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Cardiac Adaptation in Heart Failure

Risks due to myocardial phenotype changes

  • Conference proceedings
  • © 1992

Overview

Editors:
  1. J. Holtz

    1. Halle-Wittenberg Medizinische Fakultät Institut fü Pathophysiologie, Martin-Luther-Universität, Halle/Saale, Germany

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  2. H. Drexler

    1. Medizinische Universitätsklinik Innere Medizin III, Kardiologie, Albert-Ludwigs-Universität, Freiburg, Germany

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  3. H. Just

    1. Medizinische Universitätsklinik Innere Medizin III, Kardiologie, Albert-Ludwigs-Universität, Freiburg, Germany

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Table of contents (17 papers)

  1. Front Matter

    Pages I-VIII
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  2. Biological adaptation of the myocardium to a permanent change in loading conditions

    • B. Swynghedauw
    Pages 1-10

  3. Role of protein kinase system in the signal transduction of stretch-mediated myocyte growth

    • Y. Yazaki, I. Komuro
    Pages 11-18

  4. Sympathetic modulation of the cardiac myocyte phenotype: studies with a cell-culture model of myocardial hypertrophy

    • C. S. Long, K. Kariya, L. Karns, P. C. Simpson
    Pages 19-31

  5. Growth factors, growth factor response elements, and the cardiac phenotype

    • M. D. Schneider, W. Robb McLellan, F. M. Black, T. G. Parker
    Pages 33-48

  6. Signaling mechanisms for the activation of an embryonic gene program during the hypertrophy of cardiac ventricular muscle

    • K. R. Chien
    Pages 49-58

  7. Endothelial modulation of myocardial contraction: mechanisms and potential relevance in cardiac disease

    • A. M. Shah, M. J. Lewis
    Pages 59-70

  8. The regulation of calcium cycling in stressed hearts

    • N. R. Alpert, M. Periasamy, M. Arai, H. Matsui, L. A. Mulieri, G. Hasenfuss
    Pages 71-80

  9. Energetics of calcium cycling in nonfailing and failing human myocardium

    • G. Hasenfuss, L. A. Mulieri, C. Holubarsch, B. Pieske, H. Just, N. R. Alpert
    Pages 81-92

  10. Spontaneous sarcoplasmic reticulum Ca2+ release leads to heterogeneity of contractile and electrical properties of the heart

    • E. G. Lakatta, A. Talo, M. C. Capogrossi, H. A. Spurgeon, M. D. Stern
    Pages 93-104

  11. Afterdepolarizations and triggered activity

    • Harry A. Fozzard
    Pages 105-113

  12. The contribution of nonreentrant mechanisms to malignant ventricular arrhythmias

    • S. M. Pogwizd, P. B. Corr
    Pages 115-129

  13. The potential role of Ca2+ for electrical cell-to-cell uncoupling and conduction block in myocardial tissue

    • A. G. Kléber
    Pages 131-143

  14. Failure of myocardial inactivation: a clinical assessment in the hypertrophied heart

    • Walter J. Paulus, M. A. Goethals, S. U. Sys
    Pages 145-161

  15. Diastolic dysfunction in pressure-overload hypertrophy and its modification by angiotensin II: current concepts

    • Beverly H. Lorell
    Pages 163-172

  16. Mechanisms of cardiac growth. The role of the renin-angiotensin system

    • M. S. Fernandez-Alfonso, D. Ganten, M. Paul
    Pages 173-181

  17. Cardiac fibroblasts: function, regulation of gene expression, and phenotypic modulation

    • Mahboubeh Eghbali
    Pages 183-189

  18. Modulation of myocardial sarcoplasmic reticulum Ca++-ATPase in cardiac hypertrophy by angiotensin converting enzyme?

    • J. Holtz, R. Studer, H. Reinecke, H. Just, H. Drexler
    Pages 191-204

  19. Back Matter

    Pages 205-206
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Keywords

About this book

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.

Editors and Affiliations

  • Halle-Wittenberg Medizinische Fakultät Institut fü Pathophysiologie, Martin-Luther-Universität, Halle/Saale, Germany

    J. Holtz

  • Medizinische Universitätsklinik Innere Medizin III, Kardiologie, Albert-Ludwigs-Universität, Freiburg, Germany

    H. Drexler, H. Just

Bibliographic Information

  • Book Title: Cardiac Adaptation in Heart Failure

  • Book Subtitle: Risks due to myocardial phenotype changes

  • Editors: J. Holtz, H. Drexler, H. Just

  • DOI: https://doi.org/10.1007/978-3-642-72477-0

  • Publisher: Steinkopff Heidelberg

  • eBook Packages: Springer Book Archive

  • Copyright Information: Dr. Dietrich Steinkopff Verlag GmbH & Co. KG, Darmstadt 1992

  • Softcover ISBN: 978-3-642-72479-4Published: 21 December 2011

  • eBook ISBN: 978-3-642-72477-0Published: 06 December 2012

  • Edition Number: 1

  • Number of Pages: VIII, 206

  • Number of Illustrations: 26 b/w illustrations

  • Topics: Cardiology, Human Physiology

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