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Cardiac Left Ventricular Hypertrophy

  • H. E. D. J. Ter Keurs
  • J. J. Schipperheyn

Part of the Developments in Cardiovascular Medicine book series (DICM, volume 33)

Table of contents

  1. Front Matter
    Pages I-XIV
  2. Prevalence and Risks of Left Ventricular Hypertrophy

    1. Front Matter
      Pages 1-1
    2. D. D. Savage, R. D. Abbott, S. Padgett, S. J. Anderson, R. J. Garrison
      Pages 2-15
    3. R. B. Devereux, D. R. Alonso, E. M. Lutas, T. G. Pickering, G. A. Harshfield, J. H. Laragh
      Pages 16-37
  3. Etiology and Functional Aspects at the Cellular Level

    1. Front Matter
      Pages 51-51
    2. H. E. D. J. Keurs, B. J. M. Ter Mulder, V. J. A. Schouten
      Pages 66-88
  4. Etiology and functional aspects of the hypertrophied heart

  5. The Coronary Circulation in the Hypertrophied Heart

    1. Front Matter
      Pages 129-129
    2. J. I. E. Hoffman, M. T. Grattan, F. L. Hanley, L. M. Messina
      Pages 130-151
    3. J. J. Schipperheyn, J. Jonas
      Pages 152-169
    4. J. A. E. Spaan, P. Bruinsma, J. D. Laird
      Pages 170-193
  6. Diagnostic Development in Detection of Left Ventricular Hypertrophy

  7. Therapeutic Aspects of Left Ventricular Hypertrophy

    1. Front Matter
      Pages 223-223
    2. J. I. M. Drayer, M. A. Weber, J. M. Gardin
      Pages 224-237
    3. P. J. Voogd, I. Schicht, P. C. J. Van Breda Vriesman, L. K. Monsjou
      Pages 238-249
    4. A. Van Der Laarse, H. A. Huysmans
      Pages 250-265
  8. Back Matter
    Pages 283-285

About this book

Introduction

Left ventricular hypertrophy (LVH) is usually considered to be a compen­ satory adjustment of heart muscle to an inreased work load. LVH develops in the course of valvular or congenital heart disease, or when part of the myocardium is damaged by long-standing ischemia or infarction. In the hypertrophied heart the muscle fibers increase in size, not in number. The fibers are found to contain a larger number of myofibrils and the cell organelles are larger. From epidemiologic studies it is known that even mild LVH is associated with myocardial ischemia, ventricular arrhythmias, and sudden cardiac death. Most cases of LVH show focal degenerative tissue changes including cellular atrophy, myofibrillar disorganization, interstitial fibrosis, and loss of intracellular connections. Myocardial dysfunction develops and, unlike the functional adaptive changes found in pure hypertrophy, is not reversible by surgical treatment of the valvular heart disease or medical correction of hypertension. Interstitial fibrosis, intracellular changes of musc Ie cells, and loss of contract ile tissue lead to poor mechanical function and undoubtedly increase the risk of ischemia, arrhythmias, or sudden death, a well-recognized problem in patients with a variety of heart diseases. Even When successfully treated, the patients may remain at risk if the compensatory hypertrophy is not fully reversed. Epidemiologic studies conducted in the Framingham population in the early 1950' s demonstrated LVH according to electrocardiographic criteria in 1. 5% of the population; 2% of the population had LVH according to chest X-ray criteria.

Keywords

arrhythmia artery circulation congenital heart disease echocardiography heart heart disease hypertension sudden cardiac death

Editors and affiliations

  • H. E. D. J. Ter Keurs
    • 1
  • J. J. Schipperheyn
    • 1
  1. 1.Department of CardiologyLeiden University HospitalLeidenThe Netherlands

Bibliographic information

  • DOI https://doi.org/10.1007/978-94-009-6759-5
  • Copyright Information Springer Science+Business Media B.V. 1983
  • Publisher Name Springer, Dordrecht
  • eBook Packages Springer Book Archive
  • Print ISBN 978-94-009-6761-8
  • Online ISBN 978-94-009-6759-5
  • Series Print ISSN 0166-9842
  • Buy this book on publisher's site