https://caltcm.memberclicks.net/assets/documents/acc_aha_chf_2013_guidelines.pdf

2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines

Guidelines summarize and evaluate all currently available evidence on a particular issue with the aim of assisting physicians in selecting the best management strategy for an individual patient suffering from a given condition, taking into account the impact on outcome, as well as the risk–benefit ratio of particular diagnostic or therapeutic means. Guidelines are no substitutes for textbooks. The legal implications of medical guidelines have been discussed previously.

A large number of Guidelines have been issued in recent years by the European Society of Cardiology (ESC) as well as by other societies and organizations. Because of the impact on clinical practice, quality criteria for development of guidelines have been established in order to make all decisions transparent to the user. The recommendations for formulating and issuing ESC Guidelines can be found on the ESC Web Site (http://www.escardio.org/guidelines-surveys/esc-guidelines/about/Pages/rules-writing.aspx).

In brief, experts in the field are selected and undertake a comprehensive review of the published evidence for management and/or prevention of a given condition. A critical evaluation of diagnostic and therapeutic procedures is performed, including assessment of the risk–benefit ratio. Estimates of expected health outcomes for larger societies are included, where data exist. The level of evidence and the strength of recommendation of particular treatment options are weighed and graded according to pre-defined scales, as outlined in Tables 1 and 2 .

View this table:

Table 1 
Classes of recommendations



View this table:

Table 2 
Levels of evidence



The experts of the writing panels have provided disclosure statements of all relationships they may have that might be perceived as real or potential sources of conflicts of interest. These disclosure forms are kept on file at the European Heart House, headquarters of the ESC. Any changes in conflict of interest that arise during the writing period must be notified to the ESC. The Task Force report received its entire financial support from …

/pdf/guidelines-for-the-management-of-atrial-fibrillation-the-1cikaj4630.pdf

Guidelines for the management of atrial fibrillation The Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology (ESC)

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)

Supplementary Table 9, column 'Edoxaban', row 'eGFR category', '95 mL/min' (page 15). The cell should be coloured green instead of yellow. It should also read "60 mg"instead of "60 mg (use with caution in 'supranormal' renal function)."In the above-indicated cell, a footnote has also been added to state: "Edoxaban should be used in patients with high creatinine clearance only after a careful evaluation of the individual thromboembolic and bleeding risk."Supplementary Table 9, column 'Edoxaban', row 'Dose reduction in selected patients' (page 16). The cell should read "Edoxaban 60 mg reduced to 30 mg once daily if any of the following: creatinine clearance 15-50 mL/min, body weight <60 kg, concomitant use of dronedarone, erythromycin, ciclosporine or ketokonazole"instead of "Edoxaban 60 mg reduced to 30 mg once daily, and edoxaban 30 mg reduced to 15mg once daily, if any of the following: creatinine clearance of 30-50 mL/min, body weight <60 kg, concomitant us of verapamil or quinidine or dronedarone."

/pdf/2020-esc-guidelines-for-the-diagnosis-and-management-of-38dpic1xu8.pdf

2020 ESC Guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS).

Ventricular myocardium in larger mammals has been shown to be comprised of three distinct celltypes: epicardial, M, and endocardial. Epicardial and M cell action potentials differ from endocardialcells with respect to the morphology of phase 1. These cells possess a prominent I to -mediated notchresponsible for the “spike and dome” morphology of the epicardial and M cell response. M cells aredistinguished from the other cell types in that they display a smaller I Ks , but a larger late I Na andI Na-Ca . These ionic distinctions underlie the longer action potential duration (APD) and steeper APD-rate relationship of the M cell. Difference in the time course of repolarization of phase 1 and phase3 are responsible for the inscription of the electrocardiographic J wave and T wave, respectively.These repolarization gradients are sensitively modulated by electrotonic communication among thethree cells types, [ K + ] o , and the presence of drugs that either reduce or augment net repolarizingcurrent. A reduction in net repolarizing current generally leads to a preferential prolongation of theM cell action potential, responsible for a prolongation of the QT interval and an increase in transmuraldispersion of repolarization (TDR), which underlies the development of torsade de pointesarrhythmias. An increase in net repolarizing current can lead to a preferential abbreviation of theaction potential of epicardium in the right ventricle (RV), and endocardium in the left ventricle (LV).These actions also lead to a TDR that manifests as the Brugada syndrome in RV and the short QTsyndrome in LV.

Modulation of transmural repolarization.

Introduction
T-wave alternans (TWA) is characterized by beat to beat alteration in the amplitude, polarity and/or morphology of the electrocardiographic T wave. TWA has been reported in patients with the Brugada syndrome (BS) and is thought to be associated with an increased risk for development of VT/VF. The cellular mechanisms involved are not well-defined and are the subject of this investigation.

/pdf/cellular-mechanism-and-arrhythmogenic-potential-of-t-wave-j9h4spkgwy.pdf

Cellular mechanism and arrhythmogenic potential of T-wave alternans in the Brugada syndrome.

See related articles, pages 981–991 

Dispersion of repolarization across the ventricular wall has been suggested to underlie the inscription of the normal electrocardiographic T wave and when amplified to contribute prominently to the development of cardiac arrhythmias.1–3

The magnitude of transmural dispersion of repolarization (TDR) is attributable to intrinsic differences in the action potential duration (APD) of the 3 principal cell types that comprise the ventricular myocardium and the extent to which these repolarization differences are damped by electrotonic forces. An increase in tissue resistivity in the deep subepicardium,4 attributable to a sharp transition in cell orientation,3 reduced expression of connexin 435,6 and increased density of collagen7 in this region, contributes to the expression of repolarization heterogeneities across the ventricular wall by limiting the degree of electrotonic interaction between the myocardial layers. Thus, the degree of electrotonic coupling, together with the intrinsic differences in APD, determines the extent to which TDR is expressed and its impact on arrhythmogenesis, as well as on the morphology of the T wave. It is noteworthy that even in the absence of any difference in final repolarization time, electrotonic forces generated by transmural differences in the shape of the action potential can inscribe an upright T wave in the ECG. Theoretical studies have also been helpful in our understanding of the role of electrical coupling in the expression of TDR.8

TDR is in large part attributable to the presence of M cells between the endocardial and epicardial layers of the heart. The M cell, discovered in the early 1990s and named in memory of Gordon K. Moe,9,10 has as its hallmark the ability to prolong its action potential more than that of normal epicardium or endocardium in response to a slowing of rate or exposure to agents …

M Cells in the Human Heart

QT prolongation, whether congenital or acquired, is commonly associated with life-threatening torsade de pointes (TdP) arrhythmias that develop as a consequence of the amplification of electrical heterogeneities intrinsic to the ventricular myocardium. Electrophysiologic distinctions among the three predominant cell types that comprise the ventricular myocardium are responsible for the normal dispersion of repolarization and transmural voltage gradients that inscribe the J and T waves of the ECG. Differences in the response of epicardial, endocardial and M cells to pharmacologic agents and/or pathophysiological states result in amplification of these intrinsic electrical heterogeneities, thus providing a substrate and trigger for the development of reentrant arrhythmias. Transmural dispersion of repolarization secondary to disproportionate prolongation of the action potential of M cells in response to a reduction in net repolarizing current often leads to the development of a vulnerable window, long QT intervals, abnormal T waves as well as to the induction of polymorphic VT resembling torsade de pointes. The decrease in net repolarizing current also predisposes M cells and Purkinje fibres to develop early afterdepolarization-induced triggered activity, which is responsible for the generation of extrasystoles thought to precipitate TdP. Agents that prolong the QT interval but do not increase transmural dispersion of repolarization are not capable of inducing TdP. Thus, the available data suggest that that the principal problem with the long QT syndrome is not long QT intervals, but rather the dispersion of repolarization that often accompanies prolongation of the QT interval.

/pdf/heterogeneity-of-cellular-repolarization-in-lqts-the-role-of-16u98fms0k.pdf

Heterogeneity of cellular repolarization in LQTS: the role of M cells

Previous studies indicate that action potential duration (APD) alternans is initiated in the endocardial (END) and midmyocardial (MID) regions rather than the epicardium (EPI) in the canine left ve...

/pdf/cellular-and-subcellular-alternans-in-the-canine-left-3nh4h4xaqi.pdf

Charles Antzelevitch

Papers

Modulation of transmural repolarization.

Cellular mechanism and arrhythmogenic potential of T-wave alternans in the Brugada syndrome.

M Cells in the Human Heart

Heterogeneity of cellular repolarization in LQTS: the role of M cells

Cellular and subcellular alternans in the canine left ventricle.