Misinterpretation of Coronary Cholesterol Atheromata in Cholesterol-Fed Rabbits as Suitable Model for Conventional Human Coronary Plaques

  • F. Thimm
  • M. Frey
  • G. Fleckenstein-Grün
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 361)

Abstract

Occlusion of coronary arteries following arteriosclerotic plaque formation with thrombotic complications is the main etiological factor in the development of myocardial ischemia with subsequent infarction and cell necrosis. Originally, in the 16th century, arteriosclerosis was considered to be an “ossification” of arteries1. Hodgson2 was the first to report in 1815 chemical analyses of arterial plaques, which contained 65% calcium (Ca) salts and 35% organic matter. However, current concepts of the development of arteriosclerosis are overshadowed by the assumption, that the main etiological factor is an enormous accumulation of lipids, particularly cholesterol, in the arterial walls brought about by an increase in serum cholesterol3. Consequently, arterial cholesterol atheromata of cholesterol-fed rabbits are widely considered to be suitable experimental models for conventional human arteriosclerosis4. Moreover, standard anti-arteriosclerotic therapy particularly aims at the so-called “normalization” of serum lipids. Our present data, obtained from microchemical analyses of coronary artery plaques of cholesterol-fed rabbits, and humans respectively, enhance the doubts about an exclusive cholesterol hypothesis of conventional atherogenesis.

Keywords

Cholesterol Migration Graphite Acetone Ischemia 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    E.R. Long, Development of our knowledge of arteriosclerosis,in: “Cowdy’s arteriosclerosis. A survey of the problem,” H.T. Blumenthal, ed., First Edition., Charles C Thomas, Springfield/Ill USA (1933).Google Scholar
  2. 2.
    J. Hodgson. “Treatise on the diseases of arteries and veins,” (1815).Google Scholar
  3. 3.
    M.S. Brown, and J.L. Goldstein, How LDL receptors influence cholesterol and atherosclerosis. Sci Am. 251(5):58 (1984).PubMedCrossRefGoogle Scholar
  4. 4.
    N. Anitschkow, and S. Chalatow, Über experimentelle Cholesterinsteatose and ihre Bedeutung für die Entstehung einiger pathologischer Prozesse. Zentralbi. Allgemeine Pathol u Anat. 14:1 (1913).Google Scholar
  5. 5.
    G. Fleckenstein-Grün, M. Frey, F. Thimm, C. Luley, A. Czirfusz, and A. Fleckenstein, Differentiation between calcium-and cholesterol-dominated types of arteriosclerotic lesions: Antiarteriosclerotic aspects of calcium antagonists. J Cardiovasc Phan-naco1.18(Suppl 6): S1 (1991).Google Scholar
  6. 6.
    A. Fleckenstein, M. Frey, F. Thimm, and G. Fleckenstein-Grün, Excessive mural calcium overload - A predominant causal factor in the development of stenosing coronary plaques in humans. Cardiovasc Drugs and Therapy. 4:1005 (1990).CrossRefGoogle Scholar
  7. 7.
    G. Fleckenstein-Grün, and A. Fleckenstein, Calcium - A neglected key factor in arteriosclerosis. The pathogenetic role of arterial calcium overload and its prevention by calcium antagonists, Ann Med. 23:589 (1991).PubMedCrossRefGoogle Scholar
  8. 8.
    G. Fleckenstein-Grün, F. Thimm, M. Frey, and A. Czirfusz. Role of calcium in arteriosclerosis. Experimental evaluation of antiarteriosclerotic potencies of Ca antagonists, Basic Res Cardiol, accepted, in press (1993).Google Scholar
  9. 9.
    A. Fleckenstein, M. Frey, J. Zorn, and G. Fleckenstein-Grün, Calcium, a neglected key factor in hypertension and arteriosclerosis. Experimental vasoprotection with calcium antagonists or ACE inhibitors, in: “Hypertension: Pathophysiology, Diagnosis, and Mannagement.” J.H. Laragh and B.M. Brenner eds.,Raven Press, New York, 471 (1990).Google Scholar
  10. 10.
    G. Fleckenstein-Grün, M. Frey, F. Thimm, and A. Fleckenstein, Protective effects of various calcium antagonists against experimental arteriosclerosis, J Human Hypertension 6 (Suppl 1): S13Google Scholar
  11. 11.
    G. Fleckenstein-Grün, F. Thimm, A. Czirfusz, S. Matyas, and M. Frey, Experimental vasoprotection by calcium antagonists against Ca-mediated arteriosclerotic alterations. J Cardiovasc Pharmacol, accepted, in press (1993).Google Scholar
  12. 12.
    P.R. Lichtlen, P.G. Hugenholtz, W. Rafflenbeul, H. Hecker, S. Jost, P. Nikutta, J.W. Deckers, Retardation of coronary artery disease in in humans by the calcium channel blocker nifedipine: Results of the INTACT study (International Nifedipine Trial on Antiatherosclerotic Therapy). Cardiouasc Drugs and Therapy. 4: 1047 (1990).CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1994

Authors and Affiliations

  • F. Thimm
    • 1
  • M. Frey
    • 1
  • G. Fleckenstein-Grün
    • 1
  1. 1.Study Group for Calcium Antagonism Physiological InstituteUniversity of FreiburgFreiburgGermany

Personalised recommendations