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Pulsed low-energy stimulation initiates electric turbulence in cardiac tissue
- Source :
- PLoS Computational Biology, PLoS Computational Biology, Vol 17, Iss 10, p e1009476 (2021)
- Publication Year :
- 2021
- Publisher :
- Public Library of Science, 2021.
-
Abstract
- Interruptions in nonlinear wave propagation, commonly referred to as wave breaks, are typical of many complex excitable systems. In the heart they lead to lethal rhythm disorders, the so-called arrhythmias, which are one of the main causes of sudden death in the industrialized world. Progress in the treatment and therapy of cardiac arrhythmias requires a detailed understanding of the triggers and dynamics of these wave breaks. In particular, two very important questions are: 1) What determines the potential of a wave break to initiate re-entry? and 2) How do these breaks evolve such that the system is able to maintain spatiotemporally chaotic electrical activity? Here we approach these questions numerically using optogenetics in an in silico model of human atrial tissue that has undergone chronic atrial fibrillation (cAF) remodelling. In the lesser studied sub-threshold illumination régime, we discover a new mechanism of wave break initiation in cardiac tissue that occurs for gentle slopes of the restitution characteristics. This mechanism involves the creation of conduction blocks through a combination of wavefront-waveback interaction, reshaping of the wave profile and heterogeneous recovery from the excitation of the spatially extended medium, leading to the creation of re-excitable windows for sustained re-entry. This finding is an important contribution to cardiac arrhythmia research as it identifies scenarios in which low-energy perturbations to cardiac rhythm can be potentially life-threatening.<br />Author summary Electric turbulence in the heart is associated with complex spatiotemporal dynamics of nonlinear excitation waves. This life-threatening state is initiated by wavebreaks and maintained by self-organized vortices of abnormal excitation. Control over this state is achieved via defibrillation, a method whose efficacy relies on understanding the role of electric vortices in the onset and perpetuation of the turbulent state. However, in biological tissue, these vortices remain largely elusive in experiments due to limitations of visualisation. In order to study the spatiotemporal evolution of vortices in the heart precisely, reversibly and in real-time, we apply computational cardiac optogenetics on a mathematical model for human atrial tissue. Our study demonstrates a heretofore unidentified mechanism of wavebreak initiation, in the absence of standard markers of excitable medium vulnerability. This finding is an important contribution to cardiac arrhythmia research as it identifies how low-energy perturbations to cardiac rhythm can be potentially life-threatening, and render a defibrillation strategy to backfire.
- Subjects :
- Light
Physiology
Cell Membranes
Stimulation
030204 cardiovascular system & hematology
0302 clinical medicine
Low energy
Atrial Fibrillation
Medicine and Health Sciences
Chronic atrial fibrillation
Biology (General)
Physics
Light Pulses
0303 health sciences
Brain Mapping
Ecology
Turbulence
Electromagnetic Radiation
Models, Cardiovascular
Classical Mechanics
Heart
Electrophysiology
Bioassays and Physiological Analysis
Computational Theory and Mathematics
Modeling and Simulation
Physical Sciences
cardiovascular system
Cellular Structures and Organelles
Anatomy
Research Article
Wave propagation
QH301-705.5
Surgical and Invasive Medical Procedures
Fluid Mechanics
Optogenetics
Research and Analysis Methods
Sudden death
Membrane Potential
Continuum Mechanics
03 medical and health sciences
Cellular and Molecular Neuroscience
Heart Conduction System
Genetics
Humans
Heart Atria
Molecular Biology
Ecology, Evolution, Behavior and Systematics
030304 developmental biology
Functional Electrical Stimulation
Cardiac arrhythmia
Biology and Life Sciences
Computational Biology
Fluid Dynamics
Neurophysiological Analysis
Cell Biology
Electric Stimulation
Cardiovascular Anatomy
Neuroscience
Subjects
Details
- Language :
- English
- ISSN :
- 15537358 and 1553734X
- Volume :
- 17
- Issue :
- 10
- Database :
- OpenAIRE
- Journal :
- PLoS Computational Biology
- Accession number :
- edsair.doi.dedup.....10bde7b9248fb5e68c050c8bdb75502a