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A Microfluidic Technique to Probe Cell Deformability
Published on: September 3, 2014
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Percolation and tortuosity in heart-like cells.
R Rabinovitch1, Y Biton2, D Braunstein3
1Makif YudAlef, Rishon Lezion, Israel.
Scientific Reports
|June 2, 2021
Summary
This study models heart fibrosis using percolation theory, revealing wave propagation patterns similar to forest fires and Gaussian transport delays. Findings suggest ectopic sources are needed for arrhythmia, and refractory periods can prevent reentry.
Area of Science:
- Computational Biology
- Biophysics
- Cardiology
Background:
- Heart fibrosis (HF) is linked to cardiac arrhythmias like atrial tachycardia and fibrillation.
- Existing transport and percolation models lack application to action potential propagation in fibrotic heart tissue.
Purpose of the Study:
- To apply percolation and transport theories to understand action potential propagation in fibrotic heart tissue.
- To investigate the role of heart fibrosis in cardiac arrhythmia initiation.
Main Methods:
- A cellular automaton model was developed to simulate percolation and transport in a fibrotic heart-like tissue.
- The model analyzed the behavior of a single wave front and action potential delay.
Main Results:
- Wave front percolation in fibrotic tissue mirrors the forest fire model.
- Action potential transport, or delay, through fibrotic tissue exhibits Gaussian behavior on average.
- Near the percolation threshold, Gaussian parameters show critical behavior, contributing to general percolation theory.
Conclusions:
- Heart fibrosis dynamics can be effectively modeled using percolation theory.
- Arrhythmia generation in fibrotic hearts requires an ectopic source; normal sinus node operation does not induce it.
- Increased refractory periods may prevent reentry mechanisms in fibrotic cardiac tissue.
