Abstract
<jats:title>Abstract</jats:title> <jats:sec> <jats:title>BACKGROUND</jats:title> <jats:p>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.</jats:p> </jats:sec> <jats:sec> <jats:title>METHODS</jats:title> <jats:p>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.</jats:p> </jats:sec> <jats:sec> <jats:title>RESULTS</jats:title> <jats:p>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.</jats:p> </jats:sec> <jats:sec> <jats:title>CONCLUSIONS</jats:title> <jats:p>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.</jats:p> </jats:sec> <jats:sec> <jats:title>Abstract Figure</jats:title> <jats:fig id="ufig1" position="float" orientation="portrait" fig-type="figure"> <jats:graphic xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="26360016v1_ufig1" position="float" orientation="portrait"/> </jats:fig> </jats:sec> <jats:sec> <jats:title>Clinical Perspective</jats:title> <jats:sec> <jats:title>WHAT IS KNOWN?</jats:title> <jats:list list-type="bullet"> <jats:list-item> <jats:p>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.</jats:p> </jats:list-item> <jats:list-item> <jats:p>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.</jats:p> </jats:list-item> </jats:list> </jats:sec> <jats:sec> <jats:title>WHAT THE STUDY ADDS</jats:title> <jats:list list-type="bullet"> <jats:list-item> <jats:p>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.</jats:p> </jats:list-item> <jats:list-item> <jats:p>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.</jats:p> </jats:list-item> <jats:list-item> <jats:p>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.</jats:p> </jats:list-item> </jats:list> </jats:sec> </jats:sec>