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European Heart Journal 1990 11(Supplement E):174-183; doi:10.1093/eurheartj/11.suppl_E.174
Copyright © 1990 by the European Society of Cardiology.
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© 1990 The European Society of Cardiology

Lipoprotein(a) in the arterial wall

U. Beisiegel, A. Niendorf*, K. Wolf*, T. Reblin and M. Rath

Medizinische Kernklinik und Poliklinik
* Institut fur Pathologie, Universitätskrankenhaus Eppendorf Hamburg, F.R.G.

We compared CHD patients with healthy blood donors to confirm the role of Lp(a) as an independent risk factor. More important, we performed biochemical and immunohistochemical studies to evaluate the potential mechanism by which Lp(a) causes CHD. We measured the Lp(a) concentration in comparison with other lipoprotein parameters in fresh human arterial wall biopsies and, in autopsy tissue, we localized apo (a) and apo B, as well as fibrin, with immunohistochemical methodr in different vessel areas. Density gradient ultracentrifugation was used to analyse lipoprotein fractions isolated from human arterial wall.

Lp(a) accumulates in the intima, preferentially rn plaque areas, dependent on the serum Lp(a) level. Most of the Lp(a) can be located extracellularly, but apo(a) can also be detected in foam cells. A strong co-localization has been observed for apo(a) and apo B; only a few areas containing only apo B were detected. Moreover, a striking co-localization for apo(a) and fibrin was found. The possibilities for the pathways by which Lp(a) enters the arterial wall and accumulates extracellularly are discussed on the basis of the present data and recent data published by other groups.


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