Computational Evaluation of a Turbulence-like Electrical Activity Hypothesis in Atrial Fibrillation: Substrate Remodeling, Critical Wavelength Transition, and Multi-wavelet Maintenance
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BACKGROUND
Atrial fibrillation (AF) remains difficult to explain using a single focal-driver or rotor-centered mechanism across disease stages. We tested whether progressive atrial substrate remodeling can drive a critical transition toward turbulence-like, decentralized multi-wavelet electrical activity.
METHODS
We constructed a controlled two-dimensional atrial reaction-diffusion model with six graded substrate-remodeling stages. We evaluated effective wavelength, theoretical wavelet capacity, AF inducibility, vulnerable-window dynamics, spatial randomness, temporal memory, spectral dispersion, nonlinear indices, virtual ablation response and ERP-prolongation reverse mechanistic testing.
RESULTS
Progressive remodeling shortened effective wavelength from 12.0 to 2.4 cm and increased theoretical wavelet capacity from 0.69 to 17.36. Inducibility rose sigmoidally as wavelength shortened, with a model-derived transition near lambda50=4.5 cm. Advanced substrates showed increased wavebreak, spatial randomness, short-memory dynamics, broad spectral dispersion, positive nonlinear indices and resistance to random local ablation. Culprit atrial premature beats within the vulnerable window efficiently triggered AF, whereas counter-pacing at 20 to 35 ms reduced inducibility from 52% to 11% in stage 2.
CONCLUSIONS
In this controlled model, AF initiation and maintenance were linked to substrate-dependent wavelength, wavelet capacity and vulnerable-window triggering. The model-derived transition provides a testable framework for future high-density mapping, patient-specific modeling and device-based studies.
Clinical Perspective
WHAT IS KNOWN?
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Pulmonary-vein ectopy, acute autonomic or metabolic triggers and other perturbation sources can initiate paroxysmal or self-limited AF, particularly when they fall into a transient physiological atrial vulnerable window.
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Substrate remodeling with refractory-period shortening, slow conduction and fibrosis is recognized as a key determinant of AF maintenance, but a quantitative wavelength threshold separating trigger-dependent AF from self-maintaining turbulence-like AF has not been established.
WHAT THE STUDY ADDS
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In this controlled two-dimensional model, the inducibility analysis provides a quantitative estimate of an effective transition near 4.5 cm, offering a measurable framework for examining AF maintenance beyond focal-driver or rotor-centered explanations.
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The model links perturbation-source strength, physiological vulnerable-window timing and substrate capacity into a single framework, explaining how apparently physiological AF initiation can become pathological sustained AF when wavelength shortens and wavelet capacity increases.
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A virtual counter-pacing experiment shows that time-locked stimulation after a culprit atrial premature beat can pre-empt local excitability, close the vulnerable window and reduce AF inducibility, suggesting a testable trigger-interception strategy.
