Institute of Advanced Biomedical Engineering and Science, TWIns, Tokyo Women's Medical University, Shinjuku-ku, Tokyo, Japan.
Cardiac alternans (C-ALT) is a phenomenon of alternating strong and weak contractions in the heart and is considered a risk factor for the development of heart failure and arrhythmias. However, no model has been reported that can induce C-ALT in vitro using human cells, and the developmental mechanism of C-ALT has not been studied using human cells. In this study, we successfully induced C-ALT in vitro using human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs).
View Article and Find Full Text PDFBackground: Loss of stromal interaction molecule 1 (STIM1) expression in smooth muscle cells protects against ischemia-reperfusion (I/R) injury. Whether and how decreased STIM1 expression in cardiomyocytes (CM) impacts cardiac remodeling in response to I/R injury remains unknown.
Objective: To examine mechanisms by which decreased CM-STIM1 expression in the adult heart modulates cardiac function before and after I/R injury.
J Mol Cell Cardiol Plus
December 2024
Key Laboratory of Medical Electrophysiology of the Ministry of Education, Medical Electrophysiological Key Laboratory of Sichuan Province, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, Sichuan 646000, China.
Unlabelled: Abnormal regional variations in electrical and calcium homeostasis properties have been implicated in catecholaminergic polymorphic ventricular tachycardias (CPVT) attributable to abnormal RyR2-mediated store Ca release, but their underlying mechanism have not been well explored in intact hearts.
Methods: We performed in vivo and ex vivo studies including high throughput mapping of Ca transients (CaT) and transmembrane voltage (V) in murine wild-type (WT) and heterozygous -R2474S/+ hearts, before and during isoprenaline (ISO) challenge.
Results: ISO-challenged -R2474S/+ showed increased incidence of arrhythmia accompanied by abnormal Ca transients compared to WT.
bioRxiv
November 2024
Department of Physics and Astronomy, California State University, Northridge.
Curr Issues Mol Biol
November 2024
School of Systems Biology, George Mason University, Fairfax, VA 22030, USA.
Mutations in the ryanodine receptor (RyR2) gene have been linked to arrhythmia and possibly sudden cardiac death (SCD) during acute emotional stress, physical activities, or catecholamine perfusion. The most prevalent disorder is catecholaminergic polymorphic ventricular tachycardia (CPVT1). Four primary mechanisms have been proposed to describe CPVT1 with a RyR2 mutation: (a) gain-of-function, (b) destabilization of binding proteins, (c) store-overload-induced Ca release (SOICR), and (d) loss of function.
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