Excessive mural calcium overload — A predominant causal factor in the development of stenosing coronary plaques in humans


Healthy human coronary artery walls contain, over their entire lifetime, more free and total cholesterol than calcium. However, as soon as arteriosclerotic alterations set in, the calcium content increases. Thus in coronary fatty streaks (arteriosclerotic plaques of WHO stage I), calcium was increased 13 times, in stage II plaques 25 times, and in fully developed stage III plaques 80 times above normal on average. The most dramatic calcium incrustation was found in coronary stage III plaques that had produced massive fatal coronary infarction. Here, the proportion of calcium salts (particularly hydroxyapatite) may amount to almost 50% of dry weight. Thus the most excessive accumulation of calcium seems to be correlated with the highest fatality. In contrast, there is no correlation between mural coronary free or total cholesterol content, and plaque severity. Accordingly, stenosing coronary stage III plaques contain less cholesterol than do fatty streaks. Moreover, in coronary stage III plaques the proportion of free cholesterol was 1.37%, and of total cholesterol only 2.34% of the whole mass, certainly not enough for directly causing coronary occlusion. Thus the calcium-rich plaques of human coronary arteries considerably differ from the well-known cholesterol-rich plaques (stage I and II) of human aortae. Our findings justify a new prophylactic approach with suitable calcium antagonists, to interfere with deleterious calcium uptake in coronary plaque development.

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Correspondence to Professor A. Fleckenstein.

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Fleckenstein, A., Frey, M., Thimm, F. et al. Excessive mural calcium overload — A predominant causal factor in the development of stenosing coronary plaques in humans. Cardiovasc Drug Ther 4, 1005–1013 (1990). https://doi.org/10.1007/BF02018309

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Key Words

  • atherogenesis
  • calcium overload
  • coronary plaque tissue
  • severity of plaques
  • cholesterol accumulation
  • antiarteriosclerotic effects of calcium antagonists