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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.
Cellular and Molecular Pathobiology of Cardiovascular Disease focuses on the pathophysiology of common cardiovascular disease in the context of its underlying mechanisms and molecular biology. This book has been developed from the editors' experiences teaching an advanced cardiovascular pathology course for PhD trainees in the biomedical sciences, and trainees in cardiology, pathology, public health, and veterinary medicine. No other single text-reference combines clinical cardiology and cardiovascular pathology with enough molecular content for graduate students in both biomedical research and clinical departments. The text is complemented and supported by a rich variety of photomicrographs, diagrams of molecular relationships, and tables. It is uniquely useful to a wide audience of graduate students and post-doctoral fellows in areas from pathology to physiology, genetics, pharmacology, and more, as well as medical residents in pathology, laboratory medicine, internal medicine, cardiovascular surgery, and cardiology. - Explains how to identify cardiovascular pathologies and compare with normal physiology to aid research - Gives concise explanations of key issues and background reading suggestions - Covers molecular bases of diseases for better understanding of molecular events that precede or accompany the development of pathology
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.
Traditionally, cardiac hypertrophy is regarded as an adaptation of the heart to permanent mechanical overload. Regardless of the fact that many different and often unknown primary causes can result in heart failure, mechanical overload and myocardial hypertrophy is found in almost all forms of manifest chronic heart failure (apart from failure due to extramyocardial hindrances to inflow or to relaxation). However, the reactive enlargement of myocardial mass in response to an enhanced hemodynamic burden appears to be a double-edged sword. Obviously, the hypertrophy helps to reduce the enhanced ventricular wall stress in heart failure by adding contractile units to the overdistended chamber wall. However, in recent years it became clear that this adaptive hypertrophic process is rather complex and may include problematic facets. The adaptive hypertrophy includes proliferation of the nonmyocyte cardiac cells as well as substantial alterations in the phenotype of the growing myocytes due to differential changes in gene expression.
Heart failure continues to be a major public health problem in the United States with close to half a million new cases diagnosed each year. Moreover, deaths from heart failure are on the increase, in part because of advances in the treatment of other fatal diseases, and in part from the prevalence of lifestyles indifferent to the risk factors for heart disease. This is not to say that no progress has been made in the treatment of heart failure. While for many years treatment was confined to the management of the symptoms, in recent years with the advent of ACE inhibitor and ß blacker therapies, real improvements in cardiac function and life expectancy have been achieved (Volume 4B, Leier). On a more basic level, enormous advances have been made in describing many of the changes in structure and function of the heart and the parallel neurohumoral and circulatory adaptations that occur during the onset of failure. These advances have been made not only by using various animal models of heart failure, but also using fresh failing human heart tissue, which has become readily available for experimental investigation since the advent of cardiac transplantation.Understanding the significance of many of these changes that occur during the transition to failure and the role they play in the etiology of failure is, however, a much more difficult task. These are exciting times in heart failure research. It is as though many of the pieces of the jigsaw puzzle are available but the puzzle has yet to be assembled. The objective of these volumes is to bring together some advances that have been made in recent years in defining one aspect of the failing heart, that is, the role of altered metabolism, in order to facilitate assembly of the puzzle.
The latest developments in molecular biology have broadened our understanding of the pathogenesis of idiopathic dilated cardiomyopathy (IDC). In this book, written by well-known experts, a comprehensive overviewof IDC is given, including basic cellular and molecular concepts, virology, immunology, cardiac receptors and ionic channels, contractility abnormalities, microcirculation, and oxygen supply in cardiac hypertrophy. Details on basic research are supplemented by results of new clinical trials in IDC and the latest data on the epidemiology of the disease. For those who are interested in the disease, the book summarizes progress in all major fields.
Heart Hypertrophy and Failure brings together leading basic scientists and clinicians, presenting improved knowledge of the pathophysiology and treatment of the condition. The result is a synthesis of state-of-the-art information on molecular biology, cellular physiology and structure-function relationships in the cardiovascular system in health and disease. The papers presented describe fundamental mechanisms underlying changes in the cellular machinery during the development of cardiac hypertrophy and heart failure. Audience: Students, scientists, clinical and experimental cardiologists who seek to understand and manage the perplexing problems of hypertrophy and heart failure.
The tenth Henry Goldberg Workshop is an excellent occasion to recall our goals and celebrate some of our humble achievements. Vision and love of our fellow man are combined here to: 1) Foster interdisciplinary interaction between leading world scientists and clinical cardiologists so as to identify missing knowledge and catalyze new research ideas; 2) relate basic microscale, molecular and subcellular phenomena to the global clinically manifested cardiac performance; 3) apply conceptual modelling and quantitative analysis to better explore, describe, and understand cardiac physiology; 4) interpret available clinical data and design new revealing experiments; and 5) enhance international cooperation in the endless search for the secrets of life and their implication on cardiac pathophysiology. The first Goldberg Workshop, held in Haifa, in 1984, explored the interaction of mechanics, electrical activation, perfusion and metabolism, emphasizing imaging in the clinical environment. The second Workshop, in 1985, discussed the same parameters with a slant towards the control aspects. The third Goldberg Workshop, held in the USA at Rutgers University, in 1986, highlighted the transformation of the microscale activation phenomena to macro scale activity and performance, relating electrophysiology, energy metabolism and cardiac mechanics. The fourth Goldberg Workshop continued the effort to elucidate the various parameters affecting cardiac performance, with emphasis on the ischemic heart. The fifth Workshop concentrated on the effect of the inhomogeneity of the cardiac muscle on its performance. The sixth Workshop highlighted new imaging techniques which allow insight into the local and global cardiac performance.
Molecular Cardiology for the Cardiologist, Second Edition provides a short, easily readable summary of what the new biology brings to cardiology. Special efforts have been made to include comprehensive diagrams and drawings, as well as teaching tables, and also to keep the size of the second edition within the modest limits of the first edition. The book remains divided into 5 parts. The first part is a general introduction to the new terminology. The second part is devoted to the normal structure of the heart and vessels. Parts 3 and 4 deal with physiopathology. One of the important contributions of molecular biology to cardiology is a better understanding of the general process of adaptation of the heart and vessels to a permanent mechanical overloading. Such a process is generally called remodeling, and results from coordinate changes in the expression of the genes. The last part of the book includes information on gene and cellular therapy.
First multi-year cumulation covers six years: 1965-70.