Skip to main content
SpringerLink
Log in
Book cover

Cellular and Molecular Alterations in the Failing Human Heart

  • Conference proceedings
  • © 1992

Overview

Editors:
  1. G. Hasenfuss

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

    View editor publications

    You can also search for this editor in PubMed   Google Scholar

  2. Ch. Holubarsch

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

    View editor publications

    You can also search for this editor in PubMed   Google Scholar

  3. H. Just

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

    View editor publications

    You can also search for this editor in PubMed   Google Scholar

  4. N. R. Alpert

    1. Department of Physiology and Biophysics, University of Vermont, Burlington, USA

    View editor publications

    You can also search for this editor in PubMed   Google Scholar

This is a preview of subscription content, log in via an institution to check access.

Access this book

Log in via an institution
eBook USD 84.99
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book USD 109.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Other ways to access

Licence this eBook for your library

Institutional subscriptions

Table of contents (29 papers)

  1. Front Matter

    Pages I-XII
    Download chapter PDF

  2. Sarcolemma and phosphodiesterases

    1. Front Matter

      Pages XIII-XIII
      Download chapter PDF

    2. Receptor systems in the non-failing human heart

      • Otto-Erich Brodde, A. Broede, A. Daul, K. Kunde, M. C. Michel
      Pages 1-14

    3. Changes in the receptor-G protein-adenylyl cyclase system in heart failure from various types of heart muscle disease

      • Michael R. Bristow, A. M. Feldman
      Pages 15-35

    4. Quantification of Giα-proteins in the failing and nonfailing human myocardium

      • M. Böhm, P. Gierschik, E. Erdmann
      Pages 37-50

    5. Regulation and possible functional implications of G-protein mRNA expression in nonfailing and failing ventricular myocardium

      • T. Eschenhagen, U. Mende, M. Nose, W. Schmitz, H. Scholz, J. Schulte am Esch et al.
      Pages 51-64

    6. Phosphodiesterase inhibition and positive inotropy in failing human myocardium

      • W. Schmitz, T. Eschenhagen, U. Mende, F. U. Müller, J. Neumann, H. Scholz
      Pages 65-71

    7. Cardiovascular cyclic nucleotide phosphodiesterases and their role in regulating cardiovascular function

      • Edward D. Pagani, R. A. Buchholz, P. J. Silver
      Pages 73-86

    8. Na,K-ATPase expression in normal and failing human left ventricle

      • Paul D. Allen, T. A. Schmidt, J. D. Marsh, K. Kjeldsen
      Pages 87-94

  3. Excitation-contraction coupling and contractile proteins

    1. Front Matter

      Pages N3-N3
      Download chapter PDF

    2. Structural and functional diversity of human ventricular myosin

      • H. Rupp, R. Jacob
      Pages 95-106

    3. Contractile protein function in failing and nonfailing human myocardium

      • G. Hasenfuss, L. A. Mulieri, B. J. Leavitt, P. D. Allen, C. Holubarsch, H. Just et al.
      Pages 107-116

    4. Troponin T isoform expression in the normal and failing human left ventricle: a correlation with myofibrillar ATPase activity

      • Page A. W. Anderson, N. N. Malouf, A. E. Oakeley, E. D. Pagani, P. D. Allen
      Pages 117-127

    5. Effects of different expression and posttranslational modifications of myosin light chains on contractility of skinned human cardiac fibers

      • I. Morano
      Pages 129-141

    6. Responsiveness of the myofilaments to Ca2+ in human heart failure: implications for Ca2+ and force regulation

      • R. J. Hajjar, W. Grossman, Judith K. Gwathmey
      Pages 143-159

    7. The regulation of the human β myosin heavy-chain gene

      • H.-P. Vosberg, U. Horstmann-Herold, A. Wettstein
      Pages 161-173

    8. Mutations in cardiac myosin heavy-chain genes cause familial hypertrophic cardiomyopathy

      • C. E. Seidman, J. G. Seidman
      Pages 175-185

    9. The membrane proteins of the overloaded and senescent heart

      • B. Chevalier, D. Charlemagne, F. Callens-el Amrani, F. Carre, J. M. Moalic, C. Delcayre et al.
      Pages 187-197

    10. Contraction frequency dependence of twitch and diastolic tension in human dilated cardiomyopathy (Tension-frequency relation in cardiomyopathy)

      • L. A. Mulieri, B. J. Leavitt, G. Hasenfuss, P. D. Allen, N. R. Alpert
      Pages 199-212

    11. Alterations of the force-frequency relationship in the failing human heart depend on the underlying cardiac disease

      • B. Pieske, G. Hasenfuss, Ch. Holubarsch, R. Schwinger, M. Böhm, H. Just
      Pages 213-221
Back to top

Keywords

About this book

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.

Editors and Affiliations

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

    G. Hasenfuss, Ch. Holubarsch, H. Just

  • Department of Physiology and Biophysics, University of Vermont, Burlington, USA

    N. R. Alpert

Bibliographic Information

  • Book Title: Cellular and Molecular Alterations in the Failing Human Heart

  • Editors: G. Hasenfuss, Ch. Holubarsch, H. Just, N. R. Alpert

  • DOI: https://doi.org/10.1007/978-3-642-72474-9

  • Publisher: Steinkopff Heidelberg

  • eBook Packages: Springer Book Archive

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

  • Softcover ISBN: 978-3-642-72476-3Published: 06 December 2011

  • eBook ISBN: 978-3-642-72474-9Published: 06 December 2012

  • Edition Number: 1

  • Number of Pages: XII, 344

  • Topics: Cardiology, Human Physiology

Publish with us

Policies and ethics

Back to top

Search

Navigation