Literature DB >> 16050833

How the spatial frequency of polarization influences the induction of reentry in cardiac tissue.

Deborah Langrill Beaudoin1, Bradley J Roth.   

Abstract

UNLABELLED: Influences of spatial frequency of polarization.
INTRODUCTION: The mechanism by which an electric field induces a rotor during cross-field stimulation of cardiac tissue is not entirely known. Different heterogeneous aspects of cardiac tissue have been offered as possible theories, a prominent one being fiber curvature. The polarization produced when an electric field is applied to a sheet of tissue is varied over many spatial frequencies, depending upon the fiber angle. This article compares the effect of high and low spatial frequencies of polarization on reentry induction. METHODS AND
RESULTS: We incorporate a randomized fiber angle geometry into a two-dimensional active cardiac tissue model with unequal anisotropy ratios already exhibiting smooth, curving fibers. We simulate cross-field stimulation to initiate reentry in the tissue model, and compare the electric field thresholds at different S1-S2 intervals for tissue with randomized fiber angles, tissue with a smooth fiber geometry, and tissue with randomized fiber angles plus smooth, curving fibers. The tissue with both small, random fiber angles and curving fibers has a significantly lower threshold for reentry at certain intervals on the strength-interval curve than for the two cases individually.
CONCLUSION: Cardiac tissue exhibiting a random fiber geometry in conjunction with a smooth fiber geometry includes high and low spatial frequencies of polarization that may have an effect on the mechanism for reentry at certain S1-S2 intervals. Low spatial frequency regions of hyperpolarization carve out excitable pathways, and high spatial frequency regions provide the large gradient of transmembrane potential required to initiate break excitation.

Mesh:

Year:  2005        PMID: 16050833     DOI: 10.1111/j.1540-8167.2005.40651.x

Source DB:  PubMed          Journal:  J Cardiovasc Electrophysiol        ISSN: 1045-3873


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2.  A mechanism for the upper limit of vulnerability.

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