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Cardiac Adaptation in Heart Failure

Risks due to myocardial phenotype changes

  • J. Holtz
  • H. Drexler
  • H. Just

Table of contents

  1. Front Matter
    Pages I-VIII
  2. M. D. Schneider, W. Robb McLellan, F. M. Black, T. G. Parker
    Pages 33-48
  3. N. R. Alpert, M. Periasamy, M. Arai, H. Matsui, L. A. Mulieri, G. Hasenfuss
    Pages 71-80
  4. G. Hasenfuss, L. A. Mulieri, C. Holubarsch, B. Pieske, H. Just, N. R. Alpert
    Pages 81-92
  5. E. G. Lakatta, A. Talo, M. C. Capogrossi, H. A. Spurgeon, M. D. Stern
    Pages 93-104
  6. Harry A. Fozzard
    Pages 105-113
  7. Walter J. Paulus, M. A. Goethals, S. U. Sys
    Pages 145-161
  8. M. S. Fernandez-Alfonso, D. Ganten, M. Paul
    Pages 173-181
  9. Back Matter
    Pages 205-206

About these proceedings

Introduction

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.

Keywords

adaptation arrhythmia cells endothelium heart heart failure tissue

Editors and affiliations

  • J. Holtz
    • 1
  • H. Drexler
    • 2
  • H. Just
    • 2
  1. 1.Halle-Wittenberg Medizinische Fakultät Institut fü PathophysiologieMartin-Luther-UniversitätHalle/SaaleGermany
  2. 2.Medizinische Universitätsklinik Innere Medizin III, KardiologieAlbert-Ludwigs-UniversitätFreiburgGermany

Bibliographic information