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Alteration of excitation-contraction coupling in the failing human heart was deemed an interesting subject for a dialogue between basic scientists and clinical researchers in continuation of previous Gargellen Conferences concerned with the function of the normal and failing human myocardium. In 1987 basic mechanisms and clinical implications of then new insights into cardiac energetics was followed by a comprehensive review of inotropic stimulation and myocardial energetics in 1989. Here, we undertook a re-evaluation of the principles of inotropic stimulation and of its potential therapeutic value, based on new observa tions from experiments with human myocardium. In 1992 the risk due to myocardial phenotype change as a consequence of adaptation in heart failure was published. Here, alterations of subcellular structures and functions as a consequence of chronic heart failure, summarized as phenotype change, could be described as an essential characteristic of the failing human myocardium. This topic was discussed in greater depth in the volume "Cellular and Molecular Alterations in the Failing Human Heart", considering both the sarcolemma and the phosphodiesterases, as well as excitation-contraction coupling and contractile proteins, extracellular matrix, and mitrochondrial function.
The myocardium in heart failure: Cellular and subcellular alterations in the failing human myocardium. H. Just Medizinische Universitatsklinik Freiburg i. Br., Innere Medizin III - Kardiologie, FRG The syndrome of heart failure continues to be a major challenge to clinicians and scientists. Incidence and mortality of the disease are high, the patient is disabled, and is permanently threatened by the high morbidity and mortality. The clinician faces a syndrome of complex pathophysiology. Multiple causes or underlying disorders of the heart have to be differentiated from heart failure itself, which often results in exceedingly difficult diagnoses. Likewise, prognostication meets with difficulties due to problems in separating influences of the underlying disease and the heart failure syndrome itself. In chronic refractory failure annual mortality may exceed 50%. If aortic stenosis or ischemic cardiomyopathy with main stem lesions are present, this percentage may be even higher. The situation becomes particularly threatening to the patient when the reduction in cardiac performance goes along with complex ventricular arrhythmias. Therapy has remained difficult and of limited effectiveness. Major progress was achieved with the introduction of diuretic substances. Of similar importance was the introduction of va so dilating drugs into the treatment of heart failure. The principle of vasodilation has greatly improved our understanding of the disease, and has brought about a major improvement of symptoms, increase of exercise capacity, and reduc tion of mortality. This is especially true for the introduction of the angiotensin converting enzyme inhibitors.
G. HASENFUSS, E. MARBAN Heart failure embodies the central irony of modern medicine. As we have become increasingly adept at treating the major proximate causes of death in Western society, we have effectively converted acute illness into chronic malady. The last twenty years have witnessed a revolution in the treatment of acute coronary syndromes, myocardial infarction in particular. Patients who reach the hospital now have every expectation of leaving alive, but not necessarily well. Our ability to blunt the edge of ischemic insults has en gendered new problems: a new cohort of patients whose hearts function well enough to enable short-term survival, but at the cost of decreased ex ercise tolerance, dyspnea and increased long-term mortality. The irony is compounded by our increasingly sophisticated pharmacopeia for the treat ment of heart failure, which, by slowing the progression of ventricular dys function, has created a chronic illness. The fact of its chronicity makes heart failure no less deadly. In symptomatic patients, mortality exceeds 5-10% per year even with the best contemporary therapy. Not all heart failure is ischemic, of course, but the final common phenotype is eerily concordant regardless of the proximate cause. No wonder, then, that heart failure is the leading cause of hospitalization in America and in Western Europe and that the prevalence of the disease continues to rise. Drugs have indeed revolutionized heart failure therapy, ACE inhibitors and beta-adrenergic blockers having the most outstanding records to date.
How is the heartbeat generated? What controls the strength of contraction of heart muscle? What are the links between cardiac structure and function? How does our understanding of skeletal and smooth muscle and non-muscle cells influence our thinking about force development in the heart? Are there important species differences in how contraction is regulated in the heart? How do the new molecular data fit together in understanding the heart beat? What goes wrong in ischemia, hypertrophy, and heart failure? This book paints a modern `portrait' of how the heart works and in this picture the author shows a close-up of the structural, biochemical, and physiological links between excitation and contraction. The author takes the reader through a series of important, interrelated topics with great clarity and continuity and also includes many useful illustrations and tables. The book starts by considering the cellular structures involved in excitation-contraction coupling and then described the characteristics of the myofilaments as the end effector of excitation-contraction coupling. A general scheme of calcium regulation is described and the possible sources and sinks of calcium are discussed in simple, but quantitative terms. The cardiac action potential and its many underlying currents are reviewed. Then the characteristics of some key calcium transport systems (calcium channels, sodium/calcium exchange and SR calcium uptake and release) are discussed in detail. This is then built into a more integrated picture of calcium regulation in succeeding chapters by detailed discussions of excitation-calcium coupling mechanisms (in skeletal, cardiac, and smooth muscle), the interplay between calcium regulatory processes, and finally mechanisms of cardiac inotropy, calcium overload, and dysfunction (e.g., ischemia, hypertrophy, and heart failure). Excitation-Contraction Coupling and Cardiac Contractile Force – Second Edition is an invaluable source of information for anyone who is interested in how the heart beat is controlled and especially suited for students of the cardiovascular system at all levels from medical/graduate students through senior investigators in related fields.
Alteration of excitation-contraction coupling in the failing human heart was deemed an interesting subject for a dialogue between basic scientists and clinical researchers in continuation of previous Gargellen Conferences concerned with the function of the normal and failing human myocardium. In 1987 basic mechanisms and clinical implications of then new insights into cardiac energetics was followed by a comprehensive review of inotropic stimulation and myocardial energetics in 1989. Here, we undertook a re-evaluation of the principles of inotropic stimulation and of its potential therapeutic value, based on new observa tions from experiments with human myocardium. In 1992 the risk due to myocardial phenotype change as a consequence of adaptation in heart failure was published. Here, alterations of subcellular structures and functions as a consequence of chronic heart failure, summarized as phenotype change, could be described as an essential characteristic of the failing human myocardium. This topic was discussed in greater depth in the volume "Cellular and Molecular Alterations in the Failing Human Heart", considering both the sarcolemma and the phosphodiesterases, as well as excitation-contraction coupling and contractile proteins, extracellular matrix, and mitrochondrial function.
Rapid advancements in cardiac electrophysiology require today’s health care scientists and practitioners to stay up to date with new information both at the bench and at the bedside. The fully revised 7th Edition of Cardiac Electrophysiology: From Cell to Bedside, by Drs. Douglas Zipes, Jose Jalife, and William Stevenson, provides the comprehensive, multidisciplinary coverage you need, including the underlying basic science and the latest clinical advances in the field. An attractive full-color design features color photos, tables, flow charts, ECGs, and more. All chapters have been significantly revised and updated by global leaders in the field, including 19 new chapters covering both basic and clinical topics. New topics include advances in basic science as well as recent clinical technology, such as leadless pacemakers; catheter ablation as a new class I recommendation for atrial fibrillation after failed medical therapy; current cardiac drugs and techniques; and a new video library covering topics that range from basic mapping (for the researcher) to clinical use (implantations). Each chapter is packed with the latest information necessary for optimal basic research as well as patient care, and additional figures, tables, and videos are readily available online. New editor William G. Stevenson, highly regarded in the EP community, brings a fresh perspective to this award-winning text.
This title reviews current knowledge of the mechanisms contributing to heart failure. Editor Richard Walsh and an internationally renowned team of contributors discuss key advances in molecular and cell biology, biochemistry, and pharmacology, focusing on advances that have a direct bearing on current clinical studies. It highlights developments across a broad range of disciplines, with in-depth coverage of each topic providing background and perspective on current literature. By setting new advances in a broader context, this text allows readers to compare different ideas and evaluate their importance in their own areas of research or clinical practice.
Subjects in the monograph “Biophysics of the Failing Heart” include state of the art chapters considering major biophysical mechanisms for why hearts responding to acquired or inherited stressors enter into maladaptive processes eventually leading to an inability of the heart to respond efficiently to hemodynamic loads especially during exercise. The chapters describe biophysical techniques that have been applied to determine the triggers for the heart failure process as well as the mechanisms for sustaining the disorders. These techniques include measurements of active and passive mechanical properties and hemodynamics at levels of organization ranging from molecules to hearts beating in situ. Biophysical concepts and approaches are also applied to determination of signaling and signal transduction, energetics, ionic currents, transport processes, electro-chemical and chemo-mechanical coupling. By its emphasis on biophysical aspects of a prevalent clinical condition, the monograph is unique in its perspective and focus. The breadth of information in the chapters all in one place will be of value to clinicians and researchers at all levels. Modern research approaches and clinical understanding of heart failure demands integration of multiple aspects of the disorders. In most cases, combinations of clinician scientists and researchers author the chapters. A main benefit of the book is couched in its didactic approach together with its emphasis on how biophysical concepts and techniques aid in diagnosis and development of new therapies.