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).

ECG phenomena of the early ventricular repolarization have in the past often been misdiagnosed or misinterpreted. This happened mainly because of prevailing opinion of the “benign” or “innocent” nature of the early repolarization syndrome (ERS) (1,2). As an example, early repolarization changes consistent with Brugada syndrome were overlooked for decades. Clinical interest in ERS has been rekindled recently because of its similarities with the electrocardiographic manifestations of the highly arrhythmogenic Brugada syndrome and the potential for misdiagnosis (3–8).

ECG Phenomena of the Early Ventricular Repolarization

Although many factors influence the duration of ventricular repolarization and the detailed appearance of ECG (Table 1), regional differences in the configuration of action potentials across the myocardial wall are considered to be major determinants of the three-dimensional pattern of ECG waves and intervals. The QT interval is a surrogate electrocardiographic index of ventricular repolarization. Its duration under normal conditions is mainly determined by expression, properties, and balance of the repolarizing forces inward sodium and calcium, and outward potassium and chloride currents (intrinsic cardiac properties).

Short QT Interval

The Brugada syndrome is characterized by a ST-segment elevation in the right precordial leads associated with right bundle branch block (RBBB) pattern and a propensity for life-threatening ventricular arrhythmias in the absence of structural heart disease.1 Mutations in a cardiac sodium channel gene have been linked to this syndrome2.

 The mechanism underlying the RBBB and ST-segment elevation in right precordial leads in patients with the Brugada syndrome is thought to be an outward shift of the ionic currents during early repolarization causing a marked accentuation of the action potential notch in right ventricular epicardial but not endocardial cells. The outward shift of current ultimately leads to loss of the action potential dome causing marked abbreviation of the action potential in the right ventricular epicardial cells.3, 4,

Brugada-like electrocardiographic pattern.

Background 
Heart failure (HF) is a leading cause of mortality and is associated with cardiac remodeling. Vulnerability to atrial fibrillation (AF) has been shown to be greater in the early stages of HF, whereas ventricular tachycardia/fibrillation develop during late stages. Here, we explore changes in gene expression that underlie the differential development of fibrosis and structural alterations that predispose to atrial and ventricular arrhythmias.


Objective 
To study transcriptomic changes associated with the development of cardiac arrhythmias in early and late stages of heart failure.


Methods 
Dogs were tachy-paced from right ventricle (RV) for 2–3 or 5–6 weeks (early and late HF). We performed transcriptomic analysis of right atria (RA) and RV isolated from control dogs and those in early and late HF. Transcripts with mean relative log2-fold change ≥2 were included in the differential analysis with significance threshold adjusted to p<0.05.


Results 
Early HF remodeling was more prominent in RA with enrichment of extracellular matrix, circulatory system, wound healing and immune response pathways; many of these processes were not present in RA in late HF. RV showed no signs of remodeling in early HF but enrichment of extracellular matrix and wound healing in late HF.


Conclusion 
Our transcriptomic data indicate significant fibrosis-associated transcriptional changes in RA in early HF and in RV in late HF, with strong atrial predominance. These alterations in gene expression are consistent with the development of arrhythmogenesis in atria in early but not late HF and in the ventricle in late but not early HF.

/pdf/transcriptional-changes-associated-with-advancing-stages-of-16i3z0giz8.pdf

Charles Antzelevitch

Papers

ECG Phenomena of the Early Ventricular Repolarization

Short QT Interval

Brugada-like electrocardiographic pattern.

Transcriptional changes associated with advancing stages of heart failure underlie atrial and ventricular arrhythmogenesis.

Mechanisms Underlying Arrhythmogenesis in the J‐wave Syndromes