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Open AccessJournal ArticleDOI

Rotors and the Dynamics of Cardiac Fibrillation

Sandeep V. Pandit, +1 more
- 01 Mar 2013 - 
- Vol. 112, Iss: 5, pp 849-862
TLDR
Examination of recent evidence suggesting that rotors are critical in sustaining both atrial and ventricular fibrillation in the human heart and its implications for treatment with radiofrequency ablation is examined.
Abstract
The objective of this article is to present a broad review of the role of cardiac electric rotors and their accompanying spiral waves in the mechanism of cardiac fibrillation. At the outset, we present a brief historical overview regarding reentry and then discuss the basic concepts and terminologies pertaining to rotors and their initiation. Thereafter, the intrinsic properties of rotors and spiral waves, including phase singularities, wavefront curvature, and dominant frequency maps, are discussed. The implications of rotor dynamics for the spatiotemporal organization of fibrillation, independent of the species being studied, are described next. The knowledge gained regarding the role of cardiac structure in the initiation or maintenance of rotors and the ionic bases of spiral waves in the past 2 decades, as well as the significance for drug therapy, is reviewed subsequently. We conclude by examining recent evidence suggesting that rotors are critical in sustaining both atrial and ventricular fibrillation in the human heart and its implications for treatment with radiofrequency ablation.

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Citations
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The pro- or antiarrhythmic actions of polyunsaturated fatty acids and of cholesterol.

TL;DR: The pro‐ and anti‐arrhythmic effects of a diet rich in fish oil fatty acids and of hypercholesterolemia will be discussed in relation to two major mechanisms of arrhythmogenesis (triggered activity and re‐entry).
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A method for quantifying recurrent patterns of local wavefront direction during atrial fibrillation.

TL;DR: Calculation of Egm-C allows RQA to be performed on bipolar electrograms during AF and differentiates regions of spiral wave reentry from multiple wavelet breakup.
Journal ArticleDOI

Structural and functional bases of cardiac fibrillation. differences and similarities between atria and ventricles.

TL;DR: In this paper, the authors review the current understanding of the manner in which the underlying myocardial structure and function influence rotor initiation and maintenance during cardiac fibrillation and evaluate the latest clinical mapping technologies used to identify rotors in either arrhythmia.
References
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Journal ArticleDOI

Spontaneous Initiation of Atrial Fibrillation by Ectopic Beats Originating in the Pulmonary Veins

TL;DR: The pulmonary veins are an important source of ectopic beats, initiating frequent paroxysms of atrial fibrillation and these foci respond to treatment with radio-frequency ablation.
Book

Cardiac Electrophysiology : From Cell to Bedside

TL;DR: Part I - Molecular Bases Of Ion Channel Activity PART II - Biophysics and Regulation of Cardiac Ion Channels PART III - Pharmacology of Card cardiac Ion Ch channels PART IV - Cellular Electrophysiology PART V - Models of Cardiopulmonary Excitation PART VI - Neural Control ofCardiac Electrical Activity
Journal ArticleDOI

Excitation-Contraction Coupling and Cardiac Contractile Force.

TL;DR: The major cellular structures involved in E-C coupling include myofilaments, Na/Ca exchange and the sarcolemmal Ca-pump as mentioned in this paper, as well as the sources and sinks of activator calcium.
Journal ArticleDOI

A dynamic model of the cardiac ventricular action potential. I. Simulations of ionic currents and concentration changes.

TL;DR: The model provides the basis for the study of arrhythmogenic activity of the single myocyte including afterdepolarizations and triggered activity and can simulate cellular responses under different degrees of Ca2+ overload.
Journal ArticleDOI

A model of the ventricular cardiac action potential. Depolarization, repolarization, and their interaction.

TL;DR: Simulation of the membrane action potential of the mammalian ventricular cell shows the importance of the slow recovery of INa in determining the response of the cell and relates these phenomena to the underlying ionic channel kinetics.
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