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Review
. 2020 Dec;9(4):202-210.
doi: 10.15420/aer.2020.04.

Anisotropic Cardiac Conduction

Affiliations
Review

Anisotropic Cardiac Conduction

Irum Kotadia et al. Arrhythm Electrophysiol Rev. 2020 Dec.

Abstract

Anisotropy is the property of directional dependence. In cardiac tissue, conduction velocity is anisotropic and its orientation is determined by myocyte direction. Cell shape and size, excitability, myocardial fibrosis, gap junction distribution and function are all considered to contribute to anisotropic conduction. In disease states, anisotropic conduction may be enhanced, and is implicated, in the genesis of pathological arrhythmias. The principal mechanism responsible for enhanced anisotropy in disease remains uncertain. Possible contributors include changes in cellular excitability, changes in gap junction distribution or function and cellular uncoupling through interstitial fibrosis. It has recently been demonstrated that myocyte orientation may be identified using diffusion tensor magnetic resonance imaging in explanted hearts, and multisite pacing protocols have been proposed to estimate myocyte orientation and anisotropic conduction in vivo. These tools have the potential to contribute to the understanding of the role of myocyte disarray and anisotropic conduction in arrhythmic states.

Keywords: Anisotropy; anisotropic conduction; arrhythmias; conduction velocity; pacing.

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Conflict of interest statement

Disclosure: The research was supported by the National Institute for Health Research (NIHR) Clinical Research Facility at Guy’s and St Thomas’ NHS Foundation Trust and NIHR Biomedical Research Centre based at Guy’s and St Thomas’ NHS Foundation Trust and King’s College London. The views expressed are those of the authors, and not necessarily those of the NHS, the NIHR or the Department of Health. JW is supported by a Medical Research Council UK Clinical Research Training Fellowship (grant code: MR/N001877/1). The authors have no other conflicts of interest to disclose.

Figures

Figure 1:
Figure 1:. Resistor Network Demonstrating a 2D Bidomain Model
Figure 2:
Figure 2:. Cellular Features that Contribute to Conduction Velocity Anisotropy in Myocardial Tissue with Long, Cylindrical Cells
Figure 3:
Figure 3:. Activation Maps of the Epicardial Surface of The Anterior Left Ventricle Following a Premature Extra-stimulus from the Base of the Left Ventricle
Figure 4:
Figure 4:. Immunohistochemical Analysis Demonstrating Pathological Remodelling in Arrhythmogenic Right Ventricular Dysplasia
Figure 5:
Figure 5:. Functional Re-entry Circuit Demonstrating the Leading Circle Concept
Figure 6:
Figure 6:. Atrial Fibre Atlas and Activation Pattern

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