Clinical and Biochemical Aspects of Stress and Cardiomyopathy

  • Michael L. Hess
  • H. Page Mauck
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 45)


Clinically, a primary cardiomyopathy is defined as a left ventricular ejection fraction of less than 40% in the absence of coronary artery disease, valvular abnormalities or intracardiac shunts. This clinical syndrome thus represents a primary disease of cardiac muscle. The etiology of a cardiomyopathy process is often difficult to define. In the western world, the most common etiologies include ethanol, post viral, and a variety of pharmacological (e.g., anthracycline antibiotics) and toxic agents (e.g., radiation, cobalt and hydrocarbons) (1). The histopathology of all of these lesions tends to present as broad, pale staining myofibers with enlarged and peripheral nuclei and various degrees of necrosis and fibrosis (2). The role of environmental stress as a primary etiology is not well understood and is poorly documented.


Sarcoplasmic Reticulum Oxygen Free Radical Squirrel Monkey Shock Stress Anthracycline Antibiotic 
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  1. 1.
    Johnson RA, Palacious I: Dilated cardiomyopathies of the adult. New Eng J Med (307): 1119–1126, 1979.CrossRefGoogle Scholar
  2. 2.
    Fowles RE, Mason JW: Endomyocardial biopsy. Ann Int Med (97): 885–894, 1982.PubMedGoogle Scholar
  3. 3.
    Yates JC, Beamish RE, Dhalla NS: Ventricular dysfunction and necrosis produced by adrenochrome metabolite of epinephrine: relation to pathogenesis of catecholamine cardiomyopathy. Am Heart J (102): 210–221, 1981.PubMedCrossRefGoogle Scholar
  4. 4.
    Yates JC, Dhalla NS: Induction of necrosis and failure in the isolated perfused rat heart with oxidized isoproterenol. J Mol Cell Cardiol (7): 807–816, 1975.PubMedCrossRefGoogle Scholar
  5. 5.
    Corley KC, Shiel O’M F, Mauck HP, Greenhoot J: Electrocardiographic and cardiac morphological changes associated with environmental stress in squirrel monkeys. Psycho Medicine (35): 361–364, 1973.Google Scholar
  6. 6.
    Corley KC, Shell O’M F, Mauck HP, Clark LS, Barber JH: Myocardial degeneration and cardiac arrest in squirrel monkey: Physiological and psychological correlates. Psychophysiology (14): 322–328, 1977.PubMedCrossRefGoogle Scholar
  7. 7.
    Corley KC, Mauck HP, Sheil O’M F, Barbier JH, Clark LS, Blocher CR: Myocardial dysfunction and pathology associated with environmental stress in squirrel monkey: Effect of vagotomy and propranolol. Psychophysiology (16): 554–560, 1979.PubMedCrossRefGoogle Scholar
  8. 8.
    Meerson FZ, Kagan VE, Prilipko LL, Rozhitakaya II, Giber LM, Kozlov YP: Activation of lipid peroxidation during painful emotional stress. Bull Exper Biol Med (88): 1116–1119, 1979.CrossRefGoogle Scholar
  9. 9.
    Meerson FZ, Arhipenko YV, Rozhitakaya II, Kagan VE: Injury to the Ca++ -transporting system of the sarcoplasmic reticulum of the heart due to emotional and pain-induced stress. Bull Exper Biol Med (91): 433–435, 1981.CrossRefGoogle Scholar
  10. 10.
    Hess ML, Hanson NH, Okabe E: Involvement of free radicals in the pathophysiology of ischemic heart disease. Can J Physiol Pharmacol (60): 1382–1389, 1982.PubMedCrossRefGoogle Scholar
  11. 11.
    Singal PK, Beamish RE, Dhalla MS: Potential oxidative pathways of catecholamines in the formation of lipid peroxides and genesis of heart disease. Adv Exp fled Biol (161): 391–402, 1983.Google Scholar
  12. 12.
    Downing SE, Lee JC: Contribution of α-Adrenoceptor activation to the pathogenesis of norepinephrine cardiomyopathy. Circ Res (52): 471–478, 1983.PubMedGoogle Scholar

Copyright information

© Martinus Nijhoff Publishing, Boston 1985

Authors and Affiliations

  • Michael L. Hess
  • H. Page Mauck

There are no affiliations available

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