Computational Evaluation of a Turbulence-like Electrical Activity Hypothesis in Atrial Fibrillation: Substrate Remodeling, Critical Wavelength Transition, and Multi-wavelet Maintenance

BACKGROUNDAtrial 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. METHODSWe 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. RESULTSProgressive 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. CONCLUSIONSIn 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. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=87 SRC="FIGDIR/small/26360016v1_ufig1.gif" ALT="Figure 1"> View larger version (38K): org.highwire.dtl.DTLVardef@1f489d9org.highwire.dtl.DTLVardef@18637ccorg.highwire.dtl.DTLVardef@b97275org.highwire.dtl.DTLVardef@1099c38_HPS_FORMAT_FIGEXP M_FIG C_FIG Clinical PerspectiveO_ST_ABSWHAT IS KNOWN?C_ST_ABSO_LIPulmonary-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. C_LIO_LISubstrate 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. C_LI WHAT THE STUDY ADDSO_LIIn 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. C_LIO_LIThe 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. C_LIO_LIA 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. C_LI