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

https://repub.eur.nl/pub/104203/REPUB_104203-OA.pdf

2017 HRS / EHRA / ECAS / APHRS / SOLAECE expert consensus statement on catheter and surgical ablation of atrial fibrillation

Atrial fibrillation is a condition in which control of heart rhythm is taken away from the normal sinus node pacemaker by rapid activity in different areas within the upper chambers (atria) of the heart. This results in rapid and irregular atrial activity and, instead of contracting, the atria only quiver. It is the most common cardiac rhythm disturbance and contributes substantially to cardiac morbidity and mortality. For over 50 years, the prevailing model of atrial fibrillation involved multiple simultaneous re-entrant waves, but in light of new discoveries this hypothesis is now undergoing re-evaluation.

New ideas about atrial fibrillation 50 years on

Chronic atrial fibrillation (AF) is characterized by decreased atrial contractility, shortened action potential duration, and decreased accommodation of action potential duration to changes in activation rate. Studies on experimental animal models of AF implicate a reduction in L-type Ca2+ current (I(Ca)) density in these changes. To evaluate the effect of AF on human I(Ca), we compared I(Ca) in atrial myocytes isolated from 42 patients in normal sinus rhythm at the time of cardiac surgery with that of 11 chronic AF patients. I(Ca) was significantly reduced in the myocytes of patients with chronic AF (mean -3.35+/-0.5 pA/pF versus -9.13+/-1. 0 pA/pF in the controls), with no difference between groups in the voltage dependence of activation or steady-state inactivation. Although I(Ca) was lower in myocytes from the chronic AF patients, their response to maximal beta-adrenergic stimulation was not impaired. Postoperative AF frequently follows cardiac surgery. Half of the patients in the control group (19/38) of this study experienced postoperative AF. Whereas chronic AF is characterized by reduced atrial I(Ca), the patients with the greatest I(Ca) had an increased incidence of postoperative AF, independent of patient age or diagnosis. This observation is consistent with the concept that calcium overload may be an important factor in the initiation of AF. The reduction in functional I(Ca) density in myocytes from the atria of chronic AF patients may thus be an adaptive response to the arrhythmia-induced calcium overload.

Atrial L-Type Ca2+ Currents and Human Atrial Fibrillation

Although the canine atrium has proven useful in several experimental models of atrial fibrillation and for studying the effects of rapid atrial pacing on atrial electrical remodeling, it may not fully represent the human condition because of reported differences in functional ionic currents and ion channel subunit expression. In this study, we reassessed the molecular components underlying one current, the ultrarapid delayed rectifier current in canine atrium [IKur(d)], by evaluating the mRNA, protein, immunofluorescence, and currents of the candidate channels. Using reverse transcriptase-polymerase chain reaction, we found that Kv1.5 mRNA was expressed in canine atrium whereas message for Kv3.1 was not detected. Western analysis on cytosolic and membrane fractions of canine tissues, using selective antibodies, showed that Kv3.1 was only detectable in the brain preparations, whereas Kv1.5 was expressed at high levels in both atrial and ventricular membrane fractions. Confocal imaging performed on isolated canine atrial myocytes clearly demonstrated the presence of Kv1.5 immunostaining, whereas that of Kv3.1 was equivocal. Voltage- and current-clamp studies showed that 0.5 mmol/L tetraethylammonium had variable effects on sustained K+ currents, whereas a compound with demonstrated selectivity for hKv1.5 versus Kv3.1, hERG or the sodium channel, fully suppressed canine atrial IKur tail currents and depressed sustained outward K+ current. This agent also increased action potential plateau potentials and action potential duration at 20% and 50% repolarization. These results suggest that in canine atria, as in other species including human, Kv1.5 protein is highly expressed and contributes to IKur.

Kv1.5 Is an Important Component of Repolarizing K+ Current in Canine Atrial Myocytes

Ischemia Potentiates the Mechanosensitive Modulation of Atrial ATP-Sensitive Potassium Channels a

The modulation of whole cell K+ currents by the alpha 1-adrenergic agonist, phenylephrine, was studied in isolated rat atrial myocytes by use of perforated-patch whole cell recording techniques. The out ward K+ current in these myocytes consists of two inactivating components (iK,f and iK,s), which differ in the kinetics of inactivation and recovery from inactivation, and a noninactivating component, (iK,ss). Superfusion of these myocytes with 10 microM phenylephrine caused a rapid suppression of iK,ss, with little effect on the other current components. This effect of phenylephrine could be mimicked by exogenous application of 1,2-dioctanoyl-sn-glycerol (20 microM), a membrane-permeant diacylglycerol analogue; however, it was clearly distinct from the effect of 5 nM alpha-dendrotoxin, which selectively suppressed the slowly inactivating current component, iK,s, while having no effect on iK,ss. At a dose of 50 microM, phenylephrine also suppressed iK,s. There was no significant effect of phenylephrine (10 or 50 microM) or alpha-dendrotoxin (5 nM) on the rapidly inactivating current component, iK,f. The kinetic and pharmacological differences between these current components suggest that they represent the activity of distinct K+ channels.

Michelle Lamorgese

Papers

Atrial L-Type Ca2+ Currents and Human Atrial Fibrillation

Kv1.5 Is an Important Component of Repolarizing K+ Current in Canine Atrial Myocytes

Ischemia Potentiates the Mechanosensitive Modulation of Atrial ATP-Sensitive Potassium Channels a

Phenylephrine suppresses outward K+ currents in rat atrial myocytes.