Additions to the Wavelet Hypothesis of Cardiac Fibrillation

Authors

  • J.A. ABILDSKOV M.D.

    Corresponding author
    1. Nora Eccles Harrison Cardiovascular Research and Training Institute, and the Division of Cardiology, University of Utah, Salt Lake City, Utah
      J.A. Abildskov, M.D., Nora Eccles Harrison CVRTI, University of Utah, Building 500, Salt Lake City, UT 84112, Fax: 801-581-3128.
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  • This work was supported by Grunt HL35204 from the National Institute Health (National Heart, Lung, and Blood Institute); and awards from the Nora Eccles Treadwell Foundation and the Richard A. and Nora Eccles Harrison fund for Cardiovascular Research.

J.A. Abildskov, M.D., Nora Eccles Harrison CVRTI, University of Utah, Building 500, Salt Lake City, UT 84112, Fax: 801-581-3128.

Abstract

Wavelet Hypothesis. Introduction: The wavelet hypothesis of Moe relates the initiation of cardiac fibrillation to nonuniform propagation of premature responses in the presence of nonuniform recovery of excitability. Fibrillation itself is characterized by multiple spatially discrete activation fronts (wavelets) resulting in reentry at changing locations.

Methods and Results: A computer model originally used to demonstrate the hypothesis has been used in further studies of fibrillation and the findings add new details to the hypothesis. The model simulated propagation, cycle length dependent recovery of excitability, and slow propagation of premature responses. Additions to the hypothesis were definition of the different mechanisms by which refractory period (RP) range and mean duration affect vulnerability, explanation of the onset of the vulnerable period later than earliest propagation, and definition of effects of conduction defects on vulnerability. They also include evidence that RP range and duration affect the degree of nonuniform excitation required for fibrillation.

Conclusion: Findings indicate that mean RP duration affects vulnerability by means of the number of premature responses possible per unit time while RP range affects nonuniformity of propagation per premature response. They also suggest that effects of conduction defects on vulnerability depend on associated RPs and that the degree of nonuniform excitation required to initiate fibrillation varies with recovery properties. In addition, they provide an explanation for onset of (he vulnerable period after propagation is possible.

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