Background Atrial fibrillation, the most common sustained cardiac arrhythmia and a major cause of stroke, results from simultaneous reentrant wavelets. Its spontaneous initiation has not been studied. Methods We studied 45 patients with frequent episodes of atrial fibrillation (mean [±SD] duration, 344±326 minutes per 24 hours) refractory to drug therapy. The spontaneous initiation of atrial fibrillation was mapped with the use of multielectrode catheters designed to record the earliest electrical activity preceding the onset of atrial fibrillation and associated atrial ectopic beats. The accuracy of the mapping was confirmed by the abrupt disappearance of triggering atrial ectopic beats after ablation with local radio-frequency energy. Results A single point of origin of atrial ectopic beats was identified in 29 patients, two points of origin were identified in 9 patients, and three or four points of origin were identified in 7 patients, for a total of 69 ectopic foci. Three foci were in the right atrium...

https://www.nejm.org/doi/pdf/10.1056/NEJM199809033391003

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

The Task Force for the management of atrial fibrillation of the European Society of Cardiology (ESC)  

Developed with the special contribution of the European Heart Rhythm Association (EHRA) of the ESC  

Endorsed by the European Stroke Organisation (ESO)

/pdf/2016-esc-guidelines-for-the-management-of-atrial-ba0601yb9m.pdf

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

/pdf/2016-esc-guidelines-for-the-management-of-atrial-36b2cidm1x.pdf

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS: The Task Force for the management of atrial fibrillation of the European Society of Cardiology (ESC). Developed with the special contribution of the European Heart Rhythm Association (EHRA) of the ESC. Endorsed by the European Stroke Organisation (ESO)

ESC guidelines for the management of atrial fibrillation developed in collaboration with EACTS

Sidney C. Smith, Jr, MD, FACC, FAHA, FESC, Chair; Alice K. Jacobs, MD, FACC, FAHA, Vice-Chair; Cynthia D. Adams, MSN, APRN-BC, FAHA; Jeffery L. Anderson, MD, FACC, FAHA; Elliott M. Antman, MD, FACC, FAHA[‡][1]; Jonathan L. Halperin, MD, FACC, FAHA; Sharon Ann Hunt, MD, FACC, FAHA; Rick Nishimura,

/pdf/acc-aha-esc-2006-guidelines-for-the-management-of-patients-5fc8py53ut.pdf

ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society

The discontinuous nature of propagation in normal canine cardiac muscle. Evidence for recurrent discontinuities of intracellular resistance that affect the membrane currents.

1. Vector Analysis.- 2. Electrical Sources and Fields.- 3. Introduction to Membrane Biophysics.- 4. Action Potentials.- 5. Propagation.- 6. Subthreshold Stimuli.- 7. Extracellular Fields.- 8. Membrane Biophysics.- 9. The Electrophysiology of the Heart.- 10. The Neuromuscular Junction.- 11. Skeletal Muscle.- 12. Functional Neuromuscular Stimulation.

Bioelectricity: A Quantitative Approach

This paper considers a quantitative description of intracellular and transmembrane currents in anisotropic muscle, with emphasis on the factors that determine the extracellular potentials. Although Vmax of the intracellular action potential had no relation to changes in conduction velocity in anisotropic tissue with constant membrane properties, the extracellular waveforms were quite sensitive to velocity changes. Large amplitude biphasic deflection occurred in the fast areas, and in the slow areas the waveforms were of lower amplitude and triphasic in shape; i.e., negative potentials preceded the biphasic positive-negative deflection. The extracellular potentials were simulated on the bases of a model of intracellular currents, and the theoretical and measured results showed good agreement. In tissue with anisotropic conductivity, the relationship between the spatial intracellualr potential gradient and the magnitude of the extracellular potential of the excitation wave was opposite to the classical relationship in isotropic tissue. Due to the influence of the effective intracellular conductivity on the spread of intracellular currents and on conduction velocity, in anisotropic tissue the extracellular potential decreased as the intracellular potential gradient increased. The peak values of the positive and negative potentials and the spatial distribution of the potential gradients varied considerably along the activation front. These findings were accounted for by differences in the distribution and spatial extent of the transmembrane currents, which were determined by the intracellular currents. The theoretical analysis showed that intracellular and transmembrane currents were proportional to the local conduction velocities of the wavefront. Thereby, it was not possible to have a "uniform layer" of current when there were differences in conduction velocity along the length of the excitation wave. The implications of the analysis are considerable, since the gratifying agreement between the theoretical and measured results indicates that the details of the extracellular waveforms can be explained on the basis of the distribution of intracellular currents; i.e., extracellular potentials provide a sensitive index of intracellular current flow.

Extracellular potentials related to intracellular action potentials during impulse conduction in anisotropic canine cardiac muscle.

Although it has been known throughout this century that a complex sequence of electrical events is produced on the body surface by the electrophysiological properties of the heart, the question of how well these body surface events can be explained mathematically on the basis of experimental measurements of cardiac geometry and electrical activity remains unanswered. Recent advances in experimental capabilities have made possible the near simultaneous measurement of both cardiac epicardial and corresponding body surface potential distributions from in vivo animal preparations using chronically implanted electrodes to keep the volume conductor intact. This report provides a method for finding transfer coefficients that relate the epicardial and body surface potential distributions to each other. The method is based on knowing the geometric location of each electrode, and on having enough electrodes to establish the geometric shape and the potential distribution of closed epicardial and body surfaces. However, the method does not require that either the heart or body surfaces have any special shape, such as that of a sphere, or that any electrical quantities, such as voltage gradients, be known in addition to the potentials. The use of potential distributions to represent heart electrical activity is advantageous since such distributions can be directly measured experimentally, without a transformation to any other form, such as multiple current-generating dipoles, being required. This report includes a statement of the underlying integral equations, the procedure. for finding the equations' coefficients from geometry measurements, some considerations for computer algorithms, and an example.

Relating Epicardial to Body Surface Potential Distributions by Means of Transfer Coefficients Based on Geometry Measurements

The increased incidence of arrhythmias in structural heart disease is accompanied by remodeling of the cellular distribution of gap junctions to a diffuse pattern like that of neonatal cardiomyocytes. Accordingly, it has become important to know how remodeling of gap junctions due to normal growth hypertrophy alters anisotropic propagation at a cellular level (V(max)) in relation to conduction velocities measured at a macroscopic level. To this end, morphological studies of gap junctions (connexin43) and in vitro electrical measurements were performed in neonatal and adult canine ventricular muscle. When cells enlarged, gap junctions shifted from the sides to the ends of ventricular myocytes. Electrically, normal growth produced different patterns of change at a macroscopic and microscopic level. Although the longitudinal and transverse conduction velocities were greater in adult than neonatal muscle, the anisotropic velocity ratios were the same. In the neonate, mean V(max) was not different during longitudinal (LP) and transverse (TP) propagation. However, growth hypertrophy produced a selective increase in mean TP V(max) (P<0.001), with no significant change in mean LP V(max). Two-dimensional neonatal and adult cellular computational models show that the observed increases in cell size and changes in the distribution of gap junctions are sufficient to account for the experimental results. Unexpectedly, the results show that cellular scaling (cell size) is as important (or more so) as changes in gap junction distribution in determining TP properties. As the cells enlarged, both mean TP V(max) and lateral cell-to-cell delay increased. V(max) increased because increases in cell-to-cell delay reduced the electric current flowing downstream up to the time of V(max), thus enhancing V(max). The results suggest that in pathological substrates that are arrhythmogenic, maintaining cell size during remodeling of gap junctions is important in sustaining a maximum rate of depolarization.

Roger C. Barr

Papers

The discontinuous nature of propagation in normal canine cardiac muscle. Evidence for recurrent discontinuities of intracellular resistance that affect the membrane currents.

Bioelectricity: A Quantitative Approach

Extracellular potentials related to intracellular action potentials during impulse conduction in anisotropic canine cardiac muscle.

Relating Epicardial to Body Surface Potential Distributions by Means of Transfer Coefficients Based on Geometry Measurements

Electrophysiological Effects of Remodeling Cardiac Gap Junctions and Cell Size Experimental and Model Studies of Normal Cardiac Growth