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Turing instability mediated by voltage and calcium diffusion in paced cardiac cells
Yohannes Shiferaw1, Alain Karma
1UCLA Cardiovascular Research Laboratory, Department of Medicine (Cardiology), David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA. yshiferaw@mednet.ucla.edu
Summary
Calcium alternans within cardiac cells can become spatially out-of-phase due to a Turing-type instability. This phenomenon, mediated by voltage and calcium diffusion, links subcellular dynamics to cardiac disorders.
Area of Science:
- Cardiac Electrophysiology
- Computational Biology
- Biophysics
Background:
- Coupling between cell membrane voltage (V(m)) and calcium (Ca) release is vital for heart function.
- Period-doubling oscillations (alternans) in V(m) and Ca are linked to sudden cardiac death.
- While V(m) alternans are spatially synchronized, Ca alternans can be asynchronous within a cell.
Purpose of the Study:
- Investigate the conditions under which Ca alternans become spatially in-phase or out-of-phase within cardiac cells.
- Explore the mechanisms driving spatial asynchrony of Ca alternans on subcellular scales.
Main Methods:
- Utilized a spatially distributed computational model of calcium cycling coupled to V(m).
- Analyzed the interplay of V(m) and Ca diffusion dynamics.
- Identified Turing-type symmetry breaking instability as a key mechanism.
Main Results:
- Demonstrated a Turing-type instability mediated by V(m) and Ca diffusion.
- Showed that Ca alternans can spontaneously become out-of-phase at opposite ends of a cardiac cell.
- Pattern formation results from short-range Ca activation and long-range V(m)-mediated inhibition.
Conclusions:
- Cardiac Ca alternans can exhibit spontaneous spatial out-of-phase patterns due to a Turing instability.
- This instability is driven by the interaction between Ca cycling dynamics and V(m) alternans.
- Provides a potential link between subcellular dynamical instability and life-threatening cardiac disorders.