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).

We welcome Dr. Franz's comments relative to our recent publication dealing with the monophasic action potential (MAP) [1]. We agree and fully appreciate the fact that the Franz contact electrode technique has been successfully used for over 20 years by Dr. Franz and other investigators. This success stems from the fact that the two electrodes of the contact catheter are relatively close to each other so that their combined field of view is fairly localized. However, we do not agree that this success can be used as an argument against our conclusion that it is not the tip electrode that records the MAP. Our study investigated the physical principles behind the MAP recording. We started with a simple definition of voltage as the difference of potential between two points or two electrodes. To determine which of these two potentials carries time-dependent information, we placed the two electrodes at sites with different cellular activity and observed which activity is reflected in the MAP signal. The observations demonstrated in a very straightforward manner that the tip or inactivating electrode is not the recording electrode. This conclusion provides support for theories introduced as early as 1934 [2].

Response to specific comments:

The size of the canine left ventricular wedge preparation is typically between 2 × 1.5 × 0.9 cm and 3 × 2 × 1.5 cm. The schemes in Figs. 4 and 8 correctly depict the relative dimensions of the contact MAP catheter and the wedge preparation. Moreover, in the schematics shown in Figs. 5, 6 and 7, the catheter is larger than its actual dimension relative to the size of the wedge.

The pioneering study by Dower et al. [3], cited by Dr. Franz, was aimed at development of an intracellular recording technique. The authors recognized that microelectrodes with …

Biophysical basis for monophasic action potential

UNLABELLED\nCardiac arrhythmias complicate many diseases affecting the heart and the circulation, and incorporate a multiplicity of underlying mechanisms. The evolution of scientific knowledge has made the complex changes produced by cardiovascular disease sufficiently understood at the organ, cellular, and molecular levels such that there is a diversity of therapeutic targets for pharmacological therapy and/or prevention. Moreover, the approach of rational drug design in mechanism-specific and disease-specific fashion facilitates targeting of therapy via the methods of molecular, structural and translational biology. Additional approaches, employing similar drug design strategies but based on gene therapy and transcriptional and translational modification are on the horizon. Hence, there is reason to be optimistic regarding the design, testing and clinical availability of novel antiarrhythmic therapies.\n\n\nCONDENSED ABSTRACT\nThe evolution of scientific knowledge has made the effects of cardiovascular disease sufficiently understood at the organ, cellular, and molecular levels such that there is a diversity of therapeutic targets for pharmacological therapy and/or prevention. Moreover, the approach of rational drug design facilitates targeting of therapy via the methods of molecular, structural and translational biology. Additional approaches, employing similar drug design strategies but based on gene therapy and transcriptional and translational modification are on the horizon. Hence, there is reason to be optimistic regarding the design, testing and clinical availability of novel antiarrhythmic therapies.

New approaches to antiarrhythmic therapy: Emerging therapeutic applications of the cell biology of cardiac arrhythmias

Quinidine‐Induced Early Afterdepolarizations and Triggered Activity

Reflected reentry was produced in canine false tendons, mounted in a three-chamber bath, in which the central fiber segment was partially depolarized with an "ischemic" solution to provide an area of impaired conduction. Lidocaine (3-5 mg/l) added to the central chamber further impaired conduction; consequently, reflections were obtained at lower frequencies and over a wider range of stimulation cycle lengths. Complete block followed drug exposure in some preparations. At moderate stimulation rates, the drug-induced shift of the frequency-dependence of manifest reflected reentries was either arrhythmogenic or antiarrhythmic. The action of lidocaine can be explained on the basis of effects on depressed fast or slow response activity at the boundary regions of the ischemic gap. Under slow response conditions, in false tendons homogeneously exposed to a solution containing 20 mM K+ and 9 mM Ca++, lidocaine delayed propagation or induced complete block. In fibers mounted in a single sucrose gap, the drug increased the current required to reach threshold without significant changes in resting potential, threshold voltage or input resistance. The effect of lidocaine on threshold current was lost in Na+-deficient solutions. Thus, lidocaine impairs conduction through K+-depolarized false tendons, an effect that may be related to the Na+ background current.

Effects of lidocaine on conduction through depolarized canine false tendons and on a model of reflected reentry.

The J wave syndromes, including the Brugada (BrS) and early repolarization (ERS) syndromes, are characterized by the manifestation of prominent J waves in the electrocardiogram appearing as an ST segment elevation and the development of life-threatening cardiac arrhythmias. BrS and ERS differ with respect to the magnitude and lead location of abnormal J waves and are thought to represent a continuous spectrum of phenotypic expression termed J wave syndromes. Despite over 25 years of intensive research, risk stratification and the approach to therapy of these two inherited cardiac arrhythmia syndromes are still rapidly evolving. Our objective in this review is to provide an integrated synopsis of the clinical characteristics, risk stratifiers, as well as the molecular, ionic, cellular, and genetic mechanisms underlying these two syndromes that have captured the interest and attention of the cardiology community over the past two decades.

Charles Antzelevitch

Papers

Biophysical basis for monophasic action potential

New approaches to antiarrhythmic therapy: Emerging therapeutic applications of the cell biology of cardiac arrhythmias

Quinidine‐Induced Early Afterdepolarizations and Triggered Activity

Effects of lidocaine on conduction through depolarized canine false tendons and on a model of reflected reentry.

J wave syndromes as a cause of malignant cardiac arrhythmias.