Volume 4A: List of Contributors. Preface (R.A. Haworth and R.A. Altschuld). Part I Contractile Function. Structural and Functional Properties of the Hypertrophied and Failing Heart (R. Jacob, R.W. Gulch, and G. Kissling). The Role of Myocardial Force-Frequency Relation in left Ventricular Function and Progression of Human Heart Failure (L.A. Mulieri and N.R. Alpert). Calcium Homeostasis in Human Heart Failure (U. Schmidt, R.J. Hajjar, M. Carles, and J.K. Gwathmey). Adrenergic Regulation (S.E. Harding and A.R.W. Money-Kyrle). Part II Energy Supply. Energetics of the Normal and Failing Human Heart: Focus on the Creatine Kinase Reaction (J.S. Ingwall). ATP and Cytochrome C Oxidase in the Failing Human Heart (R.C. Starling, R. Liebes, D. Medeiros, and R.A. Altschuld). Phosphorylation Potential and Free Energy of ATP (H. Kammermeier). Altered Oxygen Availability and the Role of Nitric Oxide in the Development of Heart Failure (S.K. Laycock, X. Zhang, N. Seyedi, G. Zhao, R.D. Bernstein, and T.H. Hintze). Volume 4B: List of Contributors. Preface (R.A. Haworth and R.A. Altschuld). Metabolic and Mitochondrial Chages in the Failure Condition of Myocardial Hibernation: Present Understanding, Existing Controversies, and FUture Genetic Approaches (A.J. Liedtke). Part III Energy Demand. Human Heart Failure: Excitation-Contaction Coupling ECC (N.R. Alpert and L.A. Mulieri). Myocardial Oxygen Consumption in Heart Failure (M.R. Wolff). Part IV Etiology of Failure. Cardiovascular Aging in Health (M. Boluyt and E.G. Lakatta). Pathophosiology of the Renin-Angiotensin System in Heart Failure: Molecular Control through Encocrine, Paracrine, and Autocrine Pathways (D.E. Dostal and K.M. Baker). The Molecular Basis of Cardiomyopathies due to Genetic Deficiencies of Mitochondrial Proteins (A.W. Strauss and D.P. Kelly). Part V Therapeutics. Treatment of Heart Failure (C.V. Leier). Index.
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.
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- © Elsevier Science 1998
- 21st September 1998
- Elsevier Science
- eBook ISBN:
Department of Medical Biochemistry, The Ohio State University, Columbus, Ohio, USA
Department of Surgery, University of Wisconsin, Madison, Wisconsin, USA