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The Hypertrophied Heart

  • Nobuakira Takeda
  • Makoto Nagano
  • Naranjan S. Dhalla

Part of the Progress in Experimental Cardiology book series (PREC, volume 3)

Table of contents

  1. Front Matter
    Pages i-xiv
  2. Mechanisms of Cardiac Hypertrophy

    1. Front Matter
      Pages 1-1
    2. Toru Arino, Ross D. Hannan, Kiyofumi Suzuki, Lawrence I. Rothblum
      Pages 31-40
    3. Taro Murakami, Yoshiharu Shimomura, Li Zhihao, Kazuyuki Shimizu, Satoru Sugiyama
      Pages 41-49
    4. Karin Eizema, Han A. A. Van Heugten, Karel Bezstarosti, Marga C. Van Setten, Sonja Schneider-Rasp, Wolfgang C. Poller et al.
      Pages 51-66
    5. Kiyoharu Sakurai, Hiromi Sugawara, Tomoo Watanabe, Shigekazu Nakada, Hiroyuki Atsumi, Hitonobu Tomoike et al.
      Pages 67-81
    6. Tetsuya Ishikawa, Hidetoshi Kajiwara, Seibu Mochizuki, Satoshi Kurihara
      Pages 83-90
    7. Kyoko Imanaka-Yoshida, Kazuto Yokoyama, Teruyo Sakakura
      Pages 123-129
    8. Shalini Kanekar, Wayne Carver, Thomas K. Borg, Joel Atance, Louis Terracio
      Pages 131-141
    9. Martin Laser, Toshio Nagai, Vijaykumar S. Kasi, Catalin F. Baicu, Christopher D. Willey, Charlene M. Kerr et al.
      Pages 143-164
    10. Madhu B. Anand-Srivastava, Francesco Di Fusco
      Pages 165-178
    11. Atsushi Takeda, Yuusaku Hayashi, Chihiro Shikata, Yasuyuki Tanaka, Nobuakira Takeda
      Pages 179-186
    12. Makoto Okabe, Keishiro Kawamura, Fumio Terasaki, Tetsuya Hayashi, Yumiko Kanzaki, Haruhiro Toko
      Pages 187-196
    13. Bohuslav Ostadal, Vaclav Pelouch, Arnost Bass, Pavel Pucelik, Olga Novakova
      Pages 217-226
    14. Hari S. Sharma, Erik T. H. F. Peters, Ad J. J. C. Bogers
      Pages 227-241
  3. Cardiac Failure in the Hypertrophied Heart

    1. Front Matter
      Pages 251-251
    2. Yasuchika Takeishi, Thunder Jalili, Richard A. Walsh
      Pages 253-263
    3. Jianming Hao, Tracy Scammell-La Fleur, Ian M. C. Dixon
      Pages 303-320
    4. Keiko Yamauchi-Takihara, Keita Kunisada, Yasushi Fujio, Hidemasa Oh, Eiroh Tone, Tadamitsu Kishimoto
      Pages 321-331
    5. Shingo Kurokawa, Naoki Tokita, Masahiko Moriguchi, Naoto Fukuda, Youji Machida, Tohru Izumi
      Pages 355-362
    6. Yoshiki Sawa, Satoshi Taketani, Naomasa Kawaguchi, Koji Kagisaki, Shunzo Onishi, Hikaru Matsuda
      Pages 363-374
    7. Takuji Hayakawa, Hiroaki Minami, Saiji Masukawa, Tadato Nagane, Katsuro Takeuchi, Osamu Yahara et al.
      Pages 375-382
    8. Keld Kjeldsen
      Pages 393-398
    9. Uichi Ikeda, Yoshikazu Maeda, Ken-Ichi Oya, Masahisa Shimpo, Shuichi Ueno, Masashi Urabe et al.
      Pages 399-407
    10. Kazuhiro Yamamoto, Tohru Masuyama, Yasushi Sakata, Masatsugu Hori
      Pages 441-452
    11. Kenichi Masui, Takeshi Oguchi, Satoshi Kashimoto, Toshiaki Yamaguchi, Teruo Kumazawa
      Pages 453-461
  4. Back Matter
    Pages 463-469

About this book

Introduction

Whenever the heart is challenged with an increased work load for a prolonged period, it responds by increasing its muscle mass--a phenomenon known as cardiac hypertrophy. Although cardiac hypertrophy is commonly seen under physiological conditions such as development and exercise, a wide variety of pathological situa­ tions such as hypertension (pressure overload), valvular defects (volume overload), myocardial infarction (muscle loss), and cardiomyopathy (muscle disease) are also known to result in cardiac hypertrophy. Various hormones such as catecholamines, thyroid hormones, angiotensin II, endothelin, and growth factors have also been shown to induce cardiac hypertrophy. Although the exact mechanisms underlying or pathological forrns of cardiac hypertrophy are poorly under­ the physiological stood, an increase in the intraventricular pressure is believed to represent the major stimulus for the development of cardiac hypertrophy. In this regard, stretching of the cardiac muscle has been shown to induce the hypertrophic response, but the role of metabolic influences in this process cannot be ruled out. Furthermore, different hormones and other interventions in the absence of stretch have been observed to stimulate protein synthesis in both isolated cardiomyocyte and vascular myocyte preparations. Nonetheless, it is becoming dear that receptor as well as phospholipid­ linked signal transduction pathways are activated in some specific manner depend­ ing upon the initial hypertrophic stimulus, and these then result in an increase in the size and mass of cardiomyocytes.

Keywords

Angiotensin II angiogenesis cardiovascular heart hypertension vascular disease

Editors and affiliations

  • Nobuakira Takeda
    • 1
  • Makoto Nagano
    • 2
  • Naranjan S. Dhalla
    • 3
  1. 1.Department of Internal Medicine, Aoto HospitalJikei University School of MedicineTokyoJapan
  2. 2.Jikei University School of MedicineTokyoJapan
  3. 3.Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Faculty of MedicineUniversity of ManitobaWinnipegCanada

Bibliographic information

  • DOI https://doi.org/10.1007/978-1-4615-4423-4
  • Copyright Information Kluwer Academic Publishers 2000
  • Publisher Name Springer, Boston, MA
  • eBook Packages Springer Book Archive
  • Print ISBN 978-1-4613-6991-2
  • Online ISBN 978-1-4615-4423-4
  • Series Print ISSN 1389-1774
  • Buy this book on publisher's site
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