ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure).

Mariell Jessup, MD, FACC, FAHA, Chair [*][1]

William T. Abraham, MD, FACC, FAHA[†][2]

Donald E. Casey, MD, MPH, MBA[‡][3]

Arthur M. Feldman, MD, PhD, FACC, FAHA[§][4]

Gary S. Francis, MD, FACC, FAHA[§][4]

Theodore G. Ganiats, MD[∥][5]

Marvin A. Konstam, MD, FACC[¶][6]

Donna M.

/pdf/2009-focused-update-incorporated-into-the-acc-aha-2005-3z9lhvyqwq.pdf

2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: Developed in Collaboration With the International Society for Heart and Lung Transplantation

Background In this study we tested the hypothesis that atrial fibrillation (AF) causes electrophysiological changes of the atrial myocardium which might explain the progressive nature of the arrhythmia. Methods and Results Twelve goats were chronically instrumented with multiple electrodes sutured to the epicardium of both atria. Two to 3 Weeks after implantation, the animals were connected to a fibrillation pacemaker which artificially maintained AF. Whereas during control episodes of AF were short lasting (6±3 seconds), artificial maintenance of AF resulted in a progressive increase in the duration of AF to become sustained (>24 hours) after 7.1±4.8 days (10 of 11 goats). During the first 24 hours of AF the median fibrillation interval shortened from 145±18 to 108±8 ms and the inducibility of AF by a single premature stimulus increased from 24% to 76%. The atrial effective refractory period (AERP) shortened from 146±19 to 95±20 ms (−35%) (S1S1, 400 ms). At high pacing rates the shortening was less (−12%...

Atrial Fibrillation Begets Atrial Fibrillation A Study in Awake Chronically Instrumented Goats

Diastolic heart failure (DHF) currently accounts for more than 50% of all heart failure patients. DHF is also referred to as heart failure with normal left ventricular (LV) ejection fraction (HFNEF) to indicate that HFNEF could be a precursor of heart failure with reduced LVEF. Because of improved cardiac imaging and because of widespread clinical use of plasma levels of natriuretic peptides, diagnostic criteria for HFNEF needed to be updated. The diagnosis of HFNEF requires the following conditions to be satisfied: (i) signs or symptoms of heart failure; (ii) normal or mildly abnormal systolic LV function; (iii) evidence of diastolic LV dysfunction. Normal or mildly abnormal systolic LV function implies both an LVEF > 50% and an LV end-diastolic volume index (LVEDVI) 16 mmHg or mean pulmonary capillary wedge pressure >12 mmHg) or non-invasively by tissue Doppler (TD) (E/E' > 15). If TD yields an E/E' ratio suggestive of diastolic LV dysfunction (15 > E/E' > 8), additional non-invasive investigations are required for diagnostic evidence of diastolic LV dysfunction. These can consist of blood flow Doppler of mitral valve or pulmonary veins, echo measures of LV mass index or left atrial volume index, electrocardiographic evidence of atrial fibrillation, or plasma levels of natriuretic peptides. If plasma levels of natriuretic peptides are elevated, diagnostic evidence of diastolic LV dysfunction also requires additional non-invasive investigations such as TD, blood flow Doppler of mitral valve or pulmonary veins, echo measures of LV mass index or left atrial volume index, or electrocardiographic evidence of atrial fibrillation. A similar strategy with focus on a high negative predictive value of successive investigations is proposed for the exclusion of HFNEF in patients with breathlessness and no signs of congestion. The updated strategies for the diagnosis and exclusion of HFNEF are useful not only for individual patient management but also for patient recruitment in future clinical trials exploring therapies for HFNEF.

http://www.carsten-tschoepe.de/usr_files/6_Paper%2010.pdf

How to diagnose diastolic heart failure: a consensus statement on the diagnosis of heart failure with normal left ventricular ejection fraction by the Heart Failure and Echocardiography Associations of the European Society of Cardiology

Background and Methods. Although cachexia often accompanies advanced heart failure, little is known about the causes of the cachectic state. To assess the potential role of tumor necrosis factor in the pathogenesis of cardiac cachexia, we measured serum levels of the factor in 33 patients with chronic heart failure, 33 age-matched healthy controls, and 9 patients with chronic renal failure. Results. Mean (±SEM) serum levels of tumor necrosis factor were higher in the patients with heart failure (115±25 U per milliliter) than in the healthy controls (9±3 U per milliliter; P 2 SD above the mean value for the control group), whereas the remaining 14 patients had serum levels of tumor necrosis factor below this level. The patients with high levels of tumor necrosis factor were more cachectic than those with low levels (82±3 vs. 95±6 percent of ideal body weight, respectively; P...

https://www.nejm.org/doi/pdf/10.1056/NEJM199007263230405

Elevated Circulating Levels of Tumor Necrosis Factor in Severe Chronic Heart Failure

STRUCTURE, BIOCHEMISTRY, AND BIOPHYSICS Structure of the Heart and Cardiac Muscle Energetics and Energy Production Energy Utilization (Work and Heat) The Contractile Proteins The Cytoskeleton Active State, Length-Tension Relationship, and Cardiac Mechanics Excitation-Contraction Coupling: Extracellular and Intracellular Calcium Cycles SIGNAL TRANSDUCTION AND REGULATION Signal Transduction: Functional Signaling Signal Transduction: Proliferative Signaling Regulation of Cardiac Muscle Performance: Functional and Proliferative Mechanisms NORMAL PHYSIOLOGY The Heart as a Muscular Pump The Working Heart Cardiac Ion Channels The Cardiac Action Potential CLINICAL PHYSIOLOGY The Electrocardiogram Arrhythmias The Ischemic Heart Heart Failure

Physiology of the heart

Peptide Separation by Two-dimensional Chromatography and Electrophoresis

MORE than 80 years ago, Sir James MacKenzie1 noted: "The more I study the symptoms of heart failure, and the more I reflect on the part played by the heart muscle, the more convinced I am that... heart failure is due to the exhaustion of the reserve force of the heart muscle." Except for the cardiac glycosides, however, therapy for congestive heart failure generally has focused on the systemic signs and symptoms that appear when the failing heart becomes unable to meet the hemodynamic demands of the body, rather than on abnormalities in the heart muscle itself, which both cause . . .

Cardiomyopathy of overload. A major determinant of prognosis in congestive heart failure.

A ROLE for abnormal lipid metabolism in the pathogenesis of atherosclerosis was suggested over a century ago, when Virchow proposed that transport of plasma lipids into the walls of blood vessels contributed to the development of atheromatous lesions. Lipid abnormalities are now firmly established as one factor leading to ischemic heart disease, although the mechanism by which they lead to coronary artery occlusion remains incompletely understood. More recently, abnormalities of lipid metabolism have been implicated in another quite different aspect of the pathogenesis of ischemic heart disease. A large body of evidence now indicates that altered lipid metabolism can alter cardiac function by changing the properties of cardiac cell membranes, and that these functional changes may contribute to the decline in myocardial contractility, the arrhythmias, and the eventual cell death that follow coronary artery occlusion. This article will review some of these disorders in lipid metabolism and possible mechanisms by which they might modify membrane function in the ischemic heart. Disorders of Lipid Metabolism in the Ischemic Heart There are now at least three well-defined mechanisms by which lipid metabolism may be altered in the heart after coronary artery occlusion (Table 1). Each of these mechanisms has been implicated in the pathogenesis of the cardiac abnormalities seen in patients who sustain an acute myocardial infarction.

Arnold M. Katz

Papers

Physiology of the heart

Peptide Separation by Two-dimensional Chromatography and Electrophoresis

Cardiomyopathy of overload. A major determinant of prognosis in congestive heart failure.

BRIEF REVIEWS Lipid-Membrane Interactions and the Pathogenesis of Ischemic Damage in the Myocardium

Phosphorylation of a 22,000-dalton component of the cardiac sarcoplasmic reticulum by adenosine 3':5'-monophosphate-dependent protein kinase.