Pathophysiology of Severe Ischemic Myocardial Injury

  • Hans Michael Piper

Part of the Developments in Cardiovascular Medicine book series (DICM, volume 104)

Table of contents

  1. Front Matter
    Pages i-xii
  2. Introduction

  3. The role of energy deficiency

  4. The search for critical cellular structures

  5. The role of lipids

    1. Front Matter
      Pages 147-147
    2. Ger J. Van Der Vusse, Marc Van Bilsen, Trudi Sonderkamp, Robert S. Reneman
      Pages 167-193
    3. K. Schrör, T. Hohlfeld
      Pages 195-217
  6. The role of oxygen radicals

    1. Front Matter
      Pages 219-219
    2. R. Ferrari, S. Curello, A. Cargnoni, E. Condorelli, L. Comini, S. Ghielmi et al.
      Pages 221-238
    3. Wolfgang Schaper, Jutta Schaper
      Pages 269-280
  7. The role of calcium

    1. Front Matter
      Pages 281-281
    2. Herbert K. Hagler, L. Maximilian Buja
      Pages 283-296
  8. Mechanical factors: rigor and contracture

    1. Front Matter
      Pages 315-315
    2. Charles E. Ganote, Richard S. Vander Heide
      Pages 337-355
  9. The role of endothelial cells and neurons

    1. Front Matter
      Pages 357-357
    2. H. M. Piper, S. Buderus, A. KrÜtzfeldt, T. Noll, S. Mertens, R. Spahr
      Pages 359-379
    3. Albert SchÖmig, Ruth Strasser, Gert Richardt
      Pages 381-412
  10. Conclusions

    1. Front Matter
      Pages 413-413
  11. Back Matter
    Pages 423-428

About this book


In industrialized countries, ischemic heart disease is by far the most common organ-specific cause of death. The thrombotic occlusion of a coronary artery which had previously been severely altered by atherosclerosis, is the most frequent cause of ischemic deterioration of myocardial tissue, i. e. myocardial infarction. Death of the human individual occurs when myocardial ischemia causes a critical impairment of cardiac pump function. The failure of a heart with an ischemic area may be due to the amount and location of contractile tissue becoming paralyzed or even necrotic, or to arrhythmias provoked by the ischemic condition, or by a combination of both factors. Considerable progress has been made in the development of antiarrythmic therapy. Effective tools have been developed to reperfuse ischemic myocar­ dial tissue as soon as the patient reaches hospital. However, therapeutical principles for the ischemic-reperfused myocardium which would specifically interfere with the state of injury of the ischemic tissue at the onset of reperfusion, and avoid the apparent hazards of the reperfusion process itself, have yet to be established. But not only approved therapeutical concepts are lacking, the pathophysiology of myocardial cell injury in pro­ gressive ischemia and under reperfusion is in itself only partly understood.


calcium catecholamines cell cells endothelium energy fat free radicals heart hydrolysis hypoxia leukocyte neurons pathophysiology physiology

Editors and affiliations

  • Hans Michael Piper
    • 1
  1. 1.Institute of PhysiologyUniversity of DüsseldorfDüsseldorfGermany

Bibliographic information

  • DOI
  • Copyright Information Springer Science+Business Media B.V. 1990
  • Publisher Name Springer, Dordrecht
  • eBook Packages Springer Book Archive
  • Print ISBN 978-0-7923-0459-3
  • Online ISBN 978-94-009-0475-0
  • Series Print ISSN 0166-9842
  • Buy this book on publisher's site