Déjà vu in the theories of atrial fibrillation dynamics

Abstract

This brief review looks back to the major theoretical, experimental, and clinical work on the dynamics and mechanisms of atrial fibrillation (AF). Its goal is to highlight the most important issues, controversies, and advances that have driven the field of investigation into AF mechanisms at any given time during the last ∼100 years. It emphasizes that while the history of AF research has been full of controversies from the start, such controversies have led to new information, and individual scientists have learned from those that have preceded them. However, in the face of the most common sustained cardiac arrhythmia seen in clinical practice, we are yet to fully understand its fundamental mechanisms and learn how to treat it effectively. Future research into AF dynamics and mechanisms should focus on the development and validation of new numerical and animal models. Such models should be relevant to and accurately reproduce the important substrates associated with ageing and with diseases such as hypertension, heart failure, and ischaemic heart disease which cause AF in the vast majority of patients. Knowledge derived from such models may help to greatly advance the field and hopefully lead to more effective prevention and therapy.

Figure 1

A.G. Mayer's circulating movements produced in rings cut from the bells of a jellyfish. (A) Top view of Cassiopea. (B) The bell shown after cutting the marginal sense organs which normally trigger pulsations of the subumbrella. The subumbrella tissue in the periphery is a better conductor than the gelatinous substance in the centre of the bell. (C) if an annulus is insulated by a shallow scratch through the subumbrella and then a small sector, B, is isolated by shallow radial cuts, then on stimulating the large sector A at 1 and 2 with a pair of electrodes, a contraction will travel all the distance around A, but the sector B will not contract. (D) The isolated disc can be stimulated mechanically or electrically to trigger a circular wave of current which may continue doing so for hours or days. Printed from a public domain book digitized by Google.

Figure 2

(A) Lewis’ schematic representation of the excitation wave as it circulates in flutter. (B) Similar representation of the excitation wave as it circulates in fibrillation. Arrows indicate the direction of propagation. See text for further details. Reprinted from Lewis by permission of the publisher.

Figure 3

Three-dimensional plots of CV and wavelength in experimental (top) and numerical (bottom) spiral waves. (A and C) CV (red) increases as wave front curvature decreases from the centre of rotation to the periphery. (B and D) Wavelength (yellow) is also a function of distance from the core and follows the changes in APD and CV. (A) and (B) were obtained from an optical mapping experiment in a 2D monolayer of neonatal rat ventricular myocytes; (C) and (D) were obtained from a simulation using the Luo and Rudy model. Y-axis in (A) and (C) is CV relative to maximal CV. Y-axis in (B) and (D) is wavelength relative to maximal wavelength.

Figure 4

Spiral waves spin around a tiny pivoting phase singularity. (A and B) Phase singularity (yellow cross mark) shown on a phase map (A) and black and white movie snapshot (B) of the same spiral in a neonatal rat ventricular myocyte monolayer. (C and D) Similar representations from an equivalent computer simulation. The phase singularity is the point at which all phases converge in the phase map (A and C) and wave front (red) and wave tail (blue) meet.