Pathobiology of the Human Atherosclerotic Plaque

  • Seymour Glagov
  • William P. NewmanIII
  • Sheldon A. Schaffer

Table of contents

  1. Front Matter
    Pages i-xxxi
  2. Introduction

    1. Front Matter
      Pages xxxi-xxxi
  3. Cellular Contents

    1. Front Matter
      Pages 1-1
    2. Vladimir N. Smirnov, Alexander S. Antonov, Matvey E. Lukashev, Yuri A. Romanov, J. Frederic Cornhill, Ross G. Gerrity
      Pages 47-62
    3. G. R. Campbell, J. H. Campbell, A. H. Ang, I. L. Campbell, S. Horrigan, J. A. Manderson et al.
      Pages 69-92
    4. Colin J. Schwartz, Eugene A. Sprague, Anthony J. Valente, Jim L. Kelley, Ellen H. Edwards, C. Alan Suenram
      Pages 107-120
    5. Malcolm J. Mitchinson, Keri L. H. Carpenter, Richard Y. Ball
      Pages 121-128
  4. Tissue Organization and Architecture

    1. Front Matter
      Pages 3-3
    2. G. S. Berenson, B. Radhakrishnamurthy, S. R. Sinivasan, P. Vijayagopal, E. R. Dalferes Jr.
      Pages 189-208
    3. H. C. Anderson, D. H. McGregor, A. Tanimura
      Pages 235-249
    4. Rosemarie Romeo, Joan M. Augustyn, Gretchen Mandel, Assaad S. Daoud
      Pages 251-262

About these proceedings


Seymour Glagov The last meeting, devoted exclusively to an examination of the atherosclerotic plaque, took place in Chicago 25 years ago under the joint auspices of the Council on Arteriosclerosis of the American Heart Association and the Chicago Heart Association. The proceedings were published subsequently in a volume entitled "Evolution of the Atherosclerotic Plaque", edited by Richard J. Jones (1). Both experimental and human lesions were considered and several provocative new approaches to the disorder were discussed. The electron microscope was being applied systematically to the study of blood vessels at that time, so that details of the infrastructure and cellular composition of the artery wall and of atherosclerotic lesions were presented in some detail. There was, as one result of these explorations, considerable discussion of morphologic evidence suggesting that the principal cell involved in the atherogenic process was neither the fibroblast nor the macrophage, as had been supposed, but the smooth muscle cell. In particular, the findings indicated that this cell could incorporate lipid and become a foam cell.


Artherienverkalkung Bypass Lipoprotein Pathologie artery atherosclerosis cell heart pathobiology pathogenesis pathology perception platelet tissue ultrasound

Editors and affiliations

  • Seymour Glagov
    • 1
  • William P. NewmanIII
    • 2
  • Sheldon A. Schaffer
    • 3
  1. 1.The University of Chicago HospitalChicagoUSA
  2. 2.Department of PathologyLouisiana State UniversityNew OrleansUSA
  3. 3.Colestech CorporationHaywardUSA

Bibliographic information

  • DOI
  • Copyright Information Springer-Verlag New York 1990
  • Publisher Name Springer, New York, NY
  • eBook Packages Springer Book Archive
  • Print ISBN 978-1-4612-7968-6
  • Online ISBN 978-1-4612-3326-8
  • About this book